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Evaluation of the comparative efficacy of Ojokalpa Rasayana and Amruta Kayakalpa Rasayana in Bhutabhishangaja Ojokshaya (HIV infection), C.S.HANAMANTAGOUDARDepartment of Kayachikitsa, Post graduate …

Evaluation of the comparative efficacy of Ojokalpa Rasayana and Amruta Kayakalpa Rasayana in Bhutabhishangaja Ojokshaya (HIV infection), C.S.HANAMANTAGOUDARDepartment of Kayachikitsa, Post graduate studies and research center D.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE, Gadag - 582 103

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  • 1. “Evaluation of the comparative efficacy of Ojokalpa Rasayana and Amruta Kayakalpa Rasayana in Bhutabhishangaja Ojokshaya (HIV infection)” By C.S.HANAMANTAGOUDAR As partial fulfillment of post graduation degree Ayurveda Vachaspati M.D. (Kayachikitsa) Under Rajeev Gandhi University of Health Sciences, Bangalore, Karnataka Guide Dr. K. Shiva Rama Prasad M.D. (Ayu) (Osm) M.A.(Astrology), {Ph.D (Astro-medicine)} Reader in Kayachikitsa Postgraduate Studies and Research Center, Department of KayachikitsaD.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE Gadag - 582 103 Post graduate studies and research center Department of Kayachikitsa 2004
  • 2. This is to certify that the contents of this thesis entitled “Evaluation of thecomparative efficacy of Ojokalpa Rasayana and Amruta Kayakalpa Rasayana inBhutabhishangaja Ojokshaya (HIV infection)” is has been worked out byC.S.HANAMANTAGOUDAR, under my supervision with close guidance. Even though this disease, Bhutabhishangaja Ojokshaya has been mentioned inAyurvedic texts, the aetiology, pathogenesis etc., needs further evaluation and research. Itis as developed and explained by C.S.HANAMANTAGOUDAR is unique and scientific andwill definitely help in elucidation of this disease in Ayurvedic and Modern scientific parlanceand further planning with the management. This work is applied, scientific and an original contribution in the field of research inAyurveda. I am fully satisfied with the work and recommend the dissertation to be put before theM.D. (Ayurveda Vachaspathi) Kayachikitsa panel of Rajiv Gandhi University of HealthSciences, Bangalore for adjudication. Guide Dr. K. Shiva Rama Prasad M.D. (Ayu) (Osm) M.A.(Astrology), {Ph.D (Astro-medicine)} Reader in Kayachikitsa Postgraduate Studies and Research Center, Department of Kayachikitsa
  • 3. J.S.V.V. SAMSTHE’S D.G.M.AYURVEDIC MEDICAL COLLEGE POST GRADUATE STUDIES AND RESEARCH CENTER DEPARTMENT OF KAYACHIKITSA GADAG, 582 103 Certificate This is to certify that C.S.HANAMANTAGOUDAR has worked for his thesis on thetopic entitled “Evaluation of the comparative efficacy of Ojokalpa Rasayana andAmruta Kayakalpa Rasayana in Bhutabhishangaja Ojokshaya (HIV infection)”. We here with forward this thesis for the evaluation and adjudication. Dr. V.Varadacharyulu Dr. G. B. Patil M.D.(K.C)(Osm), Principal Professor & H.O.D D.G.M. Ayurvedic Medical College, DEPT. KAYACHIKITSA Gadag DGMAMC, PGS&RC, Gadag
  • 4. ACKNOWLEDGEMENT I take this glorious opportunity to acknowledge with the deep sense of gratitudeto my guide, Dr. K. Siva Rama Prasad, Reader, Department of Postgraduate Studiesand Research (Kayachikitsa), D.G.M.A.M.C., Gadag, for his valuable guidance andclose supervision during entire phase of the study. With profound sense of gratitude I express my sincere thanks to Dr. G. B. Patil,Principal, D. G. M. A. M. C, Gadag. For encouragement and facilities provided duringmy postgraduate studies. I am very much thankful to Father, Mother,Sister,Brother in law, Pavitra,Amritagouda and cousins for their affection and lots of co-operation. I wish to add my warmest thanks to my PG teaching faculty Dr. M. C. Patil, Dr.Shashidhara Doddamani, Dr. Kuber Sankh, Dr. R. V. Shetter, Dr.GirishDanappagoudar for their valuable suggestions and timely help which made me tocomplete this dissertation work successfully. I am very much thankful to Dr. B. G. Swami, Dr. K. S. Paraddi, Dr.C. S.Kudarikannur, Dr.V. M. Sajjan, Dr. V. M. Malagoudar, Dr. S. B. Govindappanavar, Dr.P.C. Chappanamath, for their encouragement and moral support during the study. I extend my gratefulness and sincere heartfelt gratitude to my colleagues,Dr. Shakuntala C. Garwad, Dr. Shankaragouda, Dr. U. V. Purad, Dr. Shyju O. Dr.mulki patil Dr. G.S. Hadimani Dr. Yasmeen Panibhandha Dr. Anilkumar Bacha, Dr.Sitaram prasad, and Dr. Vinay. Kulakarni , my friends Dr. Kallesha Murushillin and Dr.Vishwanatha Kokare, for their timely support during the course. I am very much thankful to all teaching and non teaching staff of college andspecial thanks for librarian Shri. V. M. Mundinamani and Mr. Surreban for their timelyhelp and co-operation during the study.
  • 5. Index Evaluation of the comparative efficacy of Ojokalpa Rasayana in Bhutabhishangaja Ojokshaya (HIV infection) Chapter-1 1 to 4Introduction Chapter-2 5 to 54Conceptual study – includes Shareera, Nidana, and Chikitsa indetail with respect to the disease in comparison tocontemporary medicine. Chapter-3 55 to 73Drug review – Ojokalpa Rasayana composition is discussedwith its pharmacological and pharmaco-dynamics. Chapter-4 74 to 81Material and methods Chapter-5 82 to 113Observation and results Chapter-6 114 to 130Discussion and conclusion Summary 131 to 136 Annexes References Bibliography case sheet
  • 6. List of tables Table explanation Page Number1 Combination and proportions of Ojokalpa Rasayana 552 Guna Karmas of each drug of Ojo kalp rasayan 573 Age group incidences 824 Sex ratio incidences 835 Diet incidences 846 Religion incidences 857 Economic incidence 868 Occupational incidence 879 Marital status incidence 8810 Source of infection 8911 Chief complaints 9012 Associated complaints 9113 Changes Hemoglobin percentage (HB%) 9314 Erythrocyte Sedimentation Rate (ESR) 9415 Changes in Total Lymphocyte count 9516 Changes in white Blood corpuscles 9617 Changes in Weight 9718 Changes in Platelet count 9819 Changes in Kornefsky performance score 9920 Changes in general health condition 10021 Changes in CD4 count 10122 Changes in CD8 count 10223 Observations on Chronicity 10324 Observations on Ojo vyapat lakshana 10325 Observations on Ojo Vishramsha lakshana 10526 Observations on Ojokshaya lakshana 10527 Assessments criteria - Evaluation of the comparative efficacy 106 of Ojokalpa Rasayana in Bhutabhishangaja Ojokshaya28 Assessment Parameter study of group 1 10929 Assessment Parameter study Group 2 11030 Assessment Parameter Comparative study of Group 1 and 2 11131 Result in-group 1 11332 Result in-group 2 114
  • 7. List of graphs Graph item Page number1 Age group incidences 822 Sex ratio incidences 833 Diet incidences 844 Religion incidences 855 Economic incidence 866 Occupational incidence 877 Marital status incidence 888 Result in-group 1 1139 Result in-group 2 114 List of Figures1 Life cycle of HIV 322 Structure of HIV 333 Ingredients of Ojokalparasayana 55
  • 8. AcknowledgementI am deeply indebted to several people who have helped me during the study.I acknowledge my sincere gratitude to my guide Dr. K. Shiva Rama Prasad, Reader/Asst. Professor, Post-Graduate studies and Research Center in Kayachikitsa,D.G.M.A.M.C, Gadag, for his expert comments, critical analysis and affectionateencouragement, throughout the study.I am grateful to Dr. V. Varadacharyulu, H.O.D., Post-Graduate studies and ResearchCenter in Kayachikitsa, D.G.M.A.M.C, Gadag for inspiring me to take up thisdissertation subject and supporting me with timely guidance and encouragementWords are poor substitutes for my immense feelings of gratitude for Dr. G. B. Patil,Principal, DGMAMC, Gadag. I thank him for his ever inspiring encouragement,facilities provided and for his personal interest in overall supervision of this study.
  • 9. I extend my immense gratitude to Dr. M.C. Patil, Dr. Raghavedra Shettar and Dr.Kuber Sankh, Dr. Shashidhar H. Doddamani, faculties of Post-Graduate studies andResearch Center in Kayachikitsa, D.G.M.A.M.C, Gadag.I scenically remember the co-operation and support extended by Dr. B.G. Swami, Dr.Chappanmath.P.C., Dr. V.M. Malagoudar, Dr.A.K.Panda, Dr.S.B.Govindappanavar,Dr. V.M. Sajjan, Dr. Gireesh Danappagoudar and Dr. C.S. Kudarikhannur, Dr K SParaddi, and all the staff of DGMAMC. I thank all my P.G. colleges for their constantsupport and co-operation.I am very much great full to my beloved father, mother, brother, sister, brother in lawAmrutagouda and Pavitra for their lots of affection and co-operation.I sincerely thank Mr. P.M. Nandakumar, statistician, for the statistical analysis of theresults and librarian V.M. Mundinamani and assistant librarian Sureban for theirtimely assistance.I honestly remember the co-operation and support of Dr.G.S.Hadimani, Dr.Shankaragouda, Dr. Srinivasa Reddy, Dr. A.P.Yasmin Dr. U. V. Purad, Dr.O.Shyju,and all the scholars of DGMAMC – PG branches. I thank all my P.G. colleagues andmy friends Dr Kallesha Moorashillin, Dr Vishwanatha Kokare for their constant helpand co-operation.I am very thankful to Sunil. L. Mundra, M.D., Natural Capsules Pvt. Ltd., Bangalorewho supplied Natural Vegetable and Gelatin capsules for the study. I am thankful toM/s R.Y.Shettar, Doddappa Billal and Dhanwantari Pharmacy who supplied mecomponents of my trail medicine. I am thankful to Hubli diagnostics, Hubli for theirconstant cooperation through out the study.With deep sense of gratitude I thank all the subjects who participated in this study. (C.S.Hanamantagoudar)
  • 10. As we walk in so many centuries away from descent of Ayurveda many infectiousdiseases are emerging once again to remind us about their existence as urbanizationdeveloped. Among them since two decades sudden emerge of new epidemics such asSARS and AIDS/HIV, termed in Ayurveda as Bhootopaghataja Ojokshaya. This is veryvolatile disease-entity. The etymology of words, Bhoota and Upaghata developed form theword Bhootopaghata is, Bhoota denotes as Krimi or Virus and Upaghata means as infection.So exclusively the word Bhootopaghata indicates as viral infection. Every body believes that, the Ayurveda is the mother of all medical sciences. Allmedical knowledge’s of present world has authentic information about microbes anddiseases caused by them. Acharyas of Ayurveda have explained common means of gettinginfections long ago, such as sexual intercourse, physical contact, droplet infection, food andwater, sharing the-bed, cloth, ornaments. Ancient history revels and refers massiveinfectious conditions such as AIDS through excavations. Now a day it seems to bereminding as a simple dream is that “Health for all “. If we are not accumulating all of ourhuman resources, energies, intelligence not to allow any further spread of these infectiousdiseases such as HIV or SARS it will be havoc to the mankind. If not, according to theestimation one should wonder if the slogan “Health for all” turns out as “AIDS for all”. Thenumber of people infected by HIV would have crossed 50 million and till now there were 12million deaths due to ARC (aids related complications) in entire world. In India since thedetection of HIV infection since 1986, the epidemic has been frankly out of control. As ofnow an estimated 4-6 million HIV infected cases are present in India. Within this shortperiod it has emerged as one of the most serious public health problem in the country. Introduction to Bhutabhishangaja Ojokshaya 1
  • 11. AIDS is a multi dimensional disease syndrome, affecting physical, mental, social andspiritual facets of the affected person. The virus HIV hampers the Immune system. Whereas in Ayurveda the immunity is termed as Ojas. So the vitiated Immune system is called asOjovikruti. Bhootopaghata is one of the causative factors for Ojovikruti. The unique featureof human immune-deficiency virus is that it attacks the basic defense mechanism of humanbeings and gradually destroys the system completely. Then body becomes playground forall types of microbes like viruses, bacteria, fungi, protozoa, to inter play. In absence of anycheck force the microorganisms that enter the body through various entry points. And freelymultiply to cause numerous infections, which may leads to life threatening. The Ojokshayais one among the Ojovikruti. Symptoms are also identical to the advanced AIDS sign andsymptoms for example Moorcha, Moha, Pralapa, Mrutyu, Mamsakshaya, etc. There forAcquired Immune Deficiency Syndrome can be termed as Bhootopaghata Ojokshaya. At the same time there is no specific treatment available for the AIDS /HIV infection.AZT the costly medicine is still in practice, which is use full for the preventing the ARC, andfurther duplication of HIV virus.Recent advances in medical treatment Recent advances in medical treatment have given scientists renewed strength in thestruggle against HIV-the virus that causes AIDS. Many of today’s scientists are using AZTand DDI as a source of treatment. AZT inhibits reverse transcription, which is vital for HIV toinfect its host. Since HIV is a retrovirus it must convert its RNA to DNA. AZT and DDI willstop this from occurring and thus stop the HIV virus from spreading. There are also manyscientists trying to use CD4 as a potential type of vaccine. CD4 is a membrane protein thatmany cells in our body use. Those cells include the immune system cells, blood cells, andthe nervous system cells. It has been found that HIV only infects cells with CD4. It is for thisthat HIV infects its host in only areas whose cells contain CD4 1. Introduction to Bhutabhishangaja Ojokshaya 2
  • 12. Vaccine in trial The vaccine in “Evaluation of an HIV-1 DNA Vaccine Encoding a Modified Gag-Polin Uninfected Adult Volunteers (Contact: Grace Kelly, RN)” trial, VRC 4302, is classified as agenetic vaccine. Genetic vaccines contain the genes (hereditary material) which direct theproduction of the proteins of the HIV virus. VRC 4302 contains the gene for the Gag and Polproteins of HIV. It is important to know that you cannot catch HIV or AIDS from this vaccine.Volunteers will be randomized in a blinded manner to receive either active vaccine (at one of3 doses, 0.5mg, 1.5mg or 4.0 mg) or vehicle ("control") alone. Participants will receive VRC4302 by intra-muscular injection once a month for 3 months. The injection is given using aneedle-less injection device. A total of approximately 21 individuals will be evaluated.Volunteers will be evaluated over the course of one-year (approximately 15 visits).Present study - as Ojokalpa Rasayana .Present study is a comparative study to assess two Ayurvedic combinations ofimmune builders, Immuno-modulators and acts on Ojovikruti by preventing ARC. Foodsupplements of immune modulation through well-known herbo-mineral origin, AmrutaKayaKalpa Rasayan of Amruta pharmaceuticals Hyderabad, is compared with the trail drugcombination of Bilvadi Vati and Agnikumar Vati (Sahasrayoga) as Ojokalpa Rasayana. InSahasrayoga Bilvadi vati and Agnikumar vati are indicated for Chira Atisara and Ama-Atisara, Visarpa, Garavisha and Bhoota visha, symptoms, which are appearing in ARC.Limitations of the study This study is of only 3 months period and attempt is not made to see in vitro effect oftherapy on HIV virus. The total work dwells on inferences based on both subjective andobjective parameters such as KPS score and CD4 count. With this duration, sample size anddesign, it is not possible to conclude the exact role of Ayurvedic treatment but this is a good Introduction to Bhutabhishangaja Ojokshaya 3
  • 13. beginning for further study. Serological test for HIV is not a criterion for assessment rather itis a diagnostic tool for inclusion of subjects. Viral load test (PCR) is not employed because of financial constrains, instead CD4enumeration, which is an internationally accepted surrogate marker of HIV status was undertaken.Study design So a rational combination was made to tackle cause of disease and management ofresultant condition under the shelter of Sahasra yoga. The Ojokalpa Rasayana, which hasOjovardhaka, Ama pachaka, jwarahara, and krimighna drugs in it. Recent researchers haveproved all the properties of individual drugs also. An attempt has been made to developnon-pharmacopeal methods of management of this condition by adopting Sadvritta(disciplines), do and don’ts prescribed by Charaka and other Acharyas 2. This dissertation begins with literary review of Ojokshaya and HIV infection and acomparative study of both. The basic physiology concerned with this disease, patho-physiology, causative factors, signs and symptoms, diagnostic tests involved are discussed. A detailed drug review has been done which speaks about the rationale behind thecombination. There is a chapter continued on materials and methods, which was adoptedfor this research work and in observation and results detail description of findings ofresearch are given. In discussion and conclusion, the possible mechanisms involved in thepharmacological intervention and subsequent improvement are discussed. There is a summary of over all work followed by the references and bibliography. It is a fond hope of people of this country that a successful drug will emerge out ofthis traditional knowledge and this is a humble effort to bring this much-cherished hope intoa reality. Introduction to Bhutabhishangaja Ojokshaya 4
  • 14. The normal healthy state of such a body requires normalcy of several factors. Theyare Dosha, Agni, Dhatu, and Mala along with peaceful disposition of Atma, Indriya andMana 3. For this normal functioning body requires strength, which is called as Bala. Ayurveda describes human body as seat of Chetana (consciousness) and a productof panchabhoutic vikara, existing in equilibrium. When this equilibrium gets disturbed, thatresults in defective bodily tissues. This is the beginning of any disease 4. This normal strength in the body is called as Sleshma 5, which has synonym -“Ojas”.This Ojas is transformed from the parents to the progeny through Sukra and Sonita 6, whichforms the zygote and from that moment development of foetus continues. The strength of any living is disturbed either by internal humors viz. Vata, Pitta andKapha or exogenous factors such as bacteria and virus. The virology and bacteriology is notmuch discussed from the ancient literature but the existence was not denied. Thus thepresent study which is based on the existence of the “Bhuta” described from the Vedicliterature. The principle of the disease development commences either from the endogenous orexogenous factors. The endogenous factors are grouped as physical and psychological.The physicals are of three humors and the psychological are rajas and tamas. Theexogenous factors which gives rise the disease because of Achayapurvaka prakopaultimately has to land for the vitiation of Dosha. Thus the terminus of the disease is underthe influence of the Dosha triode. Conceptual study of Bhutabhishangaja Ojokshaya 5
  • 15. Here in this concern discussed about the Ojas, Dosha and immunity as the virusmakes the deficiency of immunity and disturbs the Dosha triode.Ojas in general Man is a creature composed of millions of cells. A microbe is composed of only one.Yet, through out the ages, the microbes have had the upper hand in their ceaseless conflictwith man. The above sentence is narrated from Atharvaveda, which dates backs to 5000years. Ayurveda describes human body is seat of Chetana (consciousness) and a productof Panchabhoutika vikara, existing in equilibrium gets disturbed. That results in defectivebodily tissues. This is the beginning of any disease 7. The normal healthy state of a body requires normalcy of several factors they areDosha, Agni, and Dhatu, and Mala, Peaceful deposition of Atma, Indriya and Manas.8 fortheir normal functioning, body requires strength, which is called as Bala. The same normal 9.strength had synonym as Shlesma That is also known as Ojas. Ojokshaya is a broadunderstanding of immuno deficiency, depilated vigor and vitality. This Ojas is transformed 10from the parents to the pregnancy through Sukra and Shonita (Beeja of Purusha and Stri)at the time of zygote formation. Ojas is the essence of all the Dhatus. The Beeja isresponsible for the formation of particular organ or tissue, if it is vitiated, that results indeformity of the respective organ. If it develops undisturbed there will not be any deformityof the respective organ. There for it is clearly understood that every part of the healthy human body (Dhatuand Mala) develops according to the healthy state of the Beeja and Beejabhaga. There forthe essence of Dhatus as represented by Ojas of Pumbeeja and Stribeeja plays the majorrole in this mechanism. Conceptual study of Bhutabhishangaja Ojokshaya 6
  • 16. Ojas depends upon healthy state of Kapha. Physiologically Kapha represents apotential sour of strength and resistance to disease and decay. Those are Bala and Ojas.These terms reflect to the force and power which resists the factors responsible for decayand disease. Bala may be Sahaja (inherited), Kalaja (seasonal) and Yuktikruta (acquired) 11.But these all are equally capable of resisting the diseases. As vyadhi kshamatva is a force 12antagonistic to virulence of diseases causative factors . Susruta clarified further stating 13Balam is Ojas . As long as Dhatus are strong and healthy and are conducting their normalfunctions which their essence i.e. Ojas being both qualitatively and quantitatively effective.The body will be strong enough to resist and counter the decay and degeneration caused byeither the natural processes or disease. So in this contest this is very essential that, to knowabout etymology and normal physiology of Ojas.Nirukti (Etymology) of Ojas ‘Ojas’ the word has its root in “uj”or “vaj” dhatu. That means confer or strong (Ugra) 14.Ojas is the subanta pratyaya of word Ojas, which means Deepti, Prakasha and BalamKalidas in Raghu vamsha kavya writes ‘Rudraoujasa’ with reference to the potency of Shiva15 .Paribhasha (Definition) of Ojas Ojas is the essence of all Dhatus. Ojas is nothing but the Bala or Strength of thebody, which is the ultimate end product of the seven Dhatus starting from Rasa and ending 16at Shukra . Chakrapani contradicts this opinion and says Ojas sustains the body but doesnot nourish it. The normal healthy state of a body requires normalcy of several facts. They areDosha, Agni, Dhatu and Mala, along with peaceful deposition of Atma, Indriya and Manas.For this normal functioning body requires strength which is called as Bala. The normalstrength is called as Shlesma, which has synonym of Ojas, This Ojas is transformed from Conceptual study of Bhutabhishangaja Ojokshaya 7
  • 17. the parents to the pregnancy through Shukra and Shonita. Which is the essence of theDhatus. If a part of Beeja, which is responsible for the formation of particular organ or tissue,is vitiated, that results in deformity of the respective organ. If it develops undisturbed therewill not be any deformity of the respective organ. There for it is clearly understood that everypart of the healthy human body (Dhatu and Mala) develop according to the healthy state ofthe Beeja and Beejabhaga, there for the essence of Dhatus as represented by Ojas ofPumbeeja and Steebeeja plays the major role in this mechanism. Ojas depends upon healthy state of Kapha. Kapha in physiologically representspotential sours of strength and resistance to disease and decay of Bala and Ojas. Theseterms reflect to the force and power which resists the factors responsible for decay anddisease. Bala may be sahaj (inherited) kalaj (seasonal) and yuktikrita (acquired). But theseall are equally capable of resisting the diseases. As long as Dhatus are strong and healthyand conducting their normal functions with the essence i.e. Ojas being both qualitatively andquantitatively effective. The body will be strong enough to resist and counter the decay anddegeneration caused by either the natural processes or disease. So in this contest this isvery essential that, to know about etymology and normal physiology of Ojas.Formation of Ojas in the body 17 Ojas is the ‘Sara’ i.e. essence of all Dhatus . It is produced In the body as honey,Which is collected by bees from various flowers and fruits. Ojas is derived from all theSapta Dhatus in other words all the Dhatus contributes to its making. Ojas is the product ofthe prasada paka of Dhatvagni vyapara.That has the essence of all the Sapta Dhatus in it.Essentially Ojas depends on Ahara for its production and sustenance 18.Panchaboutic sangatan Apara Ojas is also known as slismika ojas and it is considered somatmak denotingthe predominance of Aap and prithvi mahabhootas 19. Conceptual study of Bhutabhishangaja Ojokshaya 8
  • 18. 20Physical properties of Ojas Colour:-Whitish yellow or whitish red resembling the color of Ghee Taste:-Sweet like honey Odour:- smell like fried paddy or Laja gelatin Ojasthana: Ojas is present all over the body and in each cell of the body 21 Oja Karya 22 Dosha nigrahana Sthiropachita Mamsata Cheshtasu Apratighata Svara Varna prasadhana Karananam Atma karya pratipatti Preenitaha sarvadehinah Prana yatra pratishtita Consistency 23 Snigda(unctuous), Guru (heavy),24, Pichchila (gelatinous) 25 , Mridu 26, 27, 28 29 (smooth), Sheeta, or somatmaka (mild to touch), , Stira (stable), Shukla varnam, 30 Saram 31, Viviktam,32 Guru 33 Bahalam 34 , Madhu rasam,35.Lajagandhi. 36, Lohita peetakam, 37Ojas Poshana 38 Ojas is nurrished mainly by Ahara, from the Ahara–Ahara rasa- Rasa dhatu- Rakta-Mamsa-Medha-Asthi- Majjaa-Shukra dhatusClassification of Ojas 39 There are two classifications of Ojas, made by Charaka, Susruta, Chakrapani, andby all other acharyas. Those are 1) Para Ojas and Conceptual study of Bhutabhishangaja Ojokshaya 9
  • 19. 2) Apara Ojas 40 These two types of Ojas have a direct bearing on body’s defense againstdegeneration and infection.Para Ojas Ojas marks the beginning of the formation of embryo. It is the essential nourishingfluid developed from the Rasa of the embryo. It enters the heart right at the stage of theletter’s initial formation and is permanently locates there, sustaining the life of fetus. Loss ofOjas amounts to the loss of life itself. Chakrapani comments that the above function pertainsto both the Ojas and further explains that Ojas plays a role in three different stages of the life 41of the fetus. It permeates to through Rasa in entire body and nourishes entire body andOjas is transported through the Ojovaha dhamanies. 42 1. At the time of conception it is the essence of Sukra and Shonit. 2. In the second stage it is the essence of the Rasa Sara, which provides nutrition to the embryo. 3. The third stage, when there is formation of various organs, Ojas manifests with its won action.Apara Ojas or Sleshmaka Ojas It performs the Tarpan action in the entire body. It is source of strength to theDhatus. Any loss in the quantity would cause sudden death. Commenting on function ofOjas Susruta has made a significant observation. Ojas permits entire body nourishes limbsand organs. In the absence or deficiency of Ojas in the body there will be wasting, decay,degeneration, and destruction of the body. This statement indicates the nutritive nature ofthe Apara Ojas in preventing the decay of the body. It is one of the ten seats of life. It givesfirmness to physical structures and gives strength to motor activity. Ojas spreads all over the Conceptual study of Bhutabhishangaja Ojokshaya 10
  • 20. body. In the absence of it life does not exist. The seat of Apara Ojas is the ten dhamaniesconnected with Hrudaya 43. According to Vagbhata, the function of Apara Ojas is “Dehastitanibhandana”. Which 44means it keeps the physical fitness of the body. Chandranandana clarifies that it is theprotection of the body in all the states. Hemadri also states that the changes in the Ojas arethe root cause for all the changes in the body. Ojas is Bala, which is a potential source ofresistance to disease and decay. Bala controls the Doshas that cause disease. This iscalled Vyadhi kshamatva.45.Synonyms of Ojas The term Ojas has been stated in Ayurvedic classics represents Kapha, Bala,Shleshma, Rasa and Rakta.46Sleshma in normal state apart from other confers 47. 1. It gives Weight and bulk. 2. It gives Strength to perform work 3. It resists disease and decay. 4. Promotes durability, (preserves the body from decay) 5. Promotes healing process (Ropanam) 6. It promotes tissue building.Ojas vriddhi lakshanas Increase in Ojas results in vriddi of Bala, Varna, Agni, Medha, Ayu and Sukha.Decrease results in kshaya. 48Nidana of Ojokshaya The pathological state of Oja is called as Ojokshaya .49. Charaka and all otherclassics have described this Oja vikriti as Ojokshaya. Susruta has classified this condition in 50to three different stages as 1) Ojo Vishrams, 2) Ojo Vyapat, 3) Ojokshaya, The Nidana Conceptual study of Bhutabhishangaja Ojokshaya 11
  • 21. which causes depletion of any Dhatu, can also causes depletion in the Ojas qualitatively andquantitatively. The factors influencing the Ojokshaya are as follows. 1) Ahar karana. 2) Vihar karana. 3) Manashika karana, 4) Aagantu karana.51Ahar karanas: - Alpaasha (mal nutrition) Anashana (starvation)Vihara karanas:- Vaata atapa shevana (expose to sun heat and winds) Ativyayama (excessive work beyond the capacity) Ativyavaya (excessive sex) Shonit ativartana (loss of blood) and Prajagara (keeping awake at night)Manashikakaranas: - Kopa, (anger) Shoka (grief) Chinta (worry) Bhaya (Phobia).Agantu karan: - “Sankramana” or “Upasarga” denote infection Krimi, Rakhsa, Rakshasa, yathudhana, Pishacha, Gandarva, Boota, Nishachar, presents different types of microbes, and Oja bhakshaka rajanichra. 52 Conceptual study of Bhutabhishangaja Ojokshaya 12
  • 22. Many diseases like Rajayakshma, Abhishyanda, Kushta, jwara, Upadamsha,Pooyameha, Apatantraka,Visarpa, Masoorika, Rohini, are some examples of infectiousdiseases coming to the mode infection, Bootopaghat, due to bhuta, pishacha, Rakshasa,etc. Charaka has mentioned that the Ojas is the Ahara for rakshas and if they consume theOjas, which leads to depletion of Ojas. Here Rakshasa i.e. Rajanichara 53 can be correlatedto infectious organism which spreads through Prasanga (sexual contact), Gatra samsparsha(physical touch), Nishwas (droplet infection), Saha bhojana (eating together) and Sahashayyasana, (sharing bed).Nidanartkara Vyadhi for the Oja vikriti 54 55 56, Rajayakshma , Prameha Pandu Raktarsha, Raktatisara, Kshayaja kasa, 57Kshataja kasa, Sannipata jwara , are the diseases which causes Ojakshaya in there later 58stage. Susruta pointed such possibility while dealing Abhinyasa jwara where in he usedthe term Hataujas 59 indicating the Ojokshaya. The clinical futures are low or even sub normal temperature, sub comatose state,loss of voice, cracked tongue, dry ness of throat, suppression of stools, perspiration,micturition, hardness of chest, aversion to food, dull complexion, difficulty in breathing, anddelirium. Susruta observed that disturbance of Ojas to the various parts of the body isaffected either due to leakage or loss or obstruction to the Ojas carrying tiny shrotases inSannipataja jwara, such condition is called as Oja – Nirodhaja sannipata. Inertness of thelimbs, chills, fits, loss of consciousness, delirium, etc. The acute condition referred above illustrates how the pronounced loss of Ojascontributes to an extra –ordinary state of susceptibility to increased microbial / viral activityand to toxins produced by these agents. Other clinical conditions which are slow inprogression, chronic in nature, and cause profound Dhatuksaya (wasting of body tissues)occur due to metabolic abnormalities leading to diminished production of Ojas. This will Conceptual study of Bhutabhishangaja Ojokshaya 13
  • 23. happen due to loss of structural integrity of Dhatu vaha srotas and obstruction in the supply 60system. Such other disease syndromes are Rajayaksma, Madhumeha, Ojomeha , Pandu,Sannipata jwara, and etc. Charaka has enumerated the pathological sequences very clearly while explainingthe Samprapti of Rajayaksma (both Anuloma and Pratiloma) in Charaka Chikitsa. Afterexplaining the manner in which nutrient materials are normally metabolized and assimilatedby the Dhatus he elaborates it further, due to the obstruction of srotas. As a result of adeficiency of nutrients Raktadi Dhatus, lowered functioning of dhatwagni and catabolicevents, the food ingested, which under goes pachana in kosta, is changed in to malas.Charaka in the Samprapti of Madhumeha observed that Vata by its ruksha guna. Charaka in the Samprapti of Madhumeha observed that Vata by its ruksha gunatransforms the Ojas, sweet in taste to astringent and transports it to the mutrashaya leadingto the causation of the condition known as Madhumeha. It is another disease whereOjokshaya is evident. Several other conditions creep in long with the main disease. Herethe Ojas produced in this person it self is vitiated 61. In case of Pandu roga the Samprapti is dominated by Pitta. The aggravated Doshavitiates the dhatus, which in turn loose their integrity and loss of normal colour, Bala(resistance) and Sneha, which are the gunas of Ojas are depleted by the dhosh-dhatusammurchana resulting the clinical features; impoverished Rakta, and medha dhatusleading shitilendriyata and vaivarnyata. Prameha, the urinary disorder is of two types. One caused due to endogenousfactors like Vatadi doshas, another one caused by exogenous or Agantuj factors likeindulgence in sex with the unfit and diseased partners. Agantuja prameha is infectious andcommunicable disease, transmitted through agamya, and dushita yoni samsarga (sexually Conceptual study of Bhutabhishangaja Ojokshaya 14
  • 24. transmitted). In these pramehas Ojokshaya occurs as a consequence of the passage ofOjas – mixed with urine excessively. Here Ojokshaya takes place in two different ways 62. Dosh Dhatu kshayajanya Ojaksaya. (That is depletion of the Ojas, due to theendogenous factors such as dosh, dhatu.etc.) Aupasargika / agantuja meha janyaOjokshaya (depletion due to exogenous factors like infections etc). But there is lot ofdifference in treatment between above said two entities. In case of Madatyaya, that severely affects Ojas, Bala and Prana. Madya is havingqualities exactly opposite to that of Ojas. Hence the Vyadhikshamatva is affected in it’stotally. Krimi and Visha also lead to severe loss of Ojas.Ojovisramsha Ojas mixes with Rasa dhatu in Hriday, from there it circulates trough out the body viavarious srotases. In this condition, the circulating Ojas leads leaks out or oozes out from thetiny distributing channels as a result; this vital substance may not reach certain organs /parts of the body and leads to the following signs and symptoms.Ojovyapat It is a pathological condition of Ojas because of vitiation by the Dosha as a result, theOjas looses its physiological or normal qualities and properties as described to it, this vikrutaOjas prod uses the following laxanas.Ojokshaya This is the final stage of Ojo-vikriti represents the loss and wasting of Ojas.According to Susruta 63Ojo-visramsa i. Sandi visleshana (loss of firmness of the joints) ii. Gatrosada (inertness of the extremities) Conceptual study of Bhutabhishangaja Ojokshaya 15
  • 25. iii. Doshachayana (disturbance) displacement of doshas from their own places iv. Kriyasannirodha (impairment of kaya vak-mano vyapara)Ojovyapat a. Stabdagatrata. (Heaviness and stiffness of the body and extremities.) b. Vata –shopha (oedema of vataja nature) c. Glani (malaise) d. Varna bheda (impairment of normal colour of the skin complexion) e. Tandra (drowsiness) f. NidraOjokshaya 1) Murcha (loss of conscious ness) 2) Mamsa kshaya (emaciation of mussels) 3) Moha (stupor) 4) Pralapa (delirium) 5) Marana (death)Kapha and vyadhikshamatva Health and longevity depends on the Balam as represented by kapha. Charaka hasexplained the same in the words “Baladisthanam Arogyam”. Bala denotes two vital aspectsof life process namely Vyayama Shakti. Vyadhikshamatva is further classified into threetypes – Sahaja, Kalaja and Yuktikrita.Sahaja Bala 64 The Sahaja Bala or resistance to the disease is stated to be prakriti. I.e. Inherentgenetic from of resistance existing in the individual body since birth and this also increases Conceptual study of Bhutabhishangaja Ojokshaya 16
  • 26. along with the growth of the body elements i.e. Sapta dhatus .It comprehends both shariraand satwa i.e. body and mind.Kalaja Bala 65 Kalaja Bala is influenced by the factors like seasonal variations and age of theindividuals. Thus kalaja Bala is supposed to be dissipated at its lowest leveling the Adanakala comprising of Sishira.Vasanta and Greeshma ritus. On other hand Bala is stated to beconserved and at its high peek level in the visarga kala, inceasing over Varsha, Sharat andHemanta ritus. Those are known as Sheeta kala or cooler period.Yuktikrita Bala 66. Yuktikrita Bala refers to the body’s resistance against disease, which can beenhanced by appropriate nutrition such as meat, Ghee, etc. Restorative and Rasayanatherapy in keeping with the seasonal requirements, adaptation of swastha vritta principles ofAyurveda along with Achara Rasayana also contributes the growth of Yuktikrita Bala. Dalhana in his commentary on Bala lakshanas as explained by Susruta observesOjas and Bala as synonyms, especially with Chikitsa point of view. However they are distinctin the sense the former is the essence of all the dhatus and it has physical properties likeRoopa, Rasa, Veerya etc., the later has to be determined from the power to lift heavy weightand the capacity to bear heavy loads etc. it does not possess physical properties. 67 The Vyadhikshamatva is not the same merit/order in all constitutions. In other words-This Shakti varies from individual. The same is explained in the Charaka Samhita ”Na chasarva shareerani vyadhikshamatva samarthani bhavantani.” In the discussion on factors thatinfluence Bala, held between Punarvasu Atreya and Agnivesha is recorded in the chapterVividaashitiyapeeya in the Charaka sutra sthana. This discussion throws considerableamount of light on the views held on resistance to disease. Conceptual study of Bhutabhishangaja Ojokshaya 17
  • 27. 68. Kapha is five types Those are Kledakakapha, Bodhakakapha, Tarpakakapha,Avalambakakapha and Shlesmakakapha. Each one is limited to some part or parts of bodyby their functions. They look after the functions of the Kapha locally and project the bodycollectively.The function of Kapha 69 The important functions, attributed to the Sleshma by the different Acharyas are, 1. Kapha is responsible for growth, weight, and bulk of the body. That is Brimhanam, and Gouravam. 2. It is Vrishya, a function relates to sexual stamina and productivity. 3. Sthairyam- it imparts stability and durability to the body and strength to the limbs. 4. It confers strength required to perform labors physical activity i.e. physical activity i.e. Vyayama Shakti. 5. It also provides the power to resist and overcome forces or factors, which bring about disease and decay popularly known as Vyadhikshamatva viz. Vyadhibala viroditva, Vyadhi utpadaka hetupratibhandakatvam.70. 6. Ropana- promotes healing process. 7. Ambukarma- Kapha being a repository of water, Makes this important fluid function to sub serve its vital secretary activities. 8. It has a function responsible of cohesion of various units and structures of the body.IMMUNE MECHANISM Defense mechanism of the body is classified in to two. 1. Immune 2. Non immune Conceptual study of Bhutabhishangaja Ojokshaya 18
  • 28. Immunity gives the specific response to a foreign antigen or pathogen. Andgenerally takes longer time to materialize. Memory is the key feature of the immunitytowards the antigen. Non immune host defense is not antigen specific, without memory itresponses immediately and is call inflammation also. There are cellular immunity and humoral immunity in the immune system and foreach the active principles are Thymus-derived (T) lymphocytes, and Bone marrow derived(B) lymphocytes respectively. Although both “B” and “T” lymphocytes are derived fromcommon stem called Bone marrow. Neutrophills, Esinophills, Basophiles, Natural killer cells,monocytes, and macrophages, are the mediators for this immediate response as nonimmune substances. Non specific resistance represents a wide variety of body reactionsagainst a wide range of pathogens, specific resistance or immunity involves the productionof specific anti body against specific pathogen or its toxins. Non specific resistance todisease is occurring by - Mechanical factors like • Skin and mucous membrane. • Saliva, Lacrimation, and Sebum. Chemical factors like • Gastric juice. • Enzymes. Mucous produced by glands of stomach, Nasal secretion and tissue fluids. Anti microbial substances 1. Interferon. 2. Complement. 3. Proper din with adherence and ingestion phagocytic activity. Conceptual study of Bhutabhishangaja Ojokshaya 19
  • 29. Specific resistance to the disease 1. Specific resistance to the disease is called Immunity. This destroys the particular antigen. 2. A detailed review of immunological process is desirable to understand the AIDS phenomena. Antigen and anti bodies Antigen is a chemical substance, which introduced at the time of production of antibodies. Antigen has 3 important characteristics. 1. Immunogenic. (This stimulates the formation of antibodies). 2. Reactivity(Reacts with antibodies) 3. Stimulation and reacting with antibodies. Vast majority of antigens are proteins, nucleoproteins, (nucleic acid plus proteins)lipoproteins, glycoprotein, and certain large polysaccharides. The entire microbe, such as a bacterium or virus or components of microbes may actinclude pollen, egg white, incompatible blood cells, and transplanted tissues and organs.The myriad of antigens in the environment provides many opportunities for the production ofantibodies by the body. Antibodies not form against with the whole antigen, at specificregions on the surface of the antigen, called antigenic determinant sites. Specific chemicalgroups of the antigen combine with the antibody. This combination depends up on the size and shape of the determinant. Site and themanner in that, it corresponds to the chemical structure of the antibody. Lymphocytes are key constituents of the immune system. In mammals, this systemhas the remarkable ability to produce antibodies against many millions of different foreignagents that invade the body. In addition, the immune system “remembers,” and a second Conceptual study of Bhutabhishangaja Ojokshaya 20
  • 30. exposure to a foreign substance produces a more rapid and greater Hum oral immunity isimmunity due to circulating antibodies in the globulin fraction of the plasma proteins. It is amajor defense against bacterial infections. Cellular immunity is responsible for delayed allergic reactions and rejection oftransplants of foreign tissue. It constitutes a major defense against infections due to viruses,fungi, and a few bacteria such as the tubercular bacillus. It also helps to defend againsttumors. There have been spectacular advances in immunology in recent years, and the fieldis now large and complex. Only the fundamentals are presented here.Development of the Immune System During fetal development, Iymphocyte precursors come from the bone marrow.Those that populate in the thymus become transformed by the environment in this organinto the lymphocytes responsible for cellular immunity i.e.-Imphocytes. Lymphocytesresponsible for humeral immunity are B-lymphocytes. Four different varieties of T cells havebeen identified: helper / inducer T cells suppressor T cells, cytotoxic T cells (which are alsoknown as effectors T cells or killer cells), and memory T cells. The first 2 types are involvedin the regulation of antibody production by B cells derivatives, whereas the cytotoxic T cellsdestroy transplanted and other foreign cells. Cytotoxic and suppressor T cells have on theirsurface the glycoprotein CD8, which can be detected by monoclonal antibodies, so they arefrequently called T, cells. Helper / inducer T cells have on their surface the glycoprotein CD4and are therefore called T cells. CD8 is a co receptor for MHC class I molecules and CD4 isa co receptor for MHC class II molecules. Memory B and T cells are cells those have been exposed to an antigen and arereadily converted to effectors cells by a later encounter with the same antigen. Unlike otherlymphocytes, they persist in the body for months or even years. Conceptual study of Bhutabhishangaja Ojokshaya 21
  • 31. Lymphocytes, macrophages, and other cells involved in immune responsescommunicate in part by hormone like chemical messengers called interleukins andcytokines.Major Histo – compatibility complex The genes of the major histo compatibility complex (MHC), which are located on theshort arm of human chromosome 6, encode glycoprotein that are located on the surface ofall cells and function in antibody processing and distinguishing self from non-self. They aredivided into 2 classes on the basis of tissue distribution and function. Class I antigens arecomposed of a 45-kilodalton heavy chain associated non-covalently with P, micro globulinencoded by a gene out side the MHC. Antigens can also be processed and presented to T4 cells by various types of cells inthe body in addition to macrophages. The other types of antigen presenting cells include theB cells themselves, the Langerahans cells of the skin, and specialized cells called dendriticcells in the lymph nods and spleen.Cellular Immunity T8 cells mediate cellular immunity. These cells are activated when they arepresented with antigens and MHC-1 proteins on the surfaces of antigen presenting cells.When also exposed to interleukin-2, they proliferate and differentiate into cytotoxic T cells.The cytotoxic T cells attack and destroy cells that have antigen, which activated them. Theykill by inserting pore-forming molecules (perforins) in the membranes of their target cells inthe same fashion as the complement system does. They may also act by including withinthe cells an as at undefined change that leads to death. Suppressor T cells, which developmore slowly then cytotoxic T cells, help terminate the immune response by dampening theimmune responses of T and B cells. This includes turning of the helper / inducer cells. Conceptual study of Bhutabhishangaja Ojokshaya 22
  • 32. To ensure maximal specific T cells response the antigen is linked to molecularcomponents of the HLA system (by B cells, dendritic cells and macrophages) and presentedto T cell. The transformed blast cell undergoes progressive mitotic division and each cell ofthe resulting clone has the same specific immune potential. The subsequent T cell activitiestend to remain local at the site of the antigen concentration and this cell mediated immunity(CMI) is delayed, i.e. at least 24 hours are required for a significant local concentration ofsensitized T cells.T cell functions and mechanism Overall regulation of the immune response and reactions- this is effected by helper Tcells which promote, and suppressor T cells which inhibit immune reactions. In theperipheral blood, 2/3 of the T lymphocytes are helper and 1/3 suppressor. Using monoclonalantibodies, helper cells carry the CD4 surface antigen and suppressor cells the CD8.T cell effecter mechanisms:a). Cytotoxic T cells cause antigen-specific lyses by direct cell-to-cell contact.b). Natural killer cells, again cause lyses by direct cell to cell contact but usually the killingaction is non specific.c). Delayed hypersensitivity reactions are mediated by the release of lymphokines from thespecifically activated T cells. They promote a wide range of cellular activity associated withthe promotion and control of the immune response and the inflammatory reaction.Lymphokines and cytokines Lymphocytes, macrophages, and in some instances endothelial cells, neurons, glialcells, and other types of cells secrete many hormone like chemical messengers that effectthe immune response. The messengers secreted by lymphocytes and often calledlymphokines. However, since other cells produce them as well, it seems more appropriate to Conceptual study of Bhutabhishangaja Ojokshaya 23
  • 33. call them cytokines. This field is growing very rapidly, and most of the cytokines are initiallynamed for other actions, e.g. B cell differentiating factor, B cell stimulating factor 2. There isa convention that once the amino acid sequence of a factor in humans is known its name ischanged to interleukin. Thus, for e.g. the name of B cell differentiating factor was changed to interleukin-4.However, nomenclature in this field remains somewhat confused and uncertain.Hemoglobin The red, oxygen-carrying pigment in the red blood cells of vertebrates isHemoglobin, Hemoglobin is a globular molecule made up of 4 sub units. Each sub unitcontains a hem moiety conjugated to a polypeptide. The average normal Hemoglobincontent of blood is 16g/dl in men and 14g/dl in women, all of it in red cells. In the body of a70- kg man, there is about 900gms of Hemoglobin, and 0.3gm of hemoglobin is destroyedand 0.3gm synthesized every hour.Platelets The platelets are small, granulated bodies 2-4 micrometers in diameter. There areabout 3 lakhs /µ liter platelets in circulating blood, and they normally have a half-life of about4 days. The megakaryocytes giant cells in the bone marrow, from platelets the pinching ofbits of cytoplasm and extruding them into the circulation. Platelet production is regulated bythe colony stimulating factors that cintroll the production of megakaryocytes. Between 60and 75% of the platelets that have been extruded from the bone marrow are in thecirculating blood, but the reminder are mostly in the spleen. Splenectomy causes anincrease in the platelet count (thrombocytosis). Non specific resistance represents a wide variety of body reactions against a wide ofpathogens. Specific resistance or immunity involves the production of specific antibodyagainst specific pathogen or its toxin. Conceptual study of Bhutabhishangaja Ojokshaya 24
  • 34. Pathology in Bhutabhishanga Ojokshaya (HIV infection) The acquired immune deficiency syndrome (AIDS) was first recognized in the UnitedStates in the summer of 1981, when the centers for disease control and prevention (CDC)reported the unexplained occurrence of to diseases. At first Pneumocystis carinii pneumoniain five previously healthy homosexual men in Los Angeles was reported. Soon afterKaposi’s sarcoma in 26 previously healthy homosexual men in New York, and Los Angeleswere reported. Within months, the disease became recognized in male and female InjectionDrug Users (IDUs) and soon after, in recipients of blood transfusions and in hemophiliacs.As the epidemiological pattern of the disease was unfolded it became clear that a microbetransmissible by sexual contact or blood and blood products was the most likely etiologicagent for the epidemic. In 1983, Human Immuno Deficiency Virus (HIV) was isolated from apatient with lymph-adenopathy. In 1984 it was demonstrated clearly that this virus is thecausative agent of AIDS. During the early years of 1980’s the care of HIV-infected individuals in the UnitedStates was confined to restricted groups of physicians and hospitals, in urban areas, ofnorth eastern and western seaboards. But today, every practicing physician in this countryand other parts of the world is required to have some degree of familiarity with the work up,diagnosis, management, of HIV-infected individuals. HIV-infected individuals are presentingin increasing numbers to family physicians, obstetricians, gynecologists, pediatricians andsurgeons with clinical problems that may be directly or indirectly related to their HIV-infection.HIV infection in India The first case of HIV infection was identified in India in 1986 at Chennai. Duringthese days it was limited to female sex workers. Focus was shifted from Chennai to Mumbaias hundreds of female sex workers were found to have HIV infection. It is with truck drivers, Conceptual study of Bhutabhishangaja Ojokshaya 25
  • 35. it started spreading from big cities to smaller ones. People, who travel from cities to city andthose who travel from villages to cities, were found to be more susceptible because ofunprotected, non-martial sexual contact. Even though thousands of people got infectedthrough blood transfusion during the first decade of epidemic, the heterosexual contact isthe major cause of spread. Every year 3 lakh Indians die due to AIDS. Since the beginning,amount of the death of the AIDS patients is 25 lakhs. It is second highest figurecommunicable diseases, which cause death.Definition of AIDS Any HIV-infected individual with CD4+T cell count of<200/microliter had AIDS bydefinition, regardless of the presence of symptoms or opportunistic diseases. The clinicalconditions like pulmonary tuberculosis, recurrent pneumonia, and invasive cervical cancer.While the definition of AIDS is complex and comprehensive, the clinician should not focuson presence of AIDS but should view HIV disease as a spectrum ranging from primaryinfection, with or without the acute syndrome, to the asymptomatic stage, and to advanceddisease. It is important to distinguish between being infected with HIV and having AIDS.People infected with HIV may take 5-7years or more to develop as AIDS. Some time it maybe sooner because of malnutrition and poor state of health, toxins and malnutrition out plaidfactors that stress the immune system probably cause AIDS. During this interval HIVinfected individuals may suffer from a variety of disorders and develop signs which aresuggestive of being infected with HIV. Mainly those symptoms are pain less swelling ofLymph nodes in the neck, Armpits and Groin, Fever, Night Sweats, Diarrhea, Loss of weightand infections such as Herpes, Pneumonia, etc. Conceptual study of Bhutabhishangaja Ojokshaya 26
  • 36. Etiologic agent The etiologic agent of AIDS is HIV (the Human Immuno deficiency Virus), whichbelongs to family of (Heterogenous) human retroviruses and the subfamily of Lentiviruses.Lentiviruses cause disease in other animal species, including Sheep, Horses, Goats, Cattle,Cats and Monkeys. The four recognized human retroviruses belong to two distinct groups,i.e.HIV-1 and HIV-2. The most common cause of HIV disease throughout the world is HIV-1comprises several subtypes with different geographic distribution. HIV-2 was first identifiedin 1986 in West African patients and was originally confined to this region. Electron microscopy shows that the HIV virus is an icosahedra structure containingnumerous external spikes formed by the two major envelope proteins, the external Gp120and the transmembrane Gp41.The virion buds from the surface of the infected cellincorporates a variety of host proteins, including Major Histo-compatibility Complex (MHC)class I and II, antigens into its lipid bilayer. This virus contains two Snake like single strands of Ribose Nucleic Acid (RNA), slowin nature, having reverse transcriptase enzyme. Having size about 90-120 mm. this virus isa tiny, a thousand times smaller than the thickness of a hair. Looks like a roller upporcupine. This lies firmly wrapped up in a care which resembles a cone with a dimple at itsbase. This cone is protected by an envelop that has a knob like protein sticking out itssurface. HIV is free from live, when it is out side the body. It dies immediately in dry area.It can alive in blood at 4o c, about three weeks or till the cell disintegrates.Pathology and Pathogenesis The hallmark of HIV disease is a profound immunodeficiency resulting primarily froma progressive quantitative and qualitative deficiency of the subset of T lymphocytes referredto as helper or inducer T cells. This subset of T cells is defined phenotypicaly by thepresence on its surface of the CD4 molecule. This serve as the primary cellular receptor of Conceptual study of Bhutabhishangaja Ojokshaya 27
  • 37. HIV it has recently been demonstrated that a co-receptor must be present together with CD4for effective fusion and entry of HIV-1 into its target cells. It is important appreciate that thepathogenic mechanisms of HIV disease are multi factorial and multi-phased and aredifferent at different stages of the disease. HIV has a number of mechanisms to evade elimination by the immune system. HIVhas as extraordinary ability to mutate, but this mechanism probably acts mainly after theestablishment of chronic infection and contributes to the maintenance of chronic. Since thetransmitted virus and the virus that initially becomes established as a chronic infection arerelatively homogeneous, the initial escape from immune system control likely involves othermechanisms. Molecular analysis of clono types has demonstrated that clones ofCD8+Cytolytic T Lymphocytes (CTLs) that expand greatly during primary HIV infection andlikely represent the high-affinity clones that would be expected to be more efficient ineliminating virus infected cells disappear after their initial burst of expansion.Viral Dynamics HIV-1 and HIV-2 are both viruses that belong to the same family, but vary in geneticmake up. HIV-1 was first discovered in 1983 in France and appears to be more preventionEurope and America. HIV-2 was first discovered in 1986 and is more prevalent in Africa.Both HIV-1 and HIV-2 have been detected in India and both leads to AIDS. It was originally thought that very little virus replication occurred during clinicallatency. However studies of lymphoid tissue using PCR analysis for HIV RNA and in sitehybridization for individual virus expressing cells clearly demonstrated that HIV replicationoccurs throughout the course of HIV infection, even during clinical latency. The availability ofsensitive PCR techniques leads to the demonstration that viremia present at all stages ofHIV disease. Conceptual study of Bhutabhishangaja Ojokshaya 28
  • 38. The behavior of the HIV is very much similar to poison. The HIV is fragile, once thevirus is out side the body in a dry form, it dies immediately. When stored in blood banks at4oc, it can live for about 3 weeks or till the cell is integrates.Mode of Transmission Transmission is of two types, horizontal and vertical. HIV is transmitted byhomosexual and heterosexual contact. Blood, Blood products are the important routes ofinfection. Infection spreads from mothers to infants either intrapartum, perinatally, or viabreast milk. After more than 15 years of scrutiny, there is no evidence that HIV is transmittedby casual contact or that the virus can spread by insects, such as by a mosquito bite.1) Sexual transmission:- ♦ Homo sexual: More HIV infections occur in homo sexual and bisexual men (lesbianism) who have a large number of sexual partners the sexual practice often involves anal intercourse (anal sex) and fella tic with ejection of semen in to the mouth (oral sex). ♦ Hetero sexual: Multiple, Hetero sexual contacts often prostitutes. ♦ Blood and tissue liquids: i. Contaminated blood and blood based products, ii. Blood transfusion, iii. Semen and Sperm, iv. Brest milk, v. Urine, Tear, Saliva, CSF with visual blood containing, ♦ Contaminated instruments like needles, syringes, surgical and dental. ♦ Transplantation of tissues and organs, (Kidney, Cornea, Skin, Bone marrow) Conceptual study of Bhutabhishangaja Ojokshaya 29
  • 39. ♦ Mother to child. Antenatal (In Uterus), Delivery (at birth), Postnatal (After birth by Breast feeding) HIV has been demonstrated in seminal fluid both within infected mononuclear cellsand in the cell free state. The virus appears to concentrate in the seminal fluid, particularly insituations where increased numbers of lymphocytes and monocytes are. The virus has alsobeen demonstrated in cervical smears and vaginal fluids. There is a strong association oftransmission of HIV with receptive intercourse. Owing to the fact that only a thin and fragilerectal mucosal membrane separates the deposited semen from potentially susceptible cellsin and beneath the mucosa this transmission takes place. Trauma associated with analintercourse provides at least two modalities of infection; direct inoculation into blood in casesof tears in the mucosa, and infection of susceptible target cells, such as langerhans cell, inthe mucosal layer in the absence of trauma. There is approximately a 20 fold greater chanceof transmission of HIV from a man to a woman than from a woman to a man through vaginalintercourse. This difference may be due to the prolonged exposure of the vaginal andcervical mucosa and endometrium to infected seminal fluid.2) Transmission by blood and blood products: HIV can be transmitted by blood products, both among individuals who sharecontaminated paraphemalia (needles and syringes) for injection drug use and in those whoreceive transfusions of blood and blood products. It is estimated that 90 to 100% individualswho were transfused with HIV-infected blood became infected. Transfusions of whole blood,packed red blood cells, platelets, leukocytes, and plasma are all capable of transmitting HIVinfection. The precautionary measures taken to check this: (1) the screening of all blood forp24 antigen and for HIV antibody body enzyme linked immuno-absorbent assay (ELISA), Conceptual study of Bhutabhishangaja Ojokshaya 30
  • 40. with a confirmatory western blot where applicable; (2) the self-deferral of donors on thebasis of risk behavior.3) Occupational transmission of HIV: There is a small but definite occupational risk of HIV transmission among health careworkers, laboratory personnel, and potentially others who work with HIV infected specimens,particularly when sharp objects is used. It is estimated that 250,000 to 1 million health careworkers are stuck with needles or other sharp medical instruments in each year large.4) Maternal to fetal / infant transmission (vertical): HIV infection can be transmitted from an infected mother to her fetus duringpregnancy or during delivery. This is an extremely important form of transmission of HIVinfection in developing countries, where the proportion of infected women to infected men isapproximately 1:15) Transmission by other body fluids: There is no convincing evidence that saliva can transmit HIV infection, either throughkissing or through other exposures, such as occupationally to health care workers. But bloodcontaminated saliva and wet kissing will leads to HIV infectionEpidemiology of HIV infection HIV infection and AIDS is a global pandemic, with cases reported virtually from everycountry. The current estimate of the number of cases of HIV infection among adultsworldwide is approximately 22 million, and approximately 2.6 Million HIV-infected childrenhave been born since the start of the HIV pandemic, and approximately one half of thesehave developed AIDS and have died. The global projections for the number of HIV-infectedindividuals by the year 2000 range from 40 to 100 million. Conceptual study of Bhutabhishangaja Ojokshaya 31
  • 41. Life cycle of HIV infection HIV is an RNA virus whose hallmark is the reverse transcription of its genomic RNAto DNA by the enzyme reverse transcriptase. The life cycle begins with the high affinitybinding of the Gp 120 protein via a portion of its VI region near N terminus to its receptor onthe host cell surface, the CD4 molecule. It has recently been demonstrated that the co-receptor that must be present together with the CD4 molecule for fusion and entry of T-celltropic strains of HIV-1 is a molecule termed CXCR4. Figure –1 Life cycle of HIV infection The reverse transcriptase enzyme, which is contained in the infecting Virions, thencatalyzes the reverse transcription of the genomic RNA into double-stranded DNA. The DNA Conceptual study of Bhutabhishangaja Ojokshaya 32
  • 42. trans-located to the nucleus, where it is integrated randomly into the host cell chromosomesthrough the action of another virally encoded enzyme Integrate.Morphology of HIV Electron microscopy shows that the HIV virus is an icosahedral structure containingnumerous external spikes formed by the two major envelope proteins, the external gp 120and the transmembrane gp41. The Virion buds from the surface of the infected cellincorporates a variety of host proteins, including Major Histo-compatibility complex (MHC)class I and II, antigens into its lipid bilayer. Figure –2 Structure of HIV Glycoprotein Glycoprotein GP41 GP120 Fatty (Lipid Bilayer membrane Protein P18 Protein Reverse transcriptase P24 enzymeHIV genetics HIV-1 has genes that encode the structural proteins of the virus gag encodes theproteins that from the core of the Virion (including p24 antigen) I Pol encodes the enzymes Conceptual study of Bhutabhishangaja Ojokshaya 33
  • 43. responsible for reverse transcription and integration and env encodes the envelopeglycoprotein. Molecular heterogeneity of HIV-1: Molecular analysis of various HIV isolates revealssequence variation over many parts of the viral genome.Types and Sub types There are two types of HIV-1 group M (major), which is responsible for most of theinfections in the world, and group O (outlier) a relatively rare viral form found at this time inCameroon, Gabon and France. The M group comprises at least light sequence subtypes, orclad, designated A to H.How does the HIV virus attack the immune system, Once the human immuno deficiency virus enters the body, it gets attacked to a typeof white blood cell called T lymphocytes. The RNA genetic material of the virus then getsconverted to DNA genetic material by an enzyme that the virus produces. This virus DNAthen gets incorporated in to the DNA of the T lymphocyte, and remains there for the lifetimeof individual. This infected cell knows becomes a virus factory producing more viruses whichbud out the cell, attack new T lymphocytes, and destroy them. Over a period of years, the Tcell count of the infected person drops to a critical level and the individual develops AIDS.Duration of an HIV infected person to develop AIDS. This depends on the mode of the HIV transmission and life styles of the HIV positiveperson. Persons those are infected through blood transfusion develop symptoms of anaverage from 3-5 years. With the other modes of transmission, when the dose of the virus isless, the person can remain healthy for 8-12 years or longer, if an HIV positive personimproves his or her quality of life by adopting safer sex, has a good nutrition, regularexercise, seeks immediate medical attention for any ill health. Avoids stress, continues to beactive he or she is likely to live longer. Conceptual study of Bhutabhishangaja Ojokshaya 34
  • 44. The cytokine network in the HIV pathogenesis On perturbation of the immune system by antigenic challenge, the expressions ofcytokines increase to varying degrees. Cytokines that are important components of thisimmune regulatory network have been demonstrated to play a major role in the regulation ofHIV expression in vitro. A number of in vitro model systems of chronically infected monocyteor T cell lines, primary cultures of peripheral blood or lymph node mononuclear cells fromHIV-infected individuals, and acutely infected primary cell cultures have been used todemonstrate the role of cytokines in the regulation of HIV expression. Potent modulation ofHIV expression has been demonstrated either by manipulating endogenous cytokines or byadding exogenous cytokines to culture. Cytokines that induce HIV expression in one ormore of these systems include IL-1, IL-2, IL-3, IL-6, IL-12, TNF and TNF. Macrophagecolony stimulating factor (M-CSF) and granulocyte-macrophage colony stimulating factor(GM-CSF). Among these cytokines the most consistent and potent inducer of HIVexpression are the pro-inflammatory cytokines TNF IL- and IL-6. Interferon (INF) and(INF) 2, IL-4, IL-10 and INF 3 can either induce or suppress HIV expression, depending onthe system involved.Clinical manifestation of HIV infection HIV disease can be divided empirically on the basis of the degree ofimmunodeficiency into an early stage (CD4+T cell count 200 to 500/ micro liter), anintermediate stage (CD4+T cell count 200 to 500 /micro liter) and an advanced stage(CD4+T cell count < 200 / micro liter). Most AIDS defining opportunistic infections and truemalignancies occur in the advanced stage of disease, while neurological disease andKaposi’s sarcoma are not as strictly related to the degree of immunodeficiency. The twomajor classification systems for staging HIV disease are the CDC system and the Walter Conceptual study of Bhutabhishangaja Ojokshaya 35
  • 45. reed medical center system; these are to be distinguished from the case definition for AIDS,which is used for surveillance purposes.Disease control classification system for HIV infection Group 1, Acute HIV syndrome Group 2, asymptomatic infection Group 3, Persistent genaralised lymph-adenopathy Group 4, other diseases • Constitutional disease • Neurological diseases • Secondary infectious diseases • Secondary neoplasms • Other conditionsThe acute HIV syndrome (acute Retro viral syndrome) About 50-70% of people infected with HIV usually develop acute viral fever flu likesyndrome called (ARS- acute retroviral syndrome), This occurs within 2-4 weeks after getting infected with HIV. The symptoms present are fever, body ache, and skin rashes. It is estimated that 50 to 70% of individuals with HIV infection experiences and acuteclinical syndrome approximately 2 to 4 weeks after primary infection. Varying degrees ofclinical severity have been reported, and it has been suggested that symptomatic sero-conversion leading to the seeking of medical attention indicates an increased risk for anaccelerated course of disease. Clinical findings occur along with a burst of plasma viremiaand p24 antigenemia. The syndrome is typical of an acute viral syndrome and has been linked to acuteinfections mononucleosis symptoms usually persist for 1 to several weeks and gradually Conceptual study of Bhutabhishangaja Ojokshaya 36
  • 46. subside as an immune response to HIV develops and the levels of plasma viremiadecrease. Opportunistic infections have been reported during this stage of infection,reflecting the immunodeficiency that results from reduced numbers of CD4+T cells. Totallymphocyte and T cell subsets (CD4+ and CD8+) are initially reduced. An inversion of theCD4+/CD8+ T cell ratio occurs later because of the rise in the number of CD8+T cell subsets,as determined by T cell receptor analysis. The total circulating CD8+T cell levels usuallyremain some what depressed although there may be a slight rebound towards normal.Lymph-adenopathy occurs in approximately 70% of individuals with primary HIV infection.Most patients recover spontaneously from this syndrome and have a mildly depressedCD4+T cell count that remains stable for a variable period before beginning its progressivedecline. In most patients, primary infection with or without the acute syndrome is followed bya prolonged period of clinical latency.The asymptomatic stage Clinical latency although the length of time from initial infection to the development ofclinical disease varies greatly the median time is approximately 10 years. HIV disease withactive virus replication usually progresses during this asymptomatic period. Some patientscalled long term non-progressors, show little decline in CD4+T cells counts over an extendedperiod. These patients generally have extremely low levels of HIV RNA. In these patients,the appearance of an opportunistic disease may be the first manifestation of HIV infection.Some patients otherwise asymptomatic develop persist generalized lymph-adenopathyduring this time. With few exceptions, CD4+T cell counts fall progressively during thisasymptomatic period at an average rate of approximately 50 cells / micro liter per year.When the CD4+T cell count falls below about 200/micro liter, the resulting stage ofimmunodeficiency is severe enough to place the patient at high risk for opportunisticinfections and neoplasm and hence are clinically apparent disease. Conceptual study of Bhutabhishangaja Ojokshaya 37
  • 47. Window period Even after a person is infected with HIV, he/she will remain healthy for some periodof time. Patient will have no complaints. In this time HIV tests will become negative for 6-12weeks after infection. In this period the person is highly infectious, viral load (number of virusin the body) is extremely high.Asymptomatic period After about 6 weeks of HIV infection, the HIV test will become positive. The HIVinfected person can remain healthy without any complaints for periods of up to 3-5 years.This period when the HIV test is positive but the person remains without symptoms orcomplaints is called the HIV positive asymptomatic period.HIV positive symptomatic period The HIV continues to multiply in the body.Early symptomatic disease At some point, usually after the CD4+T cell count has fallen below 500 /micro literpatients begin to develop signs and symptoms of clinical illness. Many of these problemscan be traced to minor opportunistic infections, not sufficiently indicative of a defect in cell-mediated immunity to be considered AIDS defining illness, while some of them appear to bedirect affects of long standing HIV infection. This stage of HIV infection has been given avariety of names in the past, among them pre-AIDS and AIDS-related complex (ARC),generalized lymph-adenopathy. This condition, defined as the presence of enlarged lymph nodes (1cm) in two ormore extra inguinal sites for more than 3 months without an obvious cause, it’s often theearliest symptom of HIV infection after primary infection. It is due to marked follicularhyperplasia. The nodes are generally discrete and freely moveable. This feature of HIV Conceptual study of Bhutabhishangaja Ojokshaya 38
  • 48. disease, which may be seen at any point of time, is not associated with an increasedlikelihood of developing AIDS. Paradoxically a loss in lymph-adenopathy or a decrease in lymph nodes size may bea prognostic maker of disease progression. In the early and intermediate stages of HIVinfection, the main differential diagnosis is an idiopathic form of Kaposi’s sarcoma. Late in the course of disease, differential diagnosis expands to include lymphoma,mycobacterium infection, toxoplasmosis, systemic fungal infection and bacillary angiomatosis. Lymph node biopsy is not indicated in patients with early stage disease unlessthere are science and symptoms of systemic illness such as fever and weight loss, or unlessthe nodes begin to enlarge, become fixed or coalesce.Oral lesions Oral lesions, including fresh, hairy leukoplakia-and aphous ulcers, are particularlycommon during this phase. Thrush due to Candida infection and oral hairy leukoplakia, areusually indicate of fairly advanced immunologic decline, generally occurring in patients withfever than 300 CD4+T cells/ micro liter.Herpes zoster (shingles) This condition is seen in 10 to 20% of patients. This reactivation syndrome ofvaricella zoster virus indicates a modest decline in immune function and is often the firstclinical indication of immunodeficiency.Thrombocytopenia Thrombocytopenia also may be an early consequence of HIV infection.Approximately 3% of patients with HIV infection and CD4+T counts above 400/ micro literhave platelet count fewer than 150,000/ micro liter. This incidence increases to 10%.Thrombocytopenia is really a serious clinical problem in these patients. Conceptual study of Bhutabhishangaja Ojokshaya 39
  • 49. Neurologic disease Clinical disease of the nervous system accounts for a significant degree of morbidityin a high percentage of patients. The neurologic problems that occur in HIV-infectedindividuals may be either primary to the pathogenic processes of HIV infection or secondaryto opportunistic infections or neoplasm.Opportunistic infections Opportunistic infections are late complications of HIV infection, for the most partoccurring in patients with less than 200 CD4+T cells per micro liter. While the causativeagents characteristically are opportunistic organisms, such as pneumocytis carimi,mycobacterium avium complex, CMV, and other organisms that do not ordinarily causedisease in the absence of a compromised immune system, they also include commonbacterial and mycobacterium pathogens. Opportunistic infections are the leading cause ofmorbidity and mortality I patients with HIV infection. Approximately 80% of AIDS patients dieas direct result of an infection other than HIV, with bacterial infections heading the list.Protozoal infections Pneumocystis carinii infection is one of the most common causes of infectionpatients generally present with fever and cough that is usually nonproductive or productiveof only scant amounts of white sputum. They may complain of a characteristic retro-sternalchest pain, which is usually course on inspiration and described as either sharp or burning.In more severe cases, patient usually notes dyspnoea on exertion, fatigue and weight loss.One may see a chest x-ray pattern with upper lobe cavity disease, reminiscent oftuberculosis.Protozoal diarrhea: Cryptosporidium is a well-known cause of Diarrhea in animals and may cause a self-limited Diarrheal infection in the immuno competent host. It is spread through fecal-oral Conceptual study of Bhutabhishangaja Ojokshaya 40
  • 50. contact. In HIV-infected individuals, cryptosporidial infection may present in a variety ofways, ranging from a self-limited or intermittent diarrhea illness in patients in the earlystages of HIV disease to a severe, life treating Diarrhea in severely immuno deficientindividuals. Therapy is purely symptomatic at present. Patients can minimize their risk ofdeveloping cryptosporidiosis by avoiding contact with human and animal feces and by notdrinking water from lakes or rivers.Microsporidia The main species causing disease in humans is Enterocytozoon bieneusi. In contrastto Cryptosporidia, microsporidia have been noted in a variety of extra intestinal locations,including the eye, muscle, liver and cause conjunctivitis and hepatitis. As in the cause ofcryptosporidium, no effective therapy is known and treatment is purely symptomatic.Bacterial infections Bacterial infections are the leading cause of death in HIV infected individuals.Disseminated mycobacterial infection, particularly due to Mycobacterium avium complex(MAC) is the most common opportunistic bacterial infection. Mycobacterium fartuitum, mycobacterium chelonas, mycobacterium marinum,mycobacterium scrofulceum and mycobacterium haeneophilum all causes disseminateddisease and septic arthritis. Mycobacterium gardnae, generally a nonpathogenic in humans,and mycobacterium zeropi, a colonizer of water storage tanks, may cause disseminateddisease. Therapy of the latter organisms is extremely difficult.Tuberculosis M. Tuberculosis, one thought to be on its way to extinction in United States,experienced resurgence. Tuberculosis is a particularly important problem with HIV infection.HIV disease progresses more rapidly when associated with tuberculosis, the level of plasma Conceptual study of Bhutabhishangaja Ojokshaya 41
  • 51. viremia increase during active tuberculosis and successful treatment of tuberculosis causesplasma viremia to fall back to baseline levels. Given the fact that, in contrast of HIV infection,with M. tuberculosis can be spread via respiratory droplets and close, non-sexual contact,this epidemic of tuberculosis probably represents the greatest health risk to the generalpublic and the health care profession associated with the HIV epidemic. Tuberculosis may be the earliest clinical sign of HIV infection. Patients present withfever, cough, and dyspnoea on exertion, weight loss, night sweats and a chest x-rayrevealing cavity apical disease of the upper lobes. Disseminated disease is more common with low CD4+T cell counts.Viral infections: Herpes virus infection: Human herpes virus infections present substantial problemsthroughout the course of HIV infection. Among the members of this group that areparticularly disabling of patients with HIV infection are CMV, Herpes simplex viruses,Varicella zoster, Epstein Barr virus and HIV-8. Cytomegalo virus infections: Retinitis, esophagitis, and colitis are the mostcommon manifestations of CMV infection in-patients with AIDS. Treatment for Cytomegalo: Three drugs-ganciclovir, foscarrnet and cidofavir arecurrently licensed for systematic treatment of CMV infection. Herpes simplex virus infection: Infection with herpes simplex virus (HSV) in HIVinfected individuals is associated with recurrent labial, genital, and peri anal lesions. As HIVdisease progresses and CD4+T cell count declines, these infections become more frequentand severe. Lesions often appear beefy red, are exquisitely painful and have a tendency tooccur high in the gluteal cleft. Treatment for Herpes simplex: The treatment for severe or recurrent HSV infectionis acyclovir. For most cases, 200mg is given orally five times per day 10 to 14 days. Conceptual study of Bhutabhishangaja Ojokshaya 42
  • 52. Varicella-zoster virus infections: Varicella-zoster virus (VZV), the etiologic agent of chickenpox, assumes a latent forma dorsal root ganglia following primary infection. Reactivation is associated with shingles theappearances of shingles in any patient fewer than 50 years of age should be an indicationfor work up of an underlying immuno deficiency, particularly HIV. Skin infections like, Warts, Dermophytes, Folliculitis, Seborrohoic dermatitis, mayoccur. Toxoplasmic encephalitis, CMV Rinitis, Cryptococcal meningioencephalitis, bizarreneurological features will occur as complications.Treatment for VZV Treatment is with acyclovir and hyper immune globulin. Most physicians choose totreat it with high-dose oral or intravenous acyclovir or oral famciclovir.Treatment of Neoplastic diseases A variety of neoplastic and pre-malignant diseases occur with increased frequently inHIV-infected individuals. They are Kaposi’s sarcoma, lymphoma and intraepithelial dysplasiaof the cervix and anus. These diseases are significant contributors to the morbidity andmortality of patients with HIV infection.Kaposi’s sarcoma Kaposi’s sarcoma is a multi centric neoplasm consisting of multiple vascular nodulesappearing in the skin, mucous membranes and viscera. Diagnosis of Kaposi’s sarcoma isbased on biopsy of a suspicious lesion.Diagnosis of HIV infection The diagnosis of HIV infection depends on the demonstration of antibodies to HIVand or the direct detection of HIV or one of its components. The standard screening test forHIV is the enzyme linked immuno sorbent assay (ELISA). This solid phase assay is anextremely good screening test; with a sensitivity of over 99.5% most diagnostic laboratories Conceptual study of Bhutabhishangaja Ojokshaya 43
  • 53. use a commercial ELISA kit that contains antigens from both HIV-1 and HIV-2 and that willdetect either. The most commonly used confirmatory test is the Western Blot. It takes advantage ofthe fact that multiple HIV antigens, having different molecular weights elicit the production ofspecific antibodies. These antigens can be separated on the basis of molecular weight, andantibodies to each component can be detected as discrete bands on the Western Blot. Anegative western blot is one in which no bands are present at molecular weightscorresponding to HIV gene products. In a patient with positive or indeterminate ELISA and anegative western blot, one can certainly that the ELISA reactivity was a false positive.List of some laboratory tests concerned to HIV/AIDS 1) Specific tests i. Serological tests by ELISA, Western blot and immunofluorescence test. ii. Antigen detection test using envelopand core proteins of HIV by recombinant DNA techniques. (HIV P24) iii. Virus isolation and culture in neoplastic T cell line. iv. Polymerase chain reaction (PCR) 2) Indirect tests a. CD4 and CD8 cell counts, reversal of CD4 to CD8 cell ratio b. Lymphopenia c. Lymph node biopsy d. Plate let count revealing thrombocytopenia e. Increased B2 microglobulinlevels Conceptual study of Bhutabhishangaja Ojokshaya 44
  • 54. Evaluation of CD4 Count: The relationship between clinical manifestations of HIV infection and CD4+T cellcount has made measurement of the latter quantity a routine part of the evaluation of HIVinfected individuals. CD4+T cells counts make a powerful set of tools for determiningprognosis and monitoring response to therapy while the CD4+T cell count providesinformation on the current immunologic status of the patient. This measurement is done byFlow Cytometry method. Patients with CD4+T cell counts below 200/ul are at high risk of infection withpreumocytis carini, while patients with CD4+T cell counts below 100/microliter are at highrisk of infection with cytomegalovirus and mycobacterium avium-intracellular complex.Patients with an initial diagnosis of HIV infection should have CD4+T cell measurementsperformed approximately every 6 months and more frequently if a declining trend is noted.At a minimum antiretroviral therapy is generally indicated when the CD4+T cell count fallsbelow 500/ul, and a declining CD4+T cell count may provide an indication for changingtherapy. Once the CD4+T cell count is 200/microliter these patients should be place on aregimen for carini pneumonia (PCP) prophylaxis. All effective forms of antiretroviral therapyto date have been associated with at least a transient increase in either CD4+T cell count.Direct measurements of HIV RNA Facilitated by techniques for the precise quantitation of small amounts of nucleicacids, the measurement of serum or plasma levels of HIV RNA has become the mostcommonly used approach for the direct detection of HIV. Two basic techniques are used thereverse transcriptase PCR (RT-PCR) assay and the branched DNA (b DNA) assay. The RT-PCR assay involves the PCR amplification of c DNA generated from viral RNA. The b DNAassay involves the use of solid-phase nucleic acid capture system and signal amplificationthrough successive nucleic acid hybridization to detect small quantities of HIV RNA. Both Conceptual study of Bhutabhishangaja Ojokshaya 45
  • 55. assays generate date in the form of number of copies HIV RNA per milliliter and is positivein >90% of patients. ALL effective forms of anti retroviral therapy to date have beenassociated with a drop in levels of HIV RNA.B2 Microglobulin levels B2 microglobulin is an 11 Kda protein that is expressed on the surface of mostnucleated cells. Free B2 microglobulin can be measured in the serum and urine. Levels ofB2 microglobulin are elevated in a variety of conditions characterized by lymphocyteactivation and / or lymphocyte destruction among these or lympho-proliferative syndromes,auto-immune diseases, and viral infections, including HIV infection.MANAGEMENT OF HIV INFECTION IN PARLANCEPrevention and controlling measures of HIV infection/AIDS At present due to absence of preventive vaccine and curative drud, prevention andcontrol is the only cure for AIDS.Counseling and Education These are of paramount importance in providing patients with optimal overall care.Patients must be educated about the potential transmission of their infection, including frankdiscussions concerning sexual practices and sharing of intravenous needles. The treating physician must not only be aware of the latest medications available forHIV infection and its complications but most also educate patients concerning the history oftheir illness and listen to their fears and concerns. Education, counseling and behavior modification are the corner stones of an HIVprevention strategy. Wide spread voluntary testing of individuals who practiced or arepracticing high-risk behavior, together with counseling of infected individuals, isrecommended. Information gathered from such an approach should serve as the basis forbehavior-modification programs, both for infected individuals who may be unaware of their Conceptual study of Bhutabhishangaja Ojokshaya 46
  • 56. HIV status and who could infect others for uninfected individuals practicing high-riskbehavior. Promotion of voluntary blood donation and universal testing of blood units for HIV Condom promotion and its accessibility Education to mother to prevent infant transmission Avoiding transmission through infected syringes and needles Early detection and prompt treatment of sexually transmitted diseasesAntiretroviral Therapy The cornerstone of medical management of HIV infection is antiretroviral therapy.Suppression of HIV replication is an important component in prolonging life. Nucleosideanalogues (reverse transcriptase inhibitors) are the ante retroviral agents. Ex, Zidovudine,Didanosine, Zalcitabine, Lamivudine, stavudine. Among them Zidovudine was the first drug approved for the treatment of HIVinfection. Patients treated with Zidovudine had increase in lymphocyte counts, includingCD4+T cell counts, declines in circulating levels of p24 antigen and weight gain. Initialstudies indicated that elevations of CD4+T cell counts from this approach.Non-nucleus reverse transcriptase inhibitors The non nucleoside reverse transcriptase inhibitors interfere with the function of theviral enzyme reverse transriptase by binding to regions outside the active site and causingconformational charges in the enzyme that render it inactive. Two members of this class, Nevirapine and Delavirdine are currently available foruse. Conceptual study of Bhutabhishangaja Ojokshaya 47
  • 57. Protease inhibitors The licensure of four separate HIV-1 inhibitors (Saquinavir, Ritonavir, Indinavir andNelfinavir) heralded a major change in the options available for antiretroviral therapy of HIVinfection. Unlike reverse transcriptase inhibitors, which interface with cellular DNApolymerases as well as inhibiting the transcriptase of HIV-1; the HIV protease inhibitors areexquisitely selective for the protease enzyme of HIV-1.Vaccines Given the fact that human sexual behavior is extremely difficult to change, the besthope for preventing the spread of HIV infection rests with the development of a safe andeffective vaccine. This task is extremely problematic for number of reasons including thehigh mutability of virus.AYURVEDIC PERSPECTIVE OF HIV INFECTION AS BHUTABHISHANGA OJOKSHAYASamannya Samprapti 71 Indulgence in above said Nidana leads to aggravation of Vata, Pitta and Kapha,ultimately it leads to Kapha kshaya. The aggravated doshas causes damage toOjovahasrotamsi leading to ojo visramsa (loss of Ojaswhen), when the further advancementof the disease process continues the Doshas vitiate Ojas, causing qualitative change inOjas. The further advancement of the disease leads to depletion of Ojas both quantitativelyand qualitatively.Vishesha Samprapti Bhootopaghata janya Ojakshaya manifests in a different manner. The infectiousorganisums (Bhoota) cause cell damage and entry of pathogen to the cell (Bootopaghata) isthe hallmark of this process. These pathogen causes srotorodha, which leads to Vatavriddhi and vitiation of other doshas. From this stage onwards the pathological processescontinue like samanya Samprapti. Conceptual study of Bhutabhishangaja Ojokshaya 48
  • 58. Bhoota + Upaghata Roga utpadaka jeevanu/vishanu, + Utpeedana Pathogenic agent +destruction HIV (in AIDS) +destruction HIV-destruction (first stage) = Ojovisramsa, (derangement with ordinary deficiency of Ojas or immunity) HIV –destruction (second) stage =Ojovyapat (Diffusive Ojas or immunity disorders), HIV- destruction (third stage) =Ojokshaya (complete loss of Ojas or immunity as found in AIDS) Results into deathSankhya Samprapti There are three types of Ojas vitiation mentioned as Ojovishramsh, Ojovyapat andOjokshaya. Even though there are explained as the types of Ojo vikriti. Practically they looklike the stage of Ojokshaya.Kriyakala in Bhutabhishanga Ojokshaya (HIV infection)Sanchaya This period starts from the point of exposure to acute condition phase which takeminimum 10 days. In this phase virus grow silently in the lympha and lympha glands. In the Conceptual study of Bhutabhishangaja Ojokshaya 49
  • 59. Rasavaha srotas and in the Rasavaha srotomoola the virus aggravate doshas to creat somesymptom which is called prakopam.Prakopam This condition generally occurs within 10 -30 days after exposure and resolves in 3-21 days. The person develops an acute flu like ill ness with a verity of symptoms and signsincluding lethargy. Malaise fever sore throat myalgio anorexia sweating orthalgia headachediarrhea nausea generalized lymph-adenopathy. This phase is called acute condition phasebecause prakupita doshas come out from their place and create abnormalities.Pasaram and stanasamsraya After prakopa doshas migrate in others path way. Then these dosha occupy placesother than their own place and circulate in channels other than their own. This stage ofdosha is called as stanasamsrayam. These two stages of doshas can consider as a symptomatic perio phase. The acutecondition phase followed by asymptomatic period, which may last up to 10 year after theacquisition of infection. During this phase patient is infective and the virus can be isolated forperipheral blood lymphocytes. The number of functions of lymphocytes sub population ishowever normal. Latest period a-symptomatic phase show some so0me signs ofopportunistic infections delayed healing of minor illness. Of course this can be considered as Purvaroopa of AIDS. During this periodprogressive weight loss, mild weakness, anorexia, generalized lymph-adenopathy, andoccasionally low-grade form etc. sign and symptoms observed.Vyakti and Bheda Presence of signs and symptoms is called Vyakti and difference from prakriti / natureis called Bhedam. These two parts of stages of Samprapti can be included in the Conceptual study of Bhutabhishangaja Ojokshaya 50
  • 60. symptomatic infection phase. After the perio latency commonly manifests with weight lossand weakness. Accelerated weight loss in an HIV infected patient is sign of disease progression. Nospecific cause of weight loss can be identified in most of the cases. Weakness and loss ofappetite are very frequently present. Fever is generally low grade may be accompanied bynight sweats and chills. AIDS patients have persistence diarrhea lasting more than onemonth as one of the major complaints. Among respiratory manifestations persistent cough of more than one month’sduration is found in majority of patients. It may be due to pulmonary tuberculosis.Pnemocytis cornii is common in western countries. In addition to these symptoms the patient with AIDS may suffer from variouscutaneous, neurological, oral manifestations as well as tumors and lymph-adenopathy.Upashayanupashaya 72 Depletion in Doshas and Dhatus as well as Ojas will make the person desire for suchfoods and drinks, which will increases the depleted one. The foodstuffs so desired are calledUpashaya. E.g. Sneha, Sheeta and Madhura Rasa yukta dravyas like milk, sugar, ghee etc.the Dravyas having opposite qualities like ruksha, Ushna, Katu and Kashaya Rasa Dravyasare Anupashaya.Vyavachedaka Nidana It is also possible that Lakshanas of Visramsa /Vyapat/Kshaya may be felt in variousother clinical conditions apart from Ojokshaya. Sannipataja Jwara, Vishama jwara.Rajayakshma and Kshata ksheena are the differential diagnosis of Ojokshaya. Conceptual study of Bhutabhishangaja Ojokshaya 51
  • 61. Samprapti ghataka Nidana- Mitya vihara, Pragnaparadha, Dosha- Three Dosha (specially Vata and Kapha) Dushya- Sapta dhatus, (Especially the Rasa, Rakta, Mamsa, and Ojas) Srotus- All srotus Srotodusti prakara- Sangha, Atipravritti, Vimargagamana Adhistana- Sarva shareera Agni- Kyaya (Jataragni, Dhatvagni) Rogamarga- Madyama rogamarga Satwa- Heena Bheda- Raktaja vyadi Vyadhiswaroopa- Chirakari Swabhava- Dharuna Sadhya-sadhyata- Anupakram Udbhava sthana- Rakta vaha samsthana Manas dosha - Raja and Tama In Prameha Nidana Charaka has explained the reasons for absence of disease andcausation of disease. According to particular features of Aetiology, Doshas (innate pathogenic factors),Dushyas (substratum of pathos) response occurs in the form of non-manifestation or otherwise of disorders. That When these three factors do not combine together, or if combined together aftera long time, or informed or with out all the said symptoms. On the contrary the result will becontrary. 73 Here the Vighata bhava as said by Charaka is innate immunity. Conceptual study of Bhutabhishangaja Ojokshaya 52
  • 62. Roopa (symptomatogy) Charaka has described the Ojokshaya lakshanas as follows 74 Bhaya beeta (frightened) Dowrbalya (severe fatigue) Abheekshna (stress full) Duschaaya (lost of luster) Ruksha (ematiated and dry) Vyatitendreeya (loss of sensory and motor functions) Durmana (sorrowful) Kshama (inability to talk)Ojovardhaka Chikitsa For the treatment of patients with HIV infection the physician requires not only acomprehensive knowledge of the disease processes, but also the ability to deal with theproblems of a chronic, life-threatening illness. Specific antiretroviral therapy andantimicrobial treatment and prophylaxis are critical measures in prolonging an acceptablequality of life. Since the disease is aggravated with the loss of immunity, the main theme of is toincrease Ojas in the body. The therapies used in Ayurveda for the same are - 1) Rasayana (Rejuvenation therapy), which restores and prevents, the loss ofmental power, the loss of efficiency of functioning of sense organs, dimension of mentalvigor, and restoring of normal balancing of three Doshas establishing the most effectiveinteraction between the seven body constituents recovering the vitality. 2) Vajikarana (Aprodiasic therapy) helps to increase the physical potency and Oja,vitality through increasing the quantity of Shukra dhatu, the last vital product of the sevenbody constituents. Conceptual study of Bhutabhishangaja Ojokshaya 53
  • 63. Modern system of medicines like Lavimisole, Interferon, Cytokines, Interleukin,Methotrexate, Cyclosorin, Gold salts. 3) Achara Rasayana and swasthavritta palana Choice one sexual partner Use of condoms during sexual penetration (vaginal, anal, or oral) Avoid sex partners who have rashes redness, sores and discharges. Stay away from casual relation ships Prevention of STDs would also reduce the risk of HIV transmission. Avoid blood transfusion as for as possible. Do not share razors, syringes, needles, and blades. Affected woman should avoid sex relation and next pregnancy. Brahmacharya palana, like avoiding sexual stimulating thicking, food, and circumstances, spiritual thinking Public awareness campaigns for HIV Anti retro viral therapy during pregnancy, delivery and postnatal 4) Bhootaghna therapy Due to decrease of immunity, different pathogens grow over the body more easilycreates different signs and symptoms in the body. Through Bhootaghna therapy, the actualcausative organism and the other organism which are helping to improve the diseaseprocess and producing different symptoms are ineffective. 5) Lakshanika Chikitsa Anti-tussive, anti diarrhea, antipyretic, digestive, etc treatment has to followaccording to clinical features. Conceptual study of Bhutabhishangaja Ojokshaya 54
  • 64. Drug Review The combinations for the evaluation in Bhutobhishanga Ojokshaya consideredare as follows in two groups. The first group patients receive Bilvadi vati fortified withAgnikumar vati called as in the trial as Ojokalpa Rasayana, collected from theSahasrayoga. The second group receives Amrita kayakalpa Rasayana a patientmedicine available from market prepared from Amrut pharmaceuticals, Hyderabad. Drug review of Bhutabhishangaja Ojokshaya 55
  • 65. Ojokalpa Rasayana The combination and proportions of Ojokalpa Rasayana is as follows: Table -1Sanskrit name Latin name ProportionBilva Aegle marmelos Three partsTulasi Ocimum santum Three partsHaridra Curcuma longa Three partsDaru Haridra Berberis aristata Three partsDevadaru Cedrus deodaru Three partsShunti Zingiber oficinalis One partMaricha Pipper nigram One partPippali Pipper longum One partAmalaki Phyluntus emblica One partHaritaki Terminalia chebula One partVibitaki Terminalia bilirica One partKaranja Pongomia glabra Three partsTagara Valerana wullichi Three partsVidanga Embelia ribes Three parts Agni kumar vatiKusta Saussurea lappaVacha Acorus calamusMusta Cyperus rotundus Three partsVatsanabha Aconitum feroxMaricha Pipper nigramAjamutra (Bhavana dravya) Goat Urine Q.S. Drug review of Bhutabhishangaja Ojokshaya 56
  • 66. Contents of Amrit kaya kalp rasayan1. .Suvarn bhasm 5mg2. Mandurabhasm 5mg3. Purnachandrodaya makardwaj 5mg4. Abhraka bhasm (100 puti) 5mg5. Lauve bhasma 5mg6. Vangabhasma 5mg7. Yashadabhasma 5mg8. Jayapala 10mg9. Jatiphala 2mg10. Vidarikanda 50mg11. Ashvaganda 25mg12. Katukia 15mg13. Punarnava 15mg14. Gokshura 15mg15. Shankpuspi 20mg16. Yasti madu 20mg17. Pippali 40mg18. Shatavari Q.S19. Milk Q.SFunction of the Amrita Kaya Kalpa rasayana compound. Immuno modulation Restorative tonic Aphrodisiac Nervin tonic and Haematinic. Drug review of Bhutabhishangaja Ojokshaya 57
  • 67. Table-2 Guna Karmas of each drug of Ojo kalp Rasayana Sanskrit name Botanical Guna Rasa Veerya Vipaka Name1 Bilva Aegle marmelos Ruksha Laghu Kashaya, Tikta Ushna. Katu.2 Tulasi Ocimum Laghu, Ruksha. Katu, Tikta. Ushna, Katu, santum3 Haridra Curcuma Longa Rooksha, Tikta, katu, Ushna. Katu. Laghu.4 Daru Haridra Berberis Ruksha, Laghu, Tikta, Kashaya, Ushna, Katu5 Devadaru Cedrusdeodaru Laghu, Snigda. Tikt katu. Ushna. Katu.6 Shunti Zingiber Guru, Ruksha Katu, Ushna, Madhura Oficinalis Teekshna7 Mareecha Pipper Nigram Laghu, Katu. Ushna. Madhura. Teekshna.8 Pippali Pipper Longum Laghu snigdha Katu. Anushna- Madhura. Teekshna. sheeta.9 Amalaki Phyluntus Laghu, Ruksha, Lavana varjit Sheeta. Madhura. Emblica Sheeta Pancha rasa10 Haritaki Terminalia Laghu, Pramati Lavana varjita Ushna, Madhura. Chebula Ruksha, Pancha rasa, lekhani,11 Bibitaki Terminalia Ruksha, Laghu Kashaya, Ushna Madhura, Bilirica12 Karanja Pongomia Laghu, Tikt, Katu, Ushna Katu Glabra Teekshna Kashay13 Tagara Valerana Laghu, Snighda Tikta, Katu, Ushna, Katu, wullichi Kashaya14 Vidanga Embelia Ribes Ruksha, Laghu, Katu Ushna, Katu. Teekshna15 Kusta Saussurea Laghu, Ruksha, Tikta, Katu, Ushna, Katu, luppa Teekshna, Madhura16 Vacha Acorus Laghu, Teeksn, Tikt, Katu Ushna, Katu Calamus Sara,17 Vatsanabha Aconitum ferox Ruksha, Laghu Madhura. Ushna, Madhura, Teekshna, Vyavai, Vikashi Yogavahi,18 Musta Cyperus Laghu, Ruksha, Katu, Tikta, Sheeta, Katu, Rotundus Grahi, Kashaya,19 Ajamootra Goat urine Ruksha, Laghu, Katu, Madhura, Ushna Madhura, Teekshna, Tikta Drug review of Bhutabhishangaja Ojokshaya 58
  • 68. Method of medicine preparation 15 drugs are there in the Ojokalparasayana, among them Bilva, Tulasi,Kharanja, are collected direct from the particular trees. Kusta, Triphala, Trikatu, Haridra,Daruharidra, Devadaru, Tagara, Vidanga, Musta, Vatsanabha, Vacha, are taken from themarket. All drugs are taken in equal quantity and cleaned properly then made in to finepowder separately. These fine powders are mixed together. This mixer soaked in toAjamootra and dried, this process has done for seven times. After drying the total drugmixer sieved by cloth by that drug made in to fine powder. That powder filled in to Gelatincapsules with quantity of 500mg. The Amruta Kayakalpa Rasayana is directly taken fromthe company.Laboratory test of Ojokalparasayana1. Loss on drying at 110oC. = 2.395% w/w2. Ash value = 7.68% w/w3. Acid insoluble ash = 0.338% w/w4. PH of 10% (w/w) aqueous solution = 55. Solubility = Highly soluble in water and Alcohol.6. Tests for Alkaloids a. Mayer’s test = Positive b. Hager’s test = Positive7. Test of CArbohydrates a. Molish test = Positive (Carbohydrate present) b. Benedict’s test = Positive (Reducing sugar present) c. Barfoedit’s test = Positive (Monosaccherides present)8. Average weight of Capsule = 0.4828 grams. Dose : 2 capsuls tid/day, after meals, Anupana : Jala Drug review of Bhutabhishangaja Ojokshaya 59
  • 69. 1) Bilva (Aegle marmelos)Synonyms:- Shandily (peedahar), Malura (increases the glamour), Sailusha,Sriphala, Gandhgarbha, Sadaphala. Granthila, KantakiChemical composition: - Musilase, Pectin, Glucose (4.6%), Tinin (9%), Mermelosin,Xanthotoxin, Umbelliferone, mermin, skimming, etc.Karma: - Kapha Vata shamaka, Pittakara, Balavardhaka, Jwaraghna, Deepana, 75, 76Pachana, Grahi, Krimighna, Ruksh,Pittatisara Grahani Kamala,77, use in debility of 78.mucuss membren Cronic dycentry and dyspepsiaResearch works- ♦ Anthelmintic activity- 79 ♦ Antidiarrahoeal activity 80 ♦ Bilva powder in Atisara 81 ♦ Bilva powder in pravathika 82. ♦ Bilva is also been used for treating giaradiasis 832) Tulasi (Ocimum santum)Synonyms: - 1. Bhootaghni, 2. Apetha raakshsi 3. DevadundubiChemical compositions: - Pale yellow green essential oil, which becomes crystallineover a period. It is called as Basil Camphor, Fenol (45.76%)Karma: - Kapha vata shamaka, Pittavarda hara, Jantughna. Demulcent Expectorent(Kasaghna) Anti periodic Anti` catarrhal Fragrant and Aromatic used in Skin diseaseItches Ring worms, Leprocy, Broncitis (Swasaghna) and Diarrhea, Swedajanana,Durgandha Nashaka. Acts on Heart and respiratory system, 843) Haridra (Curcuma Longa)Synonyms:-Krumighna, Yostipreeya, Nisa, Yositpriya, Hattavilasini, Krmighni, Pita,Kancani, Varavarnini, Gouri. Drug review of Bhutabhishangaja Ojokshaya 60
  • 70. Chemical compositions: -1% of volatile oil, Resin, Cur cumin is responsible for itscolour; Turmeric oil has a peculiar odour and taste. Curcumene, Curcumenone, curcone,curdione, cineole, cineole, curzerenone, epiprocurcumenol, eugenol, camphene,camphor, borneol, procurcumadiol, procurcumenol, curumins, ukonan A,B andD, β-sitosterol etc.Karma:- Raktashodhaka, Twagdoshahara, Shothahara, Deepana, Grahi, Kaphagna,Vatahara, Pratishyaya, Prameha, Kamala, Yakritvikara, Paryayika jwara,Netrabhishanda, Kaphaghna, Krimi, Peenasa, Pandu, Vrinaropaka, Varnya,Carminative and acts as vermicidal. 85Vyanga 86 Slipada and Dadru kustha 87Pistameha 88Research works♦ Antiseptic an ideal therapeutic agent in conditions of the biliary systems and gallbladder due to suppressed staphylococcal infection. 89,♦ Curcuma powder has been found to increase appreciably the mucin content of gastric juice in rabbits and thus may be useful in gastric disorder 90.♦ It was found that the antibacterial activity of C. longa against gram positive and gram- negative organism was less in degree as compared to penicillin and streptomycin 91♦ Anti-histamine or blockers, on isolated heart of guineapig, curcumin revealed a depressant effect 92.♦ Its anti-inflammatory activity is investigated with reference to the inhibition of activated proteases responsible for acute inflammatory process. The volatile oil of the plant was found to inhibit tryspin as well as hyaluroniadase enzymes 93.♦ 1.A clinical trial with C. longa was conduced in 114 patients of respiratory disease 94♦ The anti-inflammatory effect of volatile oil has been found to be greater than that of hydrocortisone 95.♦ Three curcuminoids (curcumin I,II, III) were compared for their cytotoxic, tumor reducing and anti-oxidant activities. Curcumin III was found to be more active than Drug review of Bhutabhishangaja Ojokshaya 61
  • 71. the other two in short term cytotoxic activity but inhibited the growth of tumor cells (L929) in culture at similar concentration (IC 50-1 µg. /ml). The curcuminooids also inhibited lipid peroxidation. The amount needed for 50% inhibition was 20,14,11 micro/ml for curcumin I, II and III respectively 96.4) Daru Haridra (Berberis)Synonyms: - Daru nisa, Pita daru, Pacampaca, Katankateri, Parjani, DarviChemical compositions: - B. Aristata – Karachine (a protoberberine alkaloid),taxilamine, berberine, palmatine, jatrorrhizine, and oxycanthine.C. Fenestratum – Berberine, berberrubine, jatrorrhizine. Palmattine, berlambine,oxypalmatine etc,Karma: - Balya, Poushtika, Deepana, Pachana, Grahi, Pittavirechaka, Jwarahara,Swedala, Shleshmaghna, Phiranga, Apachi, Rasayana, Twagdoshahara, Vishamajwara,Kupachana, Gandamala, Bhagandar, Pradar, Prameha, Pandu, Krimi, Peenasa, Meda 97Rasayana Raktagami Used in Eyes liver Spleen and skin Sveta pradara, Pistameha,Vrddhi (kaphaja), Mutrakrcchra.5) Devadaru (Cedrus deodaru)Synonyms: -Bhoota hari, Indra daru, Drukilinam, Bhadradaru, Surabhuruha, Amaradaru,Surahva, Bhadradri, Sura Kastha, Kilimam.Chemical compositions:-It contains dark colored oil and Resin Essential oil from wood;p-methylacetophenone, atlantone, sesquiterpenses (α and β –himochalene, himachaloletc); stem bark; deodarin, toxifolin.Karma: - Jwara, Jeerna, Amavata, Slipada, Jalodara, Kasa, Swasa, Atisara, Shotha,Asmari, Kushtha Hara, Kandu, Amahara, Tandrahara, Vibanda, Adman, Peenasa, Hikka,Prameha, Shleshma, Dustha vrina shodhana, Krimi, Anilahara, 98 Kasa 99 Sopha 100.Research works-♦ The alcoholic extract of the stem was found to have anticancer activity against human epidermal carcinoma of the nasopharynx in tissue culture 101 Drug review of Bhutabhishangaja Ojokshaya 62
  • 72. 6) Shunti (Zingiber Oficinalis)Synonyms:- Nagara, Srngavera, Visva, Visva bhesaja, Katubhadra, Mahousadha.Chemical compositions:-1/5%Yellow volatile oil, ginjerol, gingerin, (pungent resin)Carbohydretes, oil, and resin, is found just under the skin. Gingerol does not evoperateswith oil. α-aurcumene, β-D-curcumene, β-bourbornene, d-borneal, citral, d-caphenecitronellol, geraniol, gingerol, α and β-Zingiberences, zingiberol, zingerone, gingerols,paradol, gingerenone A, ginge glycolipis A,B, and C; (6) gingerdiol; gingerone B and CetcKarma:-Truptighna. Rochaka, Deepana, Pachana, Vatanulomana, Shopha, Arshoghna,Raktarsha, Chardhi, Agnimandya, Ajeerna, Kostavata, Udarashoola, Sandhivata,Swasa, Kasa, Hikka. Pratishyaya, Samanyanda Sannipata Jwara, Jeerna Jwara, Kushta,Pandu, Amavata, Vata Kapha hara, use in Vibhanda, Vrishya, Varnya, Vamana,Hridhya, Shoola, Slipada, Anaha,Udara, Seeta pitta, Grahani vikara, Guda keela hara,Atisaara, 102 Jaladosa 103 Pratisyaya 104, Kaphaja Arasa 105, Murcha 106Research works-♦ It has shown marked anti-inflammatory activity in rats, which is comparable to prednisolone 107♦ Stem bark extract showed significant anti-inflammatory activity in rat 108,♦ The alcoholic extract showed some significant activity against E. coli, Proteus vulgaris, S. typhimurium, Stap. Aurens and strep, Viridans 109♦ The aceton-extracts of Z. officinale, which contain essential oil and pungent principles, caused an increase in the bile secretion. It is also reported that 6 gingerol and 10 gingerol are mainly responsible for the chologosic effect of binger 110.♦ In a clinical study on Grahani roga, the effect of Z. officinale has been found significant in term of control of number of motions, improvement of body weight, appetite, Hb% etc 111. Drug review of Bhutabhishangaja Ojokshaya 63
  • 73. ♦ Acetone extract of ginger (100 mg/kg) significantly reduced serotonin (5-HT)- induced hypothermia. At 750 mg/kg it significantly inhibited 5-HT-induced diarrhea 112.♦ A single case report (42F) on migraine headache reveals the efficacy of Z. officinale in this condition 113.♦ Ginger juice produces anti-motion sickness action possibly by central and peripheral anticholinergic and antihistaminic effect 114.♦ Shunthi was put to trial on 111 patients with Ghrahani roga. The effect of the treatment was observed with in a short period. The regulation of bowel habits, improvement in general health including anemia and body weight and improvement in GL function was noted 115.♦ The antimicrobial activity of Z. officinale is reported 116.♦ The aqueous extract of ginger arrested with growth of M. tuberculosis in vivo 117.♦ Acetone extract of rhizomes of Z. officinale is attributed with the antioxidant property 118.7) Mareecha (Pipper Nigram)Synonyms:-krimihar Usana, Krsna, Dhanvantari, Dharmapattana, Vellaja, Sakanga,Chemical compositions:-The thin pungent skin of the fruit contains piperin, A volatilecompound 5.9%, an aromatic oil 1—2% and 7% fatty acids, The fruit pulp has a letterresin called chavicin, starch, oil, gum, fats 1%, protein 7%, and alkaloids 4%,Piperene, piperethine, Piperolein A and B, feruperine, dihydroferuperine,citronellol,cryptone, dihydrocarveol, α and β- pinene, piperonal, camphene β-caryophyllene, β-alanine, pipecolic acid, carotene, ascorbic acid, pipercide etc.Karma:-Switra, Kilasa, Pama, Naktandya, Krimi, Hriddourbalya, Pratishaya, Shwasa,Kasa, Shrtovrodha, Kapha vata shamaka, Shoola hara, Vrishya, use in ardita, Kusthahara. Kasa 119, Pama 120, Sthoulya 121 rahani -122 Drug review of Bhutabhishangaja Ojokshaya 64
  • 74. Research works-♦ The fruit extract respond to be inhibitory to each. Coli, Acrobactor aerogens, L casei, Staph, Faecalis, Staph, Aureus and Sh. Sonnei123,♦ The Essen. Oil inhibited vib, Cholerae, staph, Albus, C, Diphtheriae, Sh, Dyscenteriae, Pr. Pyogener, strep pyogenes etc, 124.♦ Essential oil also inhibited B. subtilis, Stap aureus, Sal, Typhi, Sal, Paratyphi and pestalotia Sp, 125,♦ Essential oil reported to be anti-fungal against Trich. Terrestre. Can. Albicans. Asp. Niger etc. 126.♦ Its insecticide activity is reported 127,♦ Piperine exhibits antibacterial and anti-tumor activities against pseudo, Aeoginosa and Alcaligenes F2518, Chem, 1288) Pippali (Pipper Longum)Synonyms:-Capala (giving instant action), Kana, Krsna, Kola, Capala, Tiksna Tandula,Magadhi, Vaidehi, Usana, SoundiChemical compositions:-Resin, Volatil oil, starch, gum, fatty oil, inorganic matter, andResin-piperin 1-2% Essential oil, mono-and sesquiterpenses, caryophyllene (mainly),piperine, piplartine, piperlogumine, piperloguminine, pipernonaline, piperudecalidine,pipercide, sesamin, β-sitosterol; foru aristolactams (capharanone B, aristolactum AII.Piperlactum A and piperolactam B); five 4,5-dioxoaporphines etcKarma:- Treedosha shamaka, Ajeerna, Aruchi, Agnimandya, Vibanda, Udarshoola,Arsha, use in Yakrit-Pleeha vikara, Krimi ,Hriddourballya, Pandu, Raktavikara, Kasa,Shwasa, Hikka, Ballya. 129,Kamala 130 Rasayana 131Chardi132. Svasa 133Research works-♦ The pellitorine type of isobutylamide was reported to exhibit significant antitubercular activity in vitro and the effect is about 20% of the potency of streptomycin 134 Drug review of Bhutabhishangaja Ojokshaya 65
  • 75. ♦ The crude extract of P. longum and piplartine suppressed the ciliary movements of the esophagus of frog. These findings suggest that its efficacy could be due to suppression of cough reflex 135.♦ A preliminary study conduced on the effect of alcoholic extract of Pippali rasayana, on serum proteins in rabbits showed a significant increase in body weight, serum albumin and globulin ratio was also observed 136.♦ The milk extract was report to increase the rate of respiratory flow 137♦ Piperene revealed a hypotensive effect in dogs and also produced a non-specific blockade of contractions induced by acetylcholine, histamine and serotonin in isolated intestine of guinea pig and rat. It also had milk antipyretic activity 138.♦ Significant effect in controlling the frequency and severity of the asthmatic attack was observed with P. longum powder in a clinical study 139.♦ The oil of P. longum fruit possessed anthelinintic activity 140.9) Amalaki (Phyluntus Emblica)Synonyms:-Amruta, Vrushya, Rochani, Kayasta. Abhaya, Amrta, Dhatri, Vayastha,Vayassya, Vrsya, Tisyaphala, Sitaphala.Chemical compositions:- Fruit – Vit. C, phyllemblin, linolic acid, indole, acetic acid andayxubsm trigaloylglucose, terchebin, corilagin, ellagic acid, phyllemblic acid and salts.Karma: -Dourbalya, Kshaya, Shotha, Shwasa, Kasa, Kusta, Visarphara, Soma roga141 Prameha 142 Hikka 143Research works-♦ Anti-microbial activity- Emblica fruit found to have very potent anti-bacterial activity 144♦ Isolation of anti-microbial substace phyllemblin from the stem-gall callus is reported 145♦ Antioxidant activity- the long-lived belief that the therapeutic effect of Amla is due to its rich vitamin C (L-ascorbic acid) content has thus been dispelled. The patent vitamin C-like activity (antioxidative effect against reactive O2 species, Ros) of Amla Drug review of Bhutabhishangaja Ojokshaya 66
  • 76. fruits has now been located in the Low Mr (Mol. Wt. Less than 1000) hydrolysable tannins. Four such compounds, emblicanin-A (1), emblicanin- B (2), puniglucomin and penduculgin, have been isolated from the fruit pericarp 146.♦ Hepatoprotective activity- Dry powdered pulp of fruits (1.0g/kg) reduced the levels of serum, aortic and hepatic cholesterol significantly in rabbits 147.♦ Rasayana activity – Amalaki Rasayana is said to have growth promoting effect (growth and longevity). The drug has no significant effect on the levels of serum protein fractions, yet it raises the total protein level and increases the body weight. The study also indicates that the increase in body weight is due to a positive nitrogen balance 14810) Haritaki (Terminalia Chebula)Synonyms: - Amrta, Abhaya, Kayastha, Vayastha, Pathaya, Vijaya, Siva, Jaya,HaimavatiChemical compositions: -Gylic acid, Tinic acid, Niryas, Sharkar, albumin, calcium,vitamin –C, Fruits- anthraquinone glycoside, chebulinic acid, tannic acid, terchebin,vitamin C. Fruit kernel – arachidic, behenic, lindeic, oleic, palmitic and stearic acids.Karma: -Tridoshahara, Mukharoga, Arsha, Kamala, Yakrit Pliha, Krimi, Balapradhan,Raktavikara, Pratishaya, Kasa, Swarabheda, Hikka, Kustha, Visarpa, kamalahara, 149,Twagsdoshhara, srotogamitva, vatanulomini, Medhya, Vatarakta hara, klibhya haraAjirna, Prameha, Amlapitta, Upadamsa.Research works-♦ Study of in vitro antibacterial activity of extracts from the plants of T. chebula, E. Alba and O. sanctum was carried out by the disk diffusion technique. All showed such activity against human pathogenic Gram positive and Gram-negative bacteria. The activity against Salmonella organisms was shown only by T. chebula; against shigella organism by T. chebula and E. Alba, but not by O. sanctum. The widest spectrum of antibacterial activity was shown by T. chebula. It was also most potent 150 Drug review of Bhutabhishangaja Ojokshaya 67
  • 77. ♦ Various extracts prepared from the powdered fruits have been wide antibacterial and anti-fungal spectrum 151.♦ It also inhibits growth of E. coli, the most common organism responsible for urinary tract infection 152.♦ Ether extract showed higher antioxidant activity than BHA and BHT. Acid esters present in phenolic fraction of extract were found most effective 153,♦ 46 children with diarrhea wee given T. chebula and T. vulgare decoction. 57.17% children were cured within 3 days of treatment 154.♦ Antioxidant property of T. chebula is reported. Alcoholic extract 10-20 fg/ml markedly inhibitd lipid peroxidation of mouse liver and lung homogenate and mitochondria. The above extracts effectively scavenge the oxygen free radical produced by Vβ2 plus light, and inhibit H2o2-induced red cell heamolyses. 20 fg/ml of extract significantly inhibited chemiluminescene of human leukocytes induced by TPA (20ng/ml). The extract (50fg/ml) also prevented DNA breaks of human leukocytes induced by TPA and cigarette smoke condensate 155.♦ T. Chelaula inhibited HIV-1 proteas activity at a concentration of 25 microg/ml in the flurogenic assay 156.♦ Aqueous extract of T. chebula (64-128 microg/ml concentrations) exhibited the most prominent anti HBV activities 157.11) Bibitaki (Terminalia Bilirica)Synonyms:- Aksaphala, Kalidruma, Karsaphala,Bootawasa, (animals take shelterin itsshadeChemical composition :-In fruit—Tinin 21.4%, B-sitostiral, Gylic acid, Eligic acid, Ethilgylate, Chebulagic acid, Minital, Glucose, Gylactose, Fructose, Rimanose, In pulp –38.6%, greenish colored oil is present, Fruits – Fructose, galactose, glucose, mannitol,rhamnose, β-sitosterol Drug review of Bhutabhishangaja Ojokshaya 68
  • 78. Karma: -Kapha pitta hara, Bhedhanam, Kasanashanam, Netrya, Keshya, Kriminashsana, Trisna-Chardi hara, Rasa, Rrakt, Mamsa, Medhaja dosham hanti, Madakara.158 Svitra, Asmari, Kasa and Svasa, AtisaraResearch works-♦ Out of 93 cases of cough and astma treated with T. bellerica, 22 showed complete relief, 27 were significantly relieved, while 35 cases were moderately relieved. The drug exhibited bronchodilatory, antispasmodic and antiasthamatic activities 159♦ The HIV-1 protease (PR) inhibitory activity was determined by using the fruit peal methanol extract 160♦ T. Bellerica showed significant activity against both gram positive and gram-negative bacteria. In addition it showed anti-fungal activity also 161.12) Karanja (Pongomia Glabra)Synonyms: - Karaja, Cirabilvaka, Naktamala, Gucchapuspaka, Ghrtapura, SnigdhapatraChemical compositions: - Fruit is having Pongamia oil 27-39%, Karangin, which isJantughn, is present. Pongamol. Karanjin, pongapin, 3-methaoxypongapin,pongaglabrne, kanjone, pongol, gamatin, lonchocarpin, isolonchocarpin, karanjachromene, porgachromene, isopongaflavone, pongamol, glabrin, ovalitenone, kanugin,cemethoxykanugin, pongamin, neglabrin etc.Karma: - Kustaghna, Amavataghna, Krimighna, Vrinaropaka, Kasahara, Pachana,Kanduhara, Parashrayi jeevanu nashaka, Dadru, Pama, Vicharchika, Visarpa Hara, Antiseptic, Used in Atisara Ama, Bhagandara, Raktarsha, Vidhradi.Kai 162, Granthi, visarpa,Romasanjanana, Rakta Pitta.Research works-♦ The essential oil from leaves showed marked in vitro antibacterial activity against B. antharcis, Ps. Mangiferae, sal. Typhi, B mycoides, B pumilus, Esch Coli, Sar, Lutea, Stap, Aureus, Staph, Albus etc. 163.♦ The oil of P. pinnate showed antibacterial activity against several organisms’ 164 Drug review of Bhutabhishangaja Ojokshaya 69
  • 79. ♦ Karanjin showed good antibacterial activity against M. tuberculosis H 37 Rv, leading to complete inhibition of the growth of the organism at a concentration of 10 ppm. 165♦ The essential oil from P. Pinnata showed mild anti-fungal activity 166.13) Tagara (Valerana wullichi)Chemical compositions:-Valrianica acid present,Karma: - Used in neurosis and Vatahara, Raktavisarana, Vatanadi, uttejaka,Chetanakaraka, Swapakaraka, Vatanulomana, Vedanastapaka, Vranaropaka,Apatantrakahara, Atatvabinivesha hara, Anti spasmodic Epilepsy 167.14) Vidanga (Embelia Ribes)Synonyms:-Jantu nashana, Jantughna, Krmighna, Citra, Tandula, Amogha, Vella,Kairali, Tandula, Jantuhantri, Gahvara.Chemical compositions:-Acid 2.5%, volatile oil, Stable oil coloring agent, tannin, resin,Cristebin, kshara.Karma: - Vata Kapha hara, Krimi hara, Carminative, Shoola, Aadmana, Udara, Shlesma,and Use full in Agni mandya, Aruchi, arsha. 168,15) Kusta (Saussurea luppa)Synonyms:- Utapala, Kasmira, Vapya, Gada, Agada, Ama, Amauya, Kapalam,Kouberam, Japyam, Tvakdohsa, Divya, Durnama, Padmaka, Paribhavya, Pakala,Paribhadraka, Manusanjaka, Ramam, Ruk, Rogahva.Chemical compositions: - Root contains 1.5%aromatic oil, Glucoside, Saussirin salt,Tannin, Insulin 18%, Stabel oil, Nitrate, Glucose, Roots yield 3.5% ash. It contains largequantity of manganese. Essential oil, costol, taraxas-terol, costunolide, dehydrocostuhactone, alpha cyclocostunolide, sitosterol, sesquiterpenes, Ar-curcumene,isodihydrocostuslactone, costus-lactone etc 169Karma:- Vata kapha hara, Shukrala, Visarpa, Kasa, Kustha, Hikka, Jwara, Unmadaand Apasmara, 170 Sirahsula 171 Medhya Rasayana 172. Drug review of Bhutabhishangaja Ojokshaya 70
  • 80. Research works-♦ Kokate established anthelmintic activity of S. lappa, in 1986.♦ Two active component costunolide and Dc hydrocostus lactone, show strong suppressive effect on the expression of Hepatitis B surface Antigen (HBS Ag) in human hepatoma Hep 3 B cells, but have little effect on the viability of the cells. Both fractions suppress HBSAg production by Hep 3 B cells in a dose dependent manner with IC 50s of 1.0 and 2.0 micro H respectively. 173.16) Vacha (Acorus Calamus)Synonyms:-Rakshogni, Ugra gandha, Golomi, Sataparvika, SandgrandhaChemical compositions:-Rhizome bark has1.5—3.5% volatile oil which containsAcorin, Eugenol, Asarone, Caffeine, and some amount of astringent matter are presentin Vacha. Acolamone, acorenone, acorgermacrone, acoramone, acorone, cis and trans-asarone, β and ofasarone, azulene, cadalene, calacone, calacorene, calamene,calamenol, calamone, calamenone, calamenene, calarene, β- gurjunene, caphene,eugenol, telekin, preisocalamendiol, acoric acid, calamen diol, calamenone etc.Karma:-Vata Slesm hara, Ruja, Krimi, Shakrun-mootra vishodani, Buddi vivardanam,Apasmara Hara, Mukha roga hara. 174Amalapitta 175 Apasmara 176, Sopha and Vrddi 177.Research works-♦ Volatile oil from roots inhibited the growth of M. tuberculosis in a concentration of 10µg /ml. it also inhibited the growth of gram-negative organisms in a concentration of 0.4-0.6 mg/ml. the LD 50 for guinea pigs was found to be 0.6275 ml/100g body weight 178.17) Vatsanabha (Aconitum ferox)Synonyms – Amrutam, Ugravisha, Garalam, Nagam, Nabhi, Mahoushadha,Amruta.Pranaharam, Maranam, Mahoushadham, Visham, Stokakam, Sthavaradyam, 179-187Vatsanagam, Drug review of Bhutabhishangaja Ojokshaya 71
  • 81. Chemical compositions: Aconitine (toxin) Picroeconine, Benzoil, Econine andHomonepelin. A. Ferox – Roots contain toxic alkaloids, pseudoaconitine along with 188,bikhaconitine, chasmaconitine, indaconitine veratoryl pseudoaconitine and diacetylpseudoacontitine (Manske and Rodrigo, 1979). Two new alkaloids –2 –(IH)- quinolinoneand 3,4- dihydro-6-hydroxy – 2 (IH)- quinolone189. A new diterpenoid alkaloid 14-0acetylsenbusine A; Vakognavine, Chasmaconitine, crassicauline A. falconericine,bikhaconine, pseudoaconine, neoline, senbusine A. neoline, senbusine B, isotalatizodine 190.and aconine are reported Four lipoalkaloids viz., liposeudo aconitine,lipoyunaconitine. Lipoindaconitine and lipobikhaconitine; and four-aconine viz., veratroylpseudaconine, anisoylyunaconine, benzoylindaconine and varatory ibikhaconine arealso reported 191.Karma: -Vata Kapha hara, Pranadai, Rasayanam, Brimhana, Veery vardhana, Kustha, 192.shotha, Vishanashnama, Agni mandy, Swasa, Plihodhar, Jwara, Madhu meha, Thewrithing response induced by acontine has been used for the measurement of analgesicactivity. The characteristic pattern of aconite-induced writhing response in albino micehas been found to be similar to that induced by bradykinin. Acontine-induced writhingresponse was found to be quicker than that induced by bradykinin, it lost for a longerperiod and was consistently observed at 2 mg dose level. Analgesic agents 193 blockedthe response.18) Musta (Cyperus Rotundus)Synonyms: - Krodesta, Hima, Sugandhi, Varida, Gundra, Gangeya, Ghana, Megha,Abda, Krodesta, Hima, Sugandhi, Varida, Gundra, Gangeya, Ghana, Megha, Abda.Chemical compositions: -Cineol (+) copadiene, capaene cyperen I and II, cyperenone,isopatchoulenone, cyperotudone, cyperol, cyperolone, α-cyperone, copaene, cyperen Iand II, cyperenone, isopatcoulenone, cyperotundone, cyperol, cyperolone, αcyperone,(+) epoxyguaiene, isocyperol, isokobusone, kobusone, muystakon,e patchulene, (+)rotundone, αand β-selinene, sugenul, β-sitosterol etc. Drug review of Bhutabhishangaja Ojokshaya 72
  • 82. Karma: - Kapha Pitta Shamaka, Deepana, Pachana, Jwara, Aruchi, Jantughna,Atisaraghni, Trisna hara, Sangrahi, 194 Jvara 195Atisara 196 Halimaka 197.Research works-♦ Except cyperone other fraction like cyperene II, cyperol and I have shown anti- bacterial activity against a number of the organisms (More specifically against staph. Urens) 198.♦ In a study C. rotundus is found to be more useful in GI conditions like amoebiosis and giardiosis 199.19) Ajamootra (Goat urine)Synonyms: -Bastasya mootra,Karma: -Treedoshagna, Alpa Vatakara, Shoola, Gulma, Visha, Shvasa, Kasa,Nadivikara, Vishavikara, Kamala, Pandu, Shosha hara, Pleeharoga, Udararoga hara, 200. Drug review of Bhutabhishangaja Ojokshaya 73
  • 83. Materials and methods The recent entry to the list of grave diseases is AIDS (Acquired Immuno deficiencySyndrome), which is caused by Human Immuno deficiency Virus (HIV). It is a seriousdisorder of the immune system, in which the body’s normal defense against infection breaksdown, leaving it vulnerable to host of life threatening infection including unusual 201malignancies . A long healthy life has been the cherished wish of man since ages, butoften many challenges are posed to this in the form of grave diseases. Ayurveda is able toprovide good health care by effectively managing the diseases from time to time 202. Ayurveda describes a number of drugs with the proven or proposed immuno 203modulating and immuno potentiating activities . Recent findings of anti-viral activities ofmany herbs have drawn the attention of the scientists to study the effect of Ayurvedic drugsin HIV infection. A number of herbal drugs have been individually evaluated in the treatment 204of HIV and AIDS related complex (ARC) . According to estimation the number of peopleinfected by HIV would have crossed 50 million and till now there were 12 million deaths dueto AIDS in entire world. In India since the detection of HIV infection in 1986, the epidemic Materials and Methods of Bhutabhishangaja Ojokshaya 74
  • 84. has been frankly out of control. As of now an estimated 4 to 6 million HIV infected cases arepresent in India. The present study is designed to assess the therapeutic effect of OjokalpaRasayana in HIV infected patients, which could be a safe, effective and economical drug 205and compared with the market available Amrut Kaya Kalpa Rasayana , which claims asimmuno-modulator. Ojas is the essence of all Dhatus and also called as Bala, which is responsible for 206Vyadhikshamatva or immunity against infections . The condition in which Ojas getsdepleted is called Ojokshaya. Susruta explained the stages of the depletion of Ojas as Ojo-visramsa, Ojovyapat and Ojokshaya 207. Ojokshaya can be defined as qualitative andquantitative lessening of Ojas. Ojas, the essence of all Dhatus, controls the vital functionsand immuno regulation. It is classified in to two types i.e. Para and Apara, out of whichAstabindu (Para) Ojas is depleted by the infection 208. The symptomatology of the HIV infection resembles that of Ojokshaya. Clinicalstages of HIV infection is classified in to five stages on the basis of CD4 count. The antiretro-viral drugs available now, act at different levels of the stages of the life cycle of HIVand the combination therapy of them has shown to prolong the life span and to decreaseopportunistic infections and to increase CD4 cells count. Ojokalpa Rasayana is an herbo-mineral compound rationally formulated on thebasis of Immunomodulatory effect, Antiretroviral and Antioxidant properties, Krimiharatwai.e. germ (Virus) killing property along with Rasayana (Tissue nourishment). Individual and 209cumulated properties of yoga is carefully thought about from Bilwadi vati of 210Sahasrayogam added with Agnikumaravati (Sahasrayogam), which is a jwarahara andBhuta (Virus) vishahara. Materials and Methods of Bhutabhishangaja Ojokshaya 75
  • 85. Objectives of the study1. To evaluate the efficacy of Ojokalpa Rasayana and Amrut Kayakalpa Rasayana in improving the clinical status of Ojokshaya with special reference to HIV infection2. To assess the role Ojokalpa Rasayana and Amrut Kayakalpa Rasayana on CD4 cell count, which is a marker of stages of the HIV infection along with viral load.Source of dataa) Literary: Literary aspects of the study will be collected from standard Ayurvedic texts, magazines and journals. The information regarding the disease will be updated from Internet search along with authentic textbooks.b) Drug: Ojokalpa Rasayana The ingredients of Ojokalpa Rasayana will properly identified. The standard manufacturing guidelines will be followed for the preparation. The combination and proportion of Ojokalpa Rasayana is as follows. 1. Bilwa (Aegle marmelos) 211 1 Part 2. Tulasi (Ocimum sanctum) 212 1 Part 3. Karanja (Pongamia glabra) 213 1 Part 4. Tagara (Valeriana wallichii) 214 1 Part 5. Devadaru (Cedrus deodara)215 1 Part 6. Haridra (Curcuma longa) 216 1 Part 7. Daruharidra (Berberis aristata) 217 1 Part 8. Triphala (three Myrobalams) 218 1 Part 9. Trikatu 219 1 Part 10. Vidanga (Embelia ribes) 220 1 Part 11. Agnikumara vati 221 1 Part Materials and Methods of Bhutabhishangaja Ojokshaya 76
  • 86. 222 The combination and proportion of Amrut Kayakalpa Rasayana is as follows. Swarna Bhasma 1 mg Makaradhwaja 2 mg Abhrak Bhasma (100puti) 5 mg Loha Bhasma (100puti) 5 mg Vanga Bhasma 5 mg Yashada Bhasma 5 mg Moti pisti 5 mg Kanta loha Bhasma 5 mg Swarnamakshika Bhasma 5 mg Jayaphala 10 mg Shankhapushpi 20 mg Ashwagandha 25 mg Vidarikanda 50 mg Katuki 15 mg Punarnava 15 mg Gokshura 15 mg Yastimadhu 20 mg Pippali 40 mg Milk Q.S. Shatavari Kashaya Q.Sb) Patients: Patients with Ojokshaya (HIV +ve) will be selected from O.P.D. of Post Graduation and Research center of Sri D.G.M. Ayurvedic medical college & Hospital, Gadag by preset inclusion and exclusion criteria. Materials and Methods of Bhutabhishangaja Ojokshaya 77
  • 87. The patients are included in the study after obtaining the informed consent. The identity of all the patients are kept confidentially. All Patients undergone individually and couples together for special counseling sessions before and after serological investigations and periodically during the course of treatment. Special instructions / advice given to patients: To stop smoking alcohol and other habits which can super impose infections or troubles systemic. Not to indulge in strenuous work / exercise. Not to take any other medication except the trail medication. Not to indulge in sex with life partner and also extra marital. To consume nutritious food Avoiding out side foodMethod of collection of data a) Research design: As this disease is a grave condition & of high mortality rate and there is no clinical evidence available for this particular yoga a prospective open clinical trial was conducted. All the patients received the same medicine. Even though a total of 25 patients were screened during this period, 20 patients were taken for the study. A detailed pro-forma was prepared for case taking. b) Sample size: A minimum of 20 patients c) Exclusion criteria: 1. Patients below the age of 20 years and above the age of 50 years, pregnant and lactating women will be excluded from the study. Materials and Methods of Bhutabhishangaja Ojokshaya 78
  • 88. 2. The patients having diabetes mellitus and other systemic diseases will be excluded and the patients with concomitant therapy will be excluded. d) Inclusion criteria 1. The patients with the HIV infection diagnosed by serological test and Western blot method will be taken in the study. 2. CD4 count ranging from 200 to 500/cu.mm. 3. Karnofsky Performance score 50 and above. 4. The patients are selected irrespective of Sex and race based on the clinical signs & symptoms other than that of exclusive criteria, e) Posology: 3-gm/24 hours or 50mg/Kg-body weight in divided dose orally f) Study duration: 120 days g) Follow up period: 60 days h) Assessment of result: subjective as well as objective parameters are assessed. 1. General health condition (Grade) 2. Karnofsky performance score 3. Body weight. 4. Total WBC count. 5. Total count platelets. 6. Total count lymphocytes. 7. Erythrocytes sedimentation rate. 8. CD4 cell count 9. CD8 cell count. 10. CD4 : CD8 ratio Materials and Methods of Bhutabhishangaja Ojokshaya 79
  • 89. For the assessment grades were fixed depending upon the condition. Overall assessment is made taking into consideration both subjective and objective parameters. Considering all the above parameters patients are graded in to four groups depending upon the response to Ojokalparasayan. The over all score was considered as 10 based on the subjective and objective parameters excluding the dosha and ojas assessment. An exclusive assessment is made for the Ayurvedic aspect. Out of 10 scores depending upon the score of individual patient the grading was done as follows: Grade Score range Best responded 8 to 11 Moderately responded 5 to 8 Responded 2 to 4 Static / Not responded 0&1 i) Criteria for considering for dropouts: Inability to attend two successive follow-ups. Discontinuing medication for more than five days j) Criteria for withdrawals: Deterioration of condition, which needs hospitalization Subsequence diagnosis of Aids related complications (ARC)Investigation required for the Ojokshaya All the patients were screened for HIV infection by using ELISA method. For theassessment of HIV status all the patients were investigated, for CD4 cell count, erythrocytesedimentation rate, random blood sugar and total lymphocyte count total platelet count. CD4 Materials and Methods of Bhutabhishangaja Ojokshaya 80
  • 90. cell count assay is conclusive of CDB cell count, total platelet count. CD4 cell count assay isinclusive of CD8 cell count also. All the investigations are repeated after three months of trailmedication. Those patients who had respiratory system symptoms were investigatedradiological. 1. Screening tests : Tri-dot 2. Confirmatory tests : Western Blot 3. Other tests : CD4 cell count - surrogate marker 223 : Erythrocyte Sedimentation Rate : Haemoglobin % : Random Blood Sugar : Total Leukocyte Count : Total platelet count : Total Lymphocyte Count : X-ray Chest (if necessary) : Viral load 224 (subjected to the condition of availability) Materials and Methods of Bhutabhishangaja Ojokshaya 81
  • 91. In this clinical study a total of 26 patients were reported either with known HIV status. Those who indulged in risk factors of HIV infection also reported. Outs of all patients were serologically diagnosed as having HIV infection. HIV status and intake of concurrent therapy, A total of 18 patients were enrolled in this study as they fulfilled the inclusive criteria. Out of these 26 patients 8 patients dropped out, during the trial study for various reasons including subsequent diagnosis of opportunistic infections. Remaining 18 patients have completed the total treatment schedule and follow up. ♦ Total patients reported 26 ♦ Serological test positive 26 ♦ Excluded 8 ♦ Initially included 8 ♦ Withdrawal 0 ♦ Finally included for study 18 (9 patients in each group) Each and every data pertaining to every patient was recorded in a well-designed case taking perform. The final data is divided into 3 sections for better analysis and convenience of observation.1. Data related to demography2. Data related to disease3. Data related to response to Ojokalparasayana and Amruta kayakalpa Rasayana. Observations and Results Bhutabhishangaja Ojokshaya 82
  • 92. 1) Age group incidences Table-3Sl no Age (Years) GROUP -1 GROUP -2 Number of % Number of % patients patients1 20-30 7 77.77 5 55.552 31-40 1 11.12 4 44.453 41-50 1 11.12 0 0 Total 9 9 Maximum patients with ailment were found in 20-30 years group i.e. 7 (77.77%) ingroup-1 and, (55.55%) in group-2. 31-40-age interval in-group-1 patients are 1 (11.11%) and4 patients (44.44%) in group-2. And 41-50 age group observed with 1 patient (11.11%) ingroup-1 and no patients’ in group-2 (0%). The data collected in the trail resembles withinternational observations of HIV incidences in different age groups. Graph -1 8 7 7 6 5 5 4 4 3 2 1 1 1 0 0 GROUP-1 20-30 31-40 41-50 GROUP-2 Observations and Results Bhutabhishangaja Ojokshaya 83
  • 93. 2) Sex ratio incidences Table -4Sl no Sex GROUP-1 GROUP-2 Number of % Number of % patients patients1 Male 6 66.66 6 66.662 Female 3 33.33 3 33.33 Maximum patients in this study are men and male verses female ratio is 2:1. This iscontradictory to the Indian data sex incidence. Which 1:1 this various can be due to the maledominance in the local society with rural and illiteracy background. This observationsuggests that the lack of freedom and social stigma for female in India. Graph -2 10 8 3 3 6 4 Female 6 6 Male 2 0 GROUP-1 GROUP-2 Observations and Results Bhutabhishangaja Ojokshaya 84
  • 94. 3) Diet incidences Table -5Sl no Parameters GROUP-1 GROUP-2 Number of % Number of % patients patients1 Vegetarian 0 0 0 02 Mixed diet 9 100 9 1003 Total 9 9 In the study incidence among people of two different food habits, it was interesting tonote that all the patients (100%) consume mixed diet. But is also interesting to note that noteven a single vegetarian subject was seen in this study. As Ayurvedic concept speaks aboutthe role of predisposing factors, there must be a physiological or psychological impact ofnon-vegetarian food that may be having a role to play in high incidence of HIV among non-vegetarians populations. And in further it was observed that patients who avoid non-vegetarian food during treatment improved a lot and deteriorated as they start consumptionof non-vegetarian food. Graph -3 10 8 6 9 9 Mixed diet 4 Vegetarian 2 0 0 0 GROUP-1 GROUP-2 Observations and Results Bhutabhishangaja Ojokshaya 85
  • 95. 4) Religion incidences Table -6 Sl no Religion GROUP-1 GROUP-2 Number of % Number of % patients patients 1 Hindu 7 77.77 9 100 2 Muslim 2 22.23 0 0 3 Christian 0 0 0 0 4 Others 0 0 0 0 5 Total 9 9 An attempt was made to know the incidences in deferent religions groups. 7patients of study for group-1 (77.77%) and all 9 patients (100%) in-group –2 are Hindupatients attended. 2 patients reported (22.22%) as Muslim in group-1. This may be due toreligion ratio of local population or as earlier discussed more of non-vegetarianconsumption. On the contrary there is a study that claims less incidence of sexuallytransmitted disease in subjects who under went circumcision 225. Graph –4 10 9 8 7 6 4 2 2 0 0 0 0 0 0 GROUP-1 du m n s GROUP-2 er tia li in us th ris H O M Ch Observations and Results Bhutabhishangaja Ojokshaya 86
  • 96. 5) Economic incidence Table –7 S. No ECONOMIC GROUP-1 GROUP-2 STATUS Number % Number % of patients of patients 1 Poor 3 33.33 4 44.44 2 Middle Class 5 55.55 5 55.55 3 Higher Middle 1 11.11 0 0 4 Higher 0 0 0 0 5 Total 9 9 The maximum patients were in middle class 5 patients (55.55%) in each group of 1and 2. Economically poor or B.P.L. patients are 3 (33.33%) and 4 (44.44%) in groups 1 and2. Very less i.e. only one patient (11.11%) reported in higher middle class of group-1. Itdoesn’t reveal the clear status of economical status verses infection because the study wasmade at district level and that too in small sample. It also reflects the easy acceptance ofinfection to middle class and B.P.L. Class patients, as they are economically not strong toconsume immuno-potent food. Graph –5 6 5 5 5 4 Poor 4 3 Middle Class 3 Higher Middle Higher 2 1 1 0 0 0 0 GROUP-1 GROUP-2 Observations and Results Bhutabhishangaja Ojokshaya 87
  • 97. 6) Occupational incidence Table - 8Sl no OCCUPATION GROUP-1 GROUP-21 Sex Worker 0 0 0 02 Driver 1 11.11 0 03 Businessman 2 22.22 2 22.224 Service / Agriculture 3 33.33 4 44.445 Student 0 0 0 06 House wife 3 33.33 3 33.337 Total 9 9 In this study of incidence of HIV infection is in people of different occupation, it wassurprising to note that maximum 11% drivers, 22% business, 33.33% and 44.44% of service/ Agriculture, in both 1, 2 group respectively. 33.33% house wives in-group 1 and 2. This isan alarming signal for developing countries because they have high-density labourpopulation. Graph - 6 Sex W orker 5 Driver Businessman 4 4 Service 3 3 Student 3 3 House wife 2 2 2 1 1 0 0 0 0 0 0 GROUP-1 GROUP-2 Observations and Results Bhutabhishangaja Ojokshaya 88
  • 98. 7) Marital status incidence Table - 9Sl no Marital Status Group-1 Group-21 Married 8 82 Single 1 13 Divorced 0 04 Widower 0 05 2 Or 3 Marriages 0 06 Total 9 9 It is observed that the extramarital affairs are more in the married people. Neitherdivorced nor widowers are reported with the HIV infection. In the study related to disease,maximum number of male patients (100%) got the infection from heterosexual contact. Thisdata coincides with the international data. Women usually come in contact with diseasethrough their husbands. Even though the incidence charges are more among the patientswho got it from blood transmission or intra-venous injections, in almost got it withheterosexual contact. It evidential for the high risk unsafe heterosexual practices in India. Graph -7 9 8 8 8 7 Married 6 Single 5 Divorced 4 W idower 3 2 Or 3 Marriages 2 1 1 1 0 0 0 0 0 0 0 Group-1 Group-2 Observations and Results Bhutabhishangaja Ojokshaya 89
  • 99. 8) Source of infection Table - 10Sl Infections Before After Before Afterno1 Anashana 7 0 3 02 Alpashana 8 0 4 03 Rooksha 5 0 4 04 Ahara 0 0 1 05 Pranita Ahara 6 0 4 06 Vatatapa Sevana 5 0 6 07 Ati Vyayama 8 0 6 08 Ati Vyavaya 0 0 5 09 Shonita Ativartana 6 0 1 010 Hetero Sexual 9 0 9 011 Prajagar 4 0 5 012 Kapa 5 0 2 013 Shoka 6 1 6 014 Chinta 9 0 8 015 Bhaya 6 0 5 116 Bhootopaghata 9 9 9 91) Anashana 7 (77%) and 3 (33%), 11) Shokha 6 (66%) each,2) Alpashana 8 (88%) and 4 (44%), 12) Chinta 9(99%) and 8 (88%),3) Rooksha Ahar 5 (55%) and 4 (44%), 13) Bhaya 6 (66%) and 5 (55%),4) Pramita Ahara 0% and 1(11%), 14) Bhootopaghata 9 (100%) seen in each5) Vataatapasevan 6(66%) each, group,6) Ativyayama 5 (55%) and 6 (66%), 15) Among these Vataatapasevan 1(11%),7) Ativyavaya 6(66%) and5 (55%) Shokha 1(11%) Bhootopaghata8) Shonitaataitavartana 0 and 1 (11%), 9(100%) are continued in group 1 and9) Prajagar 4 (44%) and 5 (55%), Bhya 1(11%) Bhootopaghata 9 (100%)10) Kopa 5 (55%) and 2 (22%), is continued in-group 2. Observations and Results Bhutabhishangaja Ojokshaya 90
  • 100. 9) Chief complaints Table -11 GROUP-1 Group-2Sl, no Complaints Before After Before After1 Loss Of Weight 5 0 5 02 General Weakness 9 0 8 03 Loss Of Appetite 1 0 5 04 Fever 9 0 7 05 Inertia of the Body 5 0 5 06 Loss Of Complexion 1 0 2 07 Emaciation 7 0 4 08 Looseness Of Joints 3 0 3 09 Somnolence 2 0 2 010 Delirium/Conversion 0 0 0 0 Urethral Disease, Genital Ulcer, Genital Warts, Vegetal Candlings, Drowsiness,Acne Valerian are not Seen At Any Cases. In group-1, two patients and in group-2, 1 patientis not responded, in the symptoms of oral thrush, and 1 patient of group-1 is not respond inWhite tongue. 1) Loss of weight 5 (55%) in each group, 2) General week ness (Glani) 9 (99%) and8 (88%), 3) Loss of appetite (Aruchi) 1(11%) and 5 (55%), 4) Fever (Jwara) 9 (99%) and 7(77%), 5) inertia of the body (Stabda gatrata) 5 (55%) each. 6) Loss of complexion,(Vyatitendriya) 1 (11%) and 2 (22%), 7) Emaciation (Mamsakshaya) 7 (77%) and 4(44%),8), 8) Looseness of joints (Sandhivislesha) 3 (33%) each, 9) Somnolence (Anidra) 2(22%)each, 10) Delirium/ convulsions (Pralapa) 0% in each group found respectively. Aftertreatment these symptoms are not seen in both groups. Observations and Results Bhutabhishangaja Ojokshaya 90
  • 101. 10) Associated complaints Table -12 Group 1 Group 2Sl, No Complaints Before After Before After1 Oral Thrush Vomiting 9 2 4 12 Bleeding Gums 1 0 2 03 Pain Abdomen 1 0 4 04 Dysphasia /Sore Throat 5 0 2 05 White tongue 4 1 3 06 Hairy tongue 3 0 0 07 Cough 3 0 4 08 Blood With Sputum 0 0 1 09 Breathlessness 2 0 1 010 Headach 5 0 4 011 Skin Eruption 1 0 1 012 Morlascum 1 0 0 013 Herpes Zoster 1 0 1 014 Giddiness 5 0 4 015 Palpitation 2 0 5 016 Burning Micturation 2 0 0 017 Diarrhea 3 0 3 018 Anal Itching 0 0 1 019 Cymphodenites 1 0 1 0 Observations and Results Bhutabhishangaja Ojokshaya 91
  • 102. 1) Oral thrush/ Vomiting/ Nausea 9 (99%) and 4 (44%),2) Bleeding gums1 (11%) and 2 (22%),3) Pain abdomen/distention 1 (11%) and 4 (44%),4) Dysphasia/ Sore throat 5 (55%) and 2 (22%),5) White tongue4 (44%) and 3 (33%),6) Hairy tongue 3 (33%) and 0%,7) Cough 3 (33%) and 4 (44%),8) Blood with sputum0% and 1(11%),9) Breathless ness0% each in both group,10) Chest pain 2 (22%) and 1 (11%),11) Head ache 6 (66%) and 4 (44%),12) Skin eruption1 (11%) each,13) Moluscum0% and 1(11%),14) Warts0% each in both group,15) Herpes zoster 5 (55%) and 1(11%),16) Giddiness 5 (55%) and 4 (44%),17) Palpitation 2 (22%) and 5 (55%),18) Burning micturation 2 (22%) and 0%,19) Urethral discharge 0% each,20) Diarrhea 3 (33%) in both group,21) Anal isching0% and 1(11%),22) Genital Ulcers 0% in both group,23) Genital warts 0% in both group,24) Veginal candidisis 0% in both group,25) Drowsiness0% in both group,26) Lymphedanitis 1 (11%) each,27) Acne Vulgaris 0% in both group respectively. Observations and Results Bhutabhishangaja Ojokshaya 92
  • 103. DISCUSSION ON LABORATORY INVESTIGATIONS11) Changes in Hemoglobin percentage (HB%) Table -13 Group –1 Group -2 OPD No Before After Difference OPD Before After Difference 1 216 14.2 12.8 -1.4 412 10 14 4 2 318 10.5 13 2.5 576 12.8 13 -2 3 561 10 10.8 0.8 4180 14.6 13 -1.6 4 2726 12 7.2 -4.8 5050 10.4 10 0.4 5 2784 11.0 7.0 -4 6421 12 13 1 6 3187 13.8 12.9 -0.9 6614 6.8 10.8 4 7 3427 13.5 11.0 -2.5 7187 12 11 -1 8 3434 12.8 13 0.2 8274 13.2 15 1.8 9 7221 10.2 10.2 0 8275 13 14 1.81 108 97.9 104.8 113.8 When studied hemoglobin % at individual level, in group-1 three patients (33%)increased and in group-2 five patients (55%) reported increases. One (11%) patient is staticwith hemoglobin % in group 1 and four patients (44%) in group-1 and three patients (33%) ingroup-2 decreased hemoglobin %. When compared inter group means of before after we found marked decrease of10.1 mg in group-1 and 8.41 mg increase in group-2. Observations and Results Bhutabhishangaja Ojokshaya 93
  • 104. 12) Changes in Erythrocyte Sedimentation Rate (ESR) Table -14 Group - 1 Group - 2 OPD No Before After Difference OPD Before After Difference 1 216 10 24 14 412 33 15 -18 2 318 30 32 2 576 25 25 0 3 561 40 68 28 4180 10 28 18 4 2726 25 82 57 5050 10.5 20 9.5 5 2784 20 64 44 6421 30 20 -10 6 3187 80 16 - 64 6614 38.1 35 -3 7 3427 80 38 - 42 7187 50 35 -15 8 3434 28 22 -6 8274 60 32 -28 9 7221 70 30 - 40 8275 77 24 -53 383 376 333.6 234 ESR of 1st hour measurement decreased in 4 patients (44.44%) in1st group and 6patients (66.66%) in 2nd group. This is a good prognosis for the patients. 5 (55.55%) patientsof group-1 and 2 patients of group-2 show increase in the E.S.R., which is a bad prognosis.One patient (11.11%) in the group-2 shows no change. But both groups exhibit decrease inthe mean values. Observations and Results Bhutabhishangaja Ojokshaya 94
  • 105. 13) Changes in Total Lymphocyte count Table -15 Group – 1 Group - 2 OPD Before After Difference OPD Before After Difference1 216 3300 3500 200 412 900 2300 4002 318 2200 4400 2200 576 1500 1000 -5003 561 1100 1100 0 4180 1800 1700 -1004 2726 1200 1000 -200 5050 1700 1463 -2375 2784 1470 1300 -170 6421 1700 2400 7006 3187 2600 2300 -300 6614 900 1000 1007 3427 1400 1000 -400 7187 4600 3500 -11008 3434 1900 4000 2100 8274 2300 2550 2509 7221 3200 2900 -300 8275 2700 2800 100 18370 21500 18100 18713 Total Lymphocyte count measurement decreased in 5 patients (55.55%) in 1st groupand 4 patients (44.44%) in 2nd group, which is a bad prognosis. 3 (33.33%) patients ofgroup-1 and 5 patients (55.55%) of group-2 show increase in the Total Lymphocyte count,which is a good prognosis for the patients. One patient (11.11%) in the group-1 shows nochange. But both groups exhibit increase in the mean values. Total Lymphocyte countincreased in total 200-2200 in range at 1st group and 100-400 increased in 2nd group, aftertreatment. Observations and Results Bhutabhishangaja Ojokshaya 95
  • 106. 14) Changes in white Blood corpuscles Table -16 Group - 1 Group - 2 OPD Before After Difference OPD Before After Difference1 216 8.2 7.8 -.4 412 6.5 8.3 1.82 318 5.8 7.5 1.7 576 8.9 7.5 1.43 561 5.6 5.6 0 4180 7.5 8.7 1.24 2726 6.3 4.9 -1.4 5050 13.5 6.2 -7.35 2784 10.7 9.6 -5.1 6421 10 8.7 1.36 3187 8.9 5.0 -3.9 6614 8.0 6.2 -1.87 3427 7.3 7.5 .2 7187 10.1 9.0 -1.18 3434 8.2 6.3 -1.9 8274 6.9 6.8 -19 7221 8.9 9.8 .9 8275 8.8 8.9 2.1 Total 69.9 64 80.2 70.3 It is significant that the viral activity is more in the samples and the fighting againstthe infection is continuous. Thus the WBC counts doesn’t show marked changes. Bothgroups express the reduction in the mean values as minimum, which could be a goodprognosis. Observations and Results Bhutabhishangaja Ojokshaya 96
  • 107. 15) Changes in Weight Table -17 Group - 1 Group - 2 OPD Before After Difference OPD Before After Difference1 216 60 61 1 412 46 51 52 318 58 61 3 576 64 67 33 561 40 44 4 4180 65 66 14 2726 50 54 4 5050 48 53 55 2784 56 58 2 6421 51 52 16 3187 45 47 2 6614 37 40 37 3427 58 60 2 7187 56 61 58 3434 45 45 0 8274 73 73 09 7221 53 54 1 8275 57 61 4 Total 465 484 497 524 All the patients in the group-1 exhibit 1-2 Kg increase and group-2 even up to 5-Kgweight increase. This is a good prognosis and expresses that the patient recovery is started.Usually in the HIV+ve’s weight loss is a sign reversed with the present management. Thisvariation may be due to the various factors, including inclusion of proteins in the food andAgni vardhaka herbs in the formula. Observations and Results Bhutabhishangaja Ojokshaya 97
  • 108. 16) Changes in Platelet count Table -18 Group - 1 Group - 2 OPD Before After Difference OPD Before After Difference1 216 2.05 2.14 0.9 412 1.5 1.52 .022 318 1.94 1.30 -.64 576 2.6 1.81 -.83 561 1.43 1.49 .06 4180 2.3 2.22 -.84 2726 1.07 1.26 .19 5050 1.95 2.10 +155 2784 2.23 2.60 0.37 6421 3.0 2.63 -376 3187 2.05 2.0 -.05 6614 1.36 1.20 -.167 3427 .81 1.5 +. 69 7187 2.5 3.5 1.58 3434 2.41 2.82 .41 8274 2.13 2.55 .429 7221 2.15 2.18 .03 8275 2.69 2.56 -.13 16.14 17.29 20.03 20.09 . Both groups express the reduction in the mean values of Platelet counts asminimum, which could be a good prognosis. Observations and Results Bhutabhishangaja Ojokshaya 98
  • 109. 17) Changes in Kornefsky performance score Table - 19 Group - 1 Group - 2 OPD Before After Difference OPD Before After Difference1 216 90 90 0 412 80 90 102 318 80 90 10 576 90 90 03 561 90 90 0 4180 90 90 04 2726 80 90 10 5050 80 90 105 2784 80 90 10 6421 80 90 06 3187 80 90 10 6614 80 90 107 3427 80 90 10 7187 80 90 108 3434 90 90 0 8274 90 90 09 7221 80 90 10 8275 90 90 0 750 810 60 760 810 40Kornefsky grade: - 6 (66%) increased by 10 grades and 3 (33%) were static in 1st group, 4(44%) increased by10 grades and 5 (55%) were static in 2nd group. Kornofsky performancescore (KPS) is a widely accepted parameter for evaluation of HIV-AIDS. All patients (100%)in this study have crossed the score 90, and none has reached score 80. This data is betterthan Alka Despande study 1998. It interesting to note that, Despande administered the drugfor 1 year and the mean was 89, where as in this trial drug was administered for four monthsand the mean KPS is 90 and 88. Therefore this drug is capable of controlling theopportunistic infections, which indirectly helps for raise in CD4 cell count. Observations and Results Bhutabhishangaja Ojokshaya 99
  • 110. 18) Changes in general health condition Table 20 Group - 1 Group - 2 OPD Before After Difference OPD Before After Difference1 216 2 3 +1 412 2 3 12 318 1 2 +1 576 2 3 13 561 1 1 0 4180 4 4 04 2726 1 2 +1 5050 1 2 15 2784 1 2 +1 6421 2 2 06 3187 1 2 1 6614 1 2 17 3427 1 2 1 7187 1 2 18 3434 3 3 0 8274 1 2 19 7221 2 3 1 8275 1 2 1 13 20 15 22General health condition: -7 (77%) increased and 2 (22%) static in both groups by 1 grade,There was a significant improvement in GHC of all the patients, from lower grade to uppergrades like grade 2 and grade 3 after medicatioin. This result is quite similar with K. 226 227Rajagopal entitled and Alka Deshapande entitled reference. The significant responsein general health condition may be due to the reduction in viral load, in plasma and reductionin the viral replication. Observations and Results Bhutabhishangaja Ojokshaya100
  • 111. 19) Changes in CD4 count Table 21 Group - 1 Group – 2 OPD Before After Difference OPD Before After Difference1 216 590 650 60 412 310 530 2202 318 510 700 190 576 460 310 -1503 561 320 320 0 4180 440 510 704 2726 410 310 -100 5050 480 203 -2775 2784 520 410 -110 6421 410 430 206 3187 510 590 80 6614 290 320 307 3427 440 320 -120 7187 718 233 -4858 3434 440 610 170 8274 580 490 -909 7221 630 580 -50 8275 590 350 -210 4370 4490 4278 3376 4 (44%) increased CD 4 cell count by 60-190, 4 (44%) decreased CD 4 cell countand 1 (11%) were static in 1st group for CD 4 cell count, 4 (44%) increased CD 4 cell countby 20-220 and 5 (55%) decreased CD 4 cell count in 2nd group. Observations and Results Bhutabhishangaja Ojokshaya101
  • 112. 20) Changes in CD8 count Table 22 Group - 1 Group - 2 OPD Before After Difference OPD Before After Difference1 216 1720 1800 80 412 320 1080 7602 318 1030 2380 1350 576 590 390 -2003 561 450 450 0 4180 820 680 -1404 2726 430 390 -40 5050 710 899 1895 2784 950 500 -450 6421 780 620 -1606 3187 1110 1020 -90 6614 340 380 407 3427 540 380 -160 7187 1780 578 -12028 3434 890 2190 1300 8274 1030 840 -1909 7221 1610 1420 -190 8275 1300 320 -980 8730 10530 7670 5787CD 8 cell count: - 5 (55%) decreased, 3 (33%) increase in 1st group, 6 (66%) decreased and3 (33%) increased in 2nd group,Ratio of CD4 and CD 8: - 5 (55%) increased, 3 (33%) decreased, 1, (11%) static in bothgroups, This may be due to fast acting drugs, having better bio-availability and perhaps dueto its potent viral action. Observations and Results Bhutabhishangaja Ojokshaya102
  • 113. 21) Observations on Chronicity Table 23Chronicity Group-1 Group-2Less Than 1 Year 2 21-2 Year 3 1Above 2 Year 4 5Total 9 9 Out of observations it was found that maximum number of patients appear with the 2years and above chronicity. Out of two groups together only 4 cases found 1 - 2 years ofhistory and/or less then one year for 4 patients. It evidential that the disease does not haveany cure but it is only palliative and to be managed with the symptoms presented by thepatient and to attend the patient for the opportunistic or AIDS related complications.22) Observations on Ojo vyapat lakshana Table 24 GROUP-1 GROUP-2SL.NO Symptoms Before After Before After1 Stabdagatrata 5 0 3 02 Gurugatrata 5 0 3 03 Vata Shopha 0 0 0 04 Varna Hani 2 0 1 05 Glani 7 0 3 06 Tandra 5 0 5 07 Nidra 1 0 2 1 Observations and Results Bhutabhishangaja Ojokshaya103
  • 114. 23) Observations on Ojo Vishramsha lakshana Table 25 GROUP-1 GROUP-2SL.NO Symptoms Before After Before After1 Gatra Sadana 9 0 6 02 Doshachavanama 1 0 2 03 Sandhi Vishlesha 4 0 3 04 Kriyasannirodha 5 0 1 024) Observations on Ojokshaya lakshana Table 26 GROUP-1 GROUP-2 SL.NO Symptoms Before After Before After 1 Bhaya 7 0 8 1 2 Chinta 9 0 8 0 3 Dushchata 1 0 2 0 4 Rooksha 7 0 6 0 5 Moorcha 1 0 1 0 6 Moha 1 0 1 0 7 Dourbalya 9 0 9 0 8 Vyatitendriya 4 0 1 0 9 Durmaan 2 0 0 0 10 Kshama 4 0 2 0 11 Mamsakshaya 9 0 7 2 12 Pralapa 0 0 A beneficial clinical out come cannot be expected unless there is an improvement instatus of Ojas. Because Ojas mediates the natural cellular immune response that lowers theviral load and maintains the CD4 cell count, Observations and Results Bhutabhishangaja Ojokshaya104
  • 115. 25) Observations on Vata vriddi lakshanaKarsha7 (77%) each, Karshna 6(66%) and 4(44%), Usnakamitwa 7 (77%) and 5 (55%),Kampa 0% and 1(11%), Anaha 2 (22%) and 4(44%), Shakrit griha 7(77%) and 5 (55%),Balabramsha3 (33%), Nidra bramsha 0% Pralapa 0%, Bhrama 0%, these symptoms areseen before treatment in both groups respectively,in group I Karshata in 3 Patients (33%)Karshnata in 3 (33%) Usnakamitva in 6 are seen after, and sdudy.in groupII ushnakamitva issenn in 1 (11%) only,26) Observations on Vata kshaya lakshanaAngasada 6 (66%) and 5 (55%), Alpabhasite Ahita 3 (33%) and 0%, Chesta heenta 2 (22%)and 1(11%), Vyamoha 4 (44%) and 2 (22%), sleshmavriddi 2 (22%) and 1(11%), thesesymptoms are seen before treatment and in group II angasad is seen in only one patient.27) Observations on Pitta vriddi lakshanaPeeta mootrata, Peetanetrata, Peeta twak, Atikshuda, Atidaha, were not seen in bothgroups before treatment,28) Observations on Pitta kshaya lakshanaPittakhaya lakshanas are seen as Mandagnin 2 (22%) and 1(11%), Shareerasheetatva 0%in both groups, and Prabhahani 4 (44%) and 1 (11%), were seen before treatment andthese symptoms are not observed after treatment.29) Observations on Kapha vriddi lakshanagnisada 2 (22%) and 3 (33%), Praseka 0% in both groups, Alasya 7 (77%) and 6 (66%),Gouravata 7 (77%) and 5(55%), Swetangata 1 (11%) and 0%, Sheetangata in both 0%, ineach group Shlatangata 4(44%), Shwasa 2 (22%) and 1(11%), Kasa 7 (77%) and 4 (44%),Atinidrata 0% in both groups are seen before treatment and these are subsided aftertreatment. Observations and Results Bhutabhishangaja Ojokshaya105
  • 116. 30) Observations on Kapha kshaya lakshanaBhrama 1(11%) and 3 (33%), Urahshunyata 1 (11%) in each, Shirah shunyata 0% and1(11%), Hridrava 3 (33%) in each, Sandishitilya 2 (22%) and 5 (55%), these symptoms seenbefore treatment and after treatment these are not seen.31) Assessment of Result The assessments criteria of the Evaluation of the comparative efficacy ofOjokalpa Rasayana in Bhutabhishangaja Ojokshaya (HIV infection) is as follows – Table 27 Group 1 Ojokalpa Rasayan 9.WEIGHT 5.Platelet 8.RATIO 11.GHC 10.KFS 4.WBC 1.Hb% Result 2.ESR 6.CD4 7.CD8 3.TLC count Total1 0 0 1 0 1 1 0 0 1 1 1 6 MR2 1 0 1 1 0 1 0 0 1 1 1 7 MR3 1 0 1 1 1 1 0 1 1 1 1 9 BR4 0 0 0 0 1 0 1 0 1 1 1 5 MR5 0 0 0 0 1 0 1 1 1 1 1 6 MR6 0 1 0 0 0 1 1 1 1 1 1 7 MR7 0 1 0 1 1 0 1 1 1 1 1 8 BR8 1 1 1 0 1 1 0 1 1 1 1 9 BR9 1 1 0 1 1 0 1 1 1 1 1 9 BR Group 2 Amritakayakalpa rasayana1 1 1 1 1 1 1 0 0 1 1 1 9 BR2 1 1 0 1 0 0 1 1 1 1 1 8 BR3 0 0 0 1 0 1 1 1 1 1 1 7 MR4 1 0 0 0 1 0 0 0 1 1 1 5 MR5 1 1 1 1 1 1 1 0 1 1 1 10 BR6 1 1 1 0 0 1 0 1 1 1 1 8 BR7 0 1 0 0 1 0 1 1 1 1 1 7 MR8 1 1 1 0 1 0 1 1 1 1 1 9 BR9 1 1 1 1 0 0 1 1 1 1 1 9 BR Grade Score range Best responded 8 to 11 Moderately responded 5 to 8 Responded 2 to 4 Static / Not responded 0&1 BR= Best Responded, MR= Moderately Responded, R = Responded, S = Static, NR = Not Responded Observations and Results Bhutabhishangaja Ojokshaya106
  • 117. Assessment Parameter study of group 1 Table 28No Parameter Mean S.D S.E t-Value P value Remarks Before After Difference1 Hemoglobin % 12.0 10.87 1.9 1.677 0.559 3.398 <0.01 Highly significant2 Erythrocyte sedimentation rate 42.5 41.77 33.0 21.97 7.325 4.505 <0.005 Highly significant3 Total leukocyte count 2041.11 2388.89 652.22 856.3618 285.539 2.284 >0.05 Not significant4 White blood cell count 7.766 6.667 1.722 1.731 0.577 2.984 <0.002 Highly significant5 Platelet count 1.793 1.921 0.3711 0.317 0.1056 3.514 <0.001 Highly significant6 C.D.4 cell count 485.55 498.89 97.777 59.113 19.704 4.962 <0.005 Highly significant7 C.D.8 cell Count 970.00 1170.0 406.66 536.702 178.9 2.273 >0.05 Not significant8 Ratio 0.575 0.562 0.113 0.1017 0.033 3.433 <0.01 Highly significant9 Weight 51.667 53.777 2.111 1.364 0.454 4.649 <0.005 Highly significant10 Karnofsky’s performance score 83.333 90.00 6.666 5.00 1.666 4.00 <0.005 Highly significant11 General health condition 1.444 2.222 0.777 0.440 0.146 5.32 <0.001 Highly significant Observations and Results Bhutabhishangaja Ojokshaya108
  • 118. Assessment Parameter study Group 2 Table 29No Parameter Mean S.D S.E t-Value P value Remarks Before After Difference1 Hemoglobin % 11.644 12.644 1.666 1.414 0.471 3.537 <0.01 Highly significant2 Erythrocyte sedimentation rate 37.066 26.00 17.166 15.862 5.287 3.246 <0.02 Highly significant3 Total leukocyte count 2011.11 2079.22 387.44 336.832 112.277 3.450 <0.01 Highly significant4 White blood cell count 8.688 7.811 2.011 2.064 0.688 2.922 <0.02 Highly significant5 Platelet count 2.225 2.232 0.482 0.474 0.158 3.051 <0.02 Highly significant6 C.D.4 cell count 475.333 378.444 172.44 147.317 49.105 3.511 <0.01 Highly significant7 C.D.8 cell Count 852.22 676.333 429.00 430.85 143.616 2.987 <0.02 Highly significant8 Ratio 0.653 0.686 0.195 0.259 0.086 2.273 >0.05 Not significant9 Weight 55.22 58.222 3.600 1.936 0.645 4.651 <0.005 Highly significant10 Karnofsky’s performance score 84.44 88.888 4.444 5.27 1.756 2.53 <0.05 Highly significant11 General health condition 1.666 2.222 0777 0.440 0.146 5.32 <0.001 Highly significant Observations and Results Bhutabhishangaja Ojokshaya109
  • 119. Assessment Parameter Comparative study of Group 1 and 2 Table 30No Parameter group Mean SD S.E P.S.E t-Value P value Remarks1 Hemoglobin % 1 10.877 2.3936 0.2659 Highly 0.6208 2.846 <0.02 significant 2 12.644 1.6845 0.5612 Erythrocyte sedimentation rate 1 41.777 23.504 7.834 Not 8.18 1.928 >0.05 significant 2 26.00 7.071 2.3573 Total leukocyte count 1 2388.89 1362.39 454.13 Not 535.065 0.578 >0.05 significant 2 2079.22 848.85 282.954 White blood cell count 1 6.667 1.612 0.537 Not 0.661 1.73 >0.05 significant 2 7.811 1.158 0.3865 Platelet count 1 1.921 0.567 0.189 Not 0.295 1.050 >0.05 significant 2 2.232 0.683 0.2276 C.D.4 cell count 1 498.89 157.356 52.45 Not 66.19 1.819 >0.05 significant 2 378.44 120.112 40.3757 C.D.8 cell Count 1 1170.00 85.155 268.38 Not 283.606 1.74 >0.05 significant 2 676.33 275.032 91.6778 Ratio 1 0.562 0.234 0.078 Not 0.113 1.097 >0.05 significant 2 0.686 0.248 0.08289 Weight 1 53.777 6.887 2.295 Not 4.083 1.088 >0.05 significant 2 58.222 10.133 3.37710 Karnofsky’s performance score 1 90.00 0.0 0.0 Not 1.111 1.00 >0.05 significant 2 88.88 3.33 1.1111 1 2.22 0.66 0.22 0.328 - - - General health condition 2 2.22 0726 0.242 Observations and Results Bhutabhishangaja Ojokshaya110
  • 120. 32) Statistical assessment of study The effect of two groups in all parameters are the same there is a highly significant inHB % when we compared two groups (P < 0.05) and all the after parameters and notsignificant (P>0.05). The group-1 is not significant in TLC and CD8 sell count (P>0.05) and afterparameters shows highly significant in-group II except ratio all the parameters are highlysignificant (P>0.05). Group-1 E.S.R. Platelet counts Kornefsky gradings and CD4 are highly significantwhen compared to group 2 (P<0.05 and T values). The WBC, Weight and General Health Condition are having same effect in bothgroups (by comparing P and T values). The parameter HB%, TLC and CD8 cell counts are highly significant in-group 2compared with group 1. Over all there is a more variation in group I. In-group 2, HB% EWR, TLC, WBC and CD8 are having uniform effect and in group 1platelet count CD4 and weight are having uninformed effect (by comparing co-efficient ofveriation). Observations and Results Bhutabhishangaja Ojokshaya111
  • 121. Result in-group 1 As mentioned that in the Table 27, group-1 has show the results with reference tothe grade declared in the study is as follows. The Best responded group is 4 patients(44.44%) and moderately responded are of 5 (55.55%) patients. There was no patient whodoesn’t respond for the treatment of Ojokalparasayana. Tabulation of group 1 is shown asunder in table-31 and the graphical form is displayed as under in the graph-8. Table -31 Result category Patients % Best responded 4 44.44 Moderately responded 5 55.56 Responded 0 0 Static 0 0 Not responded 0 0 Graph-8 Not Responded Static responded 0.00% 0.00% 0.00% Best Moderately responded responded 55.56% 44.44% Observations and Results Bhutabhishangaja Ojokshaya112
  • 122. Result in-group 2 As mentioned that in the Table 27 group-1 has show the results with reference to thegrade declared in the study is as follows. The Best responded group is 6 patients (66.66%)and moderately responded are of 3 (33.33%) patients. There was no patient who doesn’trespond for the treatment of Ojokalparasayana. Tabulation of group 2 is shown as under intable-32 and the graphical form is displayed as under in the graph-9. Table –32 Result category Patients % Best responded 6 66.67 Moderately responded 3 33.33 Responded 0 0 Static 0 0 Not responded 0 0 Graph-9 Static Responded Not 0.00% 0.00% responded 0.00% Moderately Best responded responded 33.33% 66.67% Observations and Results Bhutabhishangaja Ojokshaya113
  • 123. Discussion and conclusion The aim of this study is understand the explanations, scientific background of thetraditional Ayurvedic literature and practices, to give practical guidelines for the Ayurvedicmodalities of treatment and approach to the HIV infected patient. Ayurveda has bothpreventive and palliative methods of HIV management, as understood by the general studyof the literature. There are many facts yet to be unearthed. This is possible by profoundknowledge of Ayurveda with channeled efforts to explain the same in the light of modernscientific knowledge by the way if scientific research on literature, drug efficacy and othermethods of Ayurvedic management. The staggering worldwide growth of HIV pandemic is matched by the explosion ofinformation in the area of HIV virology, pathogenesis, and treatment of HIV diseaseincluding the opportunistic infectious associated with it. The information related to HIVdisease is much greater than that for any other infectious disease or immunologic disorder.It becomes almost impossible for health care personnel, to stay abreast of this literature.This study deals with the present and most current available information regardingprevalence of the disease, its pathogenesis, treatment and prevention. The existence of microorganisms is well documented from the time of Atharva Veda(5000 BC) and Ayurvedic texts too have vivid description of pathogens. On the country thescientific community believes that the knowledge of microbiology evolved after 18th century.The gap between these two periods is a vast one and it is difficult to know why suchknowledge did not grow further from the ancient times. One of the reasons may be becauseAyurveda gave more importance to host factor (Kshetra and Ambu) rather than thepathogens (Beeja) factor. Discussion and conclusion - Bhutabhishangaja Ojokshaya114
  • 124. The second factor may be due to fewer incidences of infectious diseases in thosedays. But with the changing times, these are sudden changes in environment due toindustrialization, deforestation, and pollution. Rapid explosion of population led us to usageof chemical fertilizers, chemical medicines, pesticides, insecticides etc. this brought about adevastating reduction in nutritional value of food products, human life span (Ayu) resistancepower (Vyadhi Kshamatva), and peace of mind (prasanna atma, indirya manah (is alsoseverely affected. This has lead to increased susceptibility of human beings, for infectiousdiseases associated with emergence of new infectious organisms and their rapid growth. So it is high time for all Ayurvedic practitioners to make necessary modifications intheir approach to infections diseases, in the light of changing scenario. HIV is the etiological agent for the newfound immuno deficiency, which came to lightin 1981. This infection spectrum is ranging from primary infection with or without acutesyndrome are a symptomatic stage and to an advanced disease. Immuno deficiency is refereed to as Ojokshaya in Ayurveda. Ojas is the essence ofsapthadhatus (all the bodily tissues) and it is responsible for vigor and vitality. It is theprotective mechanism against decay and degeneration, any depletion of Ojas can lead toinfection disease and death. There is clear description regarding the depletion of Ojas bymicroorganisms. The resultant Ojokshaya also goes for different pathological stages likemicroorganisms. The resultant Ojokshaya also goes for different pathological stages likeOjovishramsha, vyapath and Kshaya. But in the concept of Ojokshaya we do not find astage similar to clinical latency. The reasonfor this may be perhaps in those days thisparticular type of infections was not found or in those days there use to be a differentimmunological response to same infection. Whatever we see as symptoms of Ojokshaya,they are the general immuno deficiency symptoms. Discussion and conclusion - Bhutabhishangaja Ojokshaya115
  • 125. The HIV epidemic has occurred in ‘waves’ in different regions of world. Each wavehaving somewhat different characteristics, depending upon the demographics of the countryand region in question and the timing of the introduction of HIV into the population, In the large-scale deaths some people used to survive and Acharyas haverecognized this phenomenon as Vyadhi Ksamatva and those died has Ojokshaya as apredisposing factor. Discussing the root cause of Janapadodhawamsa, it is said “ adarma “ (bad conduct)is the reason for such fact transmission and fatality. When we analyze the basic causebehind the origin of this disease and subsequent transmission, we understand bad conductof human beings unnatural behavior of man resulted in a disease called HIV infection. HIV, a virus of green monkey of Africa started infecting human beings. The exactmethodology of this jump is highly debatable. But one this is sure, somewhere, some bodyhas behaved unnaturally and further spread speaks about the immoral conduct of a bigpopulation of the world. The transmission scenario of HIV has changed to heterosexual route as apredominant cause from a homosexual route and intravenous drug use. The change hasbeen recognized in type of people, sex and their economical background. A disease of menhas infected equal number of women, a disease of cities in commonly seen in small villages,a disease of rich and ducated is infecting most backward and uneducated population. Sex isa basic instinct of human beings and the experience says these will not change even whensociety doesn’t permit is in unnatural means. Susruta described communicable diseases in kusta chapter of Nidana stana. He hasgiven “prasanga” or sexual contact as the main cause of disease transmission. This gives usan idea about the prevalence of sexually transmitted diseases in ancient period also. But wedo not find the reference of transmission of infection from mother to child, even though there Discussion and conclusion - Bhutabhishangaja Ojokshaya116
  • 126. are references about the congenital disorders and role of genetics in occurrence ofdiseases. But there is a reference in Ayurveda about transfer of maternal Ojas to the foetusin intra-uterine life. This is significant observation with regard to vertical transmission. It is estimated that over 6 million Indians are HIV carriers, WHO and UNAIDS are theinternationally operating organizations, who do research on epidemiology of infection inIndia NACO (National AIDS Control Organization) is working on same guidelines since1987. In 1992 government of India HIV control project along with many N.G.Os. But all the activities of government and non-governmental organizations involve onlymodern medical professionals. Nowhere Ayurvedic doctor is involved in the AIDS controlprogram. On the contrary, Ayurveda is a popular medical science in India and theunqualified quacks started exploiting people in the name of Ayurveda. WHO recognized theimportance of Ayurveda 3 decades ago and since then many modern medical professionalsand scientists are doing research on Ayurvedic drugs. But these are scattered ones, and runby private people. But in most of these researches, there is no involvement of Ayurveidcscholars. To succeed in developing a framework of Ayurvedic treatment modality, thereshould be profound knowledge of Ayurveda along with scientific research methods.Ojokshaya is not a disease dealt with in Nidanastana or Chikitsa stana of any Samhita. It isnot discussed as and ‘Aristalakshana’ also rather it is a terminal condition of all debilitatingdiseases, which cause death. Acharya Charaka and Susruta dealt in chapters wheregeneral Vriddhi Kshaya Lakshanas of Dosha Dhatu and Mala are discussed. Ojokshaya ispathological condition associated with kshataja kasa, grahani, jaja yaksma, sannipahajajwara raktasha, pandu, grahani, raktaatisara, and shosha, kshayaja kasa, many of which areinfectious diseases. According Ayurveda, the Ahara (food) Vihara (activities) and Manasika vaikalya(psychological disorder) are also causes Ojokshaya. Alpashana (malnutrition), Anasana Discussion and conclusion - Bhutabhishangaja Ojokshaya117
  • 127. (starvation) are said to be nutritional factors, which directly effect the body’s, defensemechanism, against infection. In the modern parlance, it is a well-understood fact thatmalnutrition is a common cause of immuno deficiency, because protein takes part in theformation of antibodies. In Vihara (physical activities) Vatatapa sevana (exposing to windblow and hot sun) associated with Ativyayama (excessive work) lead to Ojokshaya. Extremeheat and blows of wind cause severe exhaustion, which leads to immuno deficiency in longrun. This also speaks about the socioeconomic conditions of said population, which issusceptible to this kind of Ojokshaya. The next cause, Ativyavaya or excessive indulgencein sex is also a cause for Ojokshaya. Here modern medical understanding differs. According to Ayurveda, Kshaya (emaciation) can result by two ways. The first type isanulomakshaya second one pratiloma kshaya. Anulomakshaya is caused due tomalnutrition in which bodily tissues from Rasa, Rakta, Mamsa progressively undergodepletion this is caused due to anashana, alpasana, vatatapa sevana type of causes.Pratiloma kshaya is caused due to shukra kshaya (depletion of shukra dhatu) due to overindulgence in sex. This is a reverse or opposite type of depletion of bodily tissues. Accordingto this principle loss of Shukra causes immuno deficiency and modern science doesn’t relatesex and immuno deficiency. Rather there are studies, which revel that sex does immunomodulation. For this reason, ayurveda explains seasonal sexual schedule where as modernscience does not believe in this. This ayurveda has recognized brahmacharya (celibacy) asone of the sub-pillars of the life where as modern science does not attach any importance tocelibacy in sustaining life. Prajagara (sleeplessness) has been considered as a cause of Ojokshaya. Modernscience also believes in this and a good sleep increases ones immunity. The next set of causes is manasika karanas (Psychological reason). They are kopa(anger), shoka (grief), chinta (worry) and bhaya (phobia). In modern pariance the new Discussion and conclusion - Bhutabhishangaja Ojokshaya118
  • 128. branch of medicine, i.e. psycho-neuro-imunology speaks about the role of psychologicalcauses like stress etc, as causative factors for immunodeficiency. It is also proved that CD4count depletes under stressful conditions and increases by meditation, chanting mantras. Susruta explains about “abhigata” or injury as a cause of Ojokshaya. If we look it inmodern angle, apart from the tissue loss in injury, there is a scope or increased susceptibilityfor infection after an injury. Very specifically an injury in sexual organs or anus is a high riskfactor for transmission of HIV infection. When we a serve the signs and symptoms of Ojokshaya we lot of similarities in bothsystems of medicine. Charaka does not explain the signs and symptoms of Ojokshaya,whereas Susruta then explained different stages of Ojokshaya. The descriptions of Susrutaare more elaborate in this regard. He has classified the Ojovikruthi is in three stages asvishramsha as a direct loss, vyapat as a vitiation, and Kshaya as depletion. But Charakahas summarized them in one condition “Ojokshaya” and we don’t get the advancing stagesof diseases. The symptomatologies given here are not in order, but “marana” or deathcomes at the end. When we see the modern classification of HIV disease there are 4 stages of HIVinfection, which results in death at the end. The first stage is primary infection or acute sero-conversion stage. This happens after the primary infection followed by an incubation periodof 2-6 weeks in which 50% of individual feels acute viral syndrome characterized by highfever, lymph adenopathy, myalgia etc. this lasts for 1-2 weeks, not responding to any line oftreatment. This is usually the uninvestigated phase of HIV infection. In many individuals thisstage may go unnoticed. During this phase there will be sever CD4 lymphopaenia. Thisparticular stage of HIV infection can not be correlated to the stages of Ojokshaya. This canbe correlated to sannipatika type of jwara, in which there will be a sudden depletion in Ojas,which is limited to Ojo-visramsa. At this stage body repairs on its own with the help of Kapha Discussion and conclusion - Bhutabhishangaja Ojokshaya119
  • 129. (Bala), and this results in to the temporary reduction in Ojo-visramsa Lakshanas. Butbecause virus survives and camouflages, it enters in to chronic phase of infection and theslow damage of Ojas continues. In the II stage of HIV infection there will be occasional symptoms of fever, loss ofappetite, loss of body weight, asthenia, diarrhoea, cough etc. this stage can be compared toOjovishramsha stage with special reference to the sequence of symptomatology explainedin sannipataja Jwara where there ill be interns of limbs, chills, looseness of limbs, low gradefever, body pain etc. it may not be as severe as a acute phase of sunnipathaja Jwara. In the stage of III of HIV infection along with the above mentioned symptoms therewill be further immuno deficiency due to which many opportunistic infections like herpessimplex, herpes zooster, oral Candidiasis, tuberculosis, hairy leukoplakia. In second stage of Ojovikriti natural properties of Ojas under the influence of vitiatedDoshas goes for vyapath phase chih given rise to stabha gurugatrata, vatasopha, 228varnabedha, glani, tandra and nidra . Even though there is no mention of opportunisticinfection in Ojovyapat the symptomatology resembles as infectious conditions leading tocoma. In the last stage of HIV infection there are, many neurological symptoms likedementia and altered personality, convulsion, ataxia, visual impairment, neurologicvaldeficits, hemiplegia followed by death. In Ojokshaya (3rd stage) there will be moorcha (lossof consciousness) mamasakshaya (wasting of muscies) moha (stupor) Pralapa (delirium)and vyathithendriyata (loss of motor and sensory perception) followed by marana (death)this is in the strict sense of Susruta’s classification of Ojokshaya stages. None of the classics described the exact Samprapti of Ojokshaya. Regarding theSamprapti of Ojokshaya, there are two different methodologies explained in differentcontexts. The Ojokshaya occurred due to general causes apart from infection and that Discussion and conclusion - Bhutabhishangaja Ojokshaya120
  • 130. caused due to infection are of two different Samprapti. The description about general 229 230Samprapti can be summarized as sited by Charaka in madhumeha and panduroga .Vitiated Doshas (either Vata or Pitta) vitiate Dhatus, which later loose integrity and getdepleted and subsequently results in depletion of Ojas. This is also called asAnulomakshaya. The autoimmune mechanism resembles this type of Ojovikriti. TheSamprapti of Ojokshaya caused by infection can be summarized with the available 231 232references in the context of Rajayakshma and Sannipata Jwara . Here in theindividuals who have basic susceptibility for infection, when get infected due to alreadydiscussed causes, get Bhootopaghata a damage of cells (carrying CD4 makers) followed byabhishanga (penetration) and entry of viral materiel into the cell. This foreign toxic materialworks like jangama visha (poison of animal origin) 233, but as virus is a live matter with RNAgenome instead of causing immediate death if replicates here getting sustenance frombodily cells. Those cells where virus replicates become reservoirs of virus. This virus iscapable of causing srothorodha, raktadi Dhatu Kshaya. Due to the lowered functioning ofdhatwagni resulting inAma and apachaya (catabolic activity) due to the deficiency ofnutrition, which further leads of Ojokshaya 234. The Ama so formed causes further Vata Vriddhi associated with Vikrita Pitta leads tosannipathika Jwara. Vitiated Vata and Pitta cause damage to Dhatu vaha srotamsi and thisleads to Ojo-visramsa, vypth and Kshaya in due course of time. So in this way pathologicalevents following bhootopaghata correlate with modern understanding of HIV infection.Sadhyasadhayata Susruta has clearly said the Ojovishramasha and vyapth can be managed byrasayana and vajeekarana Chikitsa along with appropriate diet, which increases Bala and 235antagonistic to the causative factors of Ojokshaya . Further it is said, as Ojokshaya willnot be reversed with rasayana or Vajikarana Chikitsa. The prognosis of diseases as Discussion and conclusion - Bhutabhishangaja Ojokshaya121
  • 131. explained in Ayurveda and modern science are similar as the early stages of HIV infectioncan be managed with antiviral and immuno modulators and advanced stage will not improvewith any available treatment.Chikitsa sutra General management of Ojokshaya is by rasayana and Vajikarana, which are 236Ojokara in nature . But the management of Ojokshaya caused by infection needs anadditional line of treatment, which can be developed on the basis of Krimi Chikitsa anexplained in Charaka Vimana 7th chapter. Among 3 major principles of Krimi Chikitsa, theprakriti vighata type suits the present context of HIV infection. This can be achieved byusage of drugs having Krimi prakriti vagata property.The Selection of drugs Keeping the Samprapti of Ojokshaya in mind, there is a need for both Ojoskara(immuno-stimulant) and Krimigna (anti-viral) and protecting and cures for the Aids relatedcomplications along with potent action. The conceptualization of ideal drug should alsoinvolved drugs having faster action and better cell penetration capacity. An attempt is madein the formulation of Ojokalparasayana for the management of the HIV infection. The mainingredients are Bilva, Tulashi, Haridra, Daru haridra, Devadaru, Trikatu, Triphala, Karanja,Tagara. To get additive values and fortify the drug action Vidanga and Agnikumara vati. Thevidanga is krimighna and Agnikumara vati is anti-pyrexial. Ajamootra is used as Bhavanadravya for the bilwadivati as directed in the text. The composition of Agni kumar vati isKusta, Vacha, Musta, Vatsanabha, Maricha. Therapeutic effect of Agni kumar vati isjwarahara, Atisara shamaka and also prevents and cures upper respiratory tract infections. Another drug undertaken for the comparison is Amruta kayakalpa Rasayanaestablished immuno-modulator, manufactured by a well-known company Amruta Herbs,Hyderabad. Discussion and conclusion - Bhutabhishangaja Ojokshaya122
  • 132. Plan of the study In this study a total is 9 patients each in two groups were included out of 26 casesreported during this period for comparative clinical trial. For the general analysis of overall condition of the subject, all the subjects wereinvestigated for hemoglobin percentage, Erythrocyte Sedimentation Rate. A total count wascarried out because of financial constraints. Instead CD4 and CD8 along with peripherallymphocyte and platelet counts are taken as surrogate makers of the immuno status. This isin tune with internationally practiced research parameters. All the patients have undergone these investigations before startingOjokalparasayana and Amruta kayakalparasayana that to soon after the completion of fourmonths schedule. The effect of both Ojokalparasayana and Amruta kayakalparasayana on each of theparameters was assessed with base line data. The Ayurvedic assessment was done withdetailed clinical analysis of Dosha status and Ojas status on the basis presenting symptomsusing darshana sparshana and prasna methodology. This was done before and soon aftercompletion of both trials on both compounds.General observations From the initial inclusion of 26 patients, 8 patients dropped out during the study. Dueto the decision by these patients to take medicine from a so-called AIDS specialist who hadreleased and advertisement in local newspaper, claiming a cure of HIV disease. Maximum number patients in this study are men and male verses female ratio is 2:1.This is contradictory to the Indian data sex incidence. Which 1:1 this various can be due tothe male dominance in the local society with rural and illiteracy background, 22% Muslim patients in the study may be due to religion ratio of local population andthere is a study that claims less incidence of sexually transmitted disease in subjects whounder went circumcision 237. Discussion and conclusion - Bhutabhishangaja Ojokshaya123
  • 133. The maximum patients were in middle class 55% followed by poor 33%, and 11% inhigher middle class reflect the socioeconomic status of the particular area. It also reflects theeasy acceptance of free treatment of middle class and poor class. It is interesting to note that not even a single vegetarian subject was seen in thisstudy. As Ayurvedic concepts talk about the role of predisposing factors, there must be aphysiological or psychological impact of non-vegetarian food that may be having a role toplay in high incidence of HIV among non-vegetarians populations. Coming to the study related to disease, maximum number of patients (100%) got theinfection from heterosexual contact. This data coincides with the international data. Even though the incidence changes are more among the patients who got it fromblood transmission and intra-venous drug intake, but more patients got it from heterosexualcontact only. This clearly shows the high rate of unsafe heterosexual practices in our societypopulation.Aids stages Stages of HIV infection are well understood. It is a proven fact that HIV causes AIDSand AIDS related complex. The mathematical and statically evaluated is often used toexplain the biological phenomena, through the years of studying the HIVI disease. Theinvestigation of CD4 and CD8 cells along with lymphocyte count is very much helpful in theprediction of stages of HIV infection. CD4 count cell is a surrogate marker of immuno-deficiency because lower HIV RNA level and higher CD4 cell counts correlates with long 238.time survivors in both adult and children In this study maximum patients were in earlysymptomatic stage 0% in-group I and group II respectively followed by 88% in second stageat both groups. Discussion and conclusion - Bhutabhishangaja Ojokshaya124
  • 134. Efficacy of Ojokalpa Rasayana Ojokalpa Rasayana is said with so many cumulative properties with respect to theingredients included in it. Thus the properties are classified according to the Srotas in theAyurveda is as follows.As Rasayana Amalaki, Haritaki, Daruhariudra, Pippali, kusta and Vatsanabha are well-establishedRasayana dravyas in Ayurveda. These drugs act through rasadi dhatu ayanam i.e.nourishing and fortifying the structural and functional aspect of individual tissue materials inthe body.As Ama hara Ama is one of the components of Vyadhi Samprapti. Thus Samprapti vighatana isessential through Ama hara dravya. Ama in comparison as free radicals flown in blood to beretarded and regulated otherwise they pretend the normal and unregulated functions in thebody. Thus the Ama hara dravyas are used in this combination are Devadaru, Shunti andHareetaki.Some of the properties elicited by the pharmacologists are furnished here under. As antioxident - Amalaki, Shunti and Haritaki Anti tubercular - Pippali, Karanja and Vacha Anti bacterial -Amalaki, vibhitaki, Karanja, Musta, Maricha and Haritaki Anti fungal - Haritaki. Vibhitaki and KaranjaPranavaha Srotas Many patients repeatedly reported with the upper respiratory tract infections and inlate stages with the Tuberculosis (Rajayakshama). Tulasi, Devadaru, Shunit, Maricha,Pippali, Amalaki, Haritaki, Vibhitaki, Karanja, Kusta and Vatsanabha combat these Discussion and conclusion - Bhutabhishangaja Ojokshaya125
  • 135. symptoms with the herbs in the composition. The bhavana dravya, Aja mutra is also a bestcomponent to relieve dyspnoeas.Annavaha Srotas: Almost all dravyas have deepana and pachana effect, which makes sence to theconcept Agni Chikitsa is the modality management in the Ayurveda. Bilwa, Haridra,Daruharidra, Shunti and Musta are reported with the Deepana and Pachana effect.Main symptoms from the gastro-intestinal tract commonly reported are nausea and vomiting.This is controlled with the Shunti, Pippali and Vibhitaki.Pureeshavaha Srotas Diarrhea is common symptom managed by the composition such as Bilwa, Tulasi,Devadaru, Shunti, Vibhitaki, Musta and Haridra. All other conditions which develop from thisSrotas is also managed.Rasavaha Srotas Bilwa, Haridra, Daru haridra, Shunti, Pipplai, Kusta, Vatsanabha and Musta are thebest alliterative and anti pyrexial herbs included in the combination. These herbs not onlyanti-pyrexial but also assists to potentiate the rasavaha sroto moola.Raktavaha Srotas Commonly observed skin conditions revile the inclusion of skin and its importance inHIV infectious conditions. Few drugs included in the combination for the prevention andcurative aspect are Amalaki, Haritaki, Tulasi, Maricha, Vatsanabha, Karanja, Kusta,Daruharidra, Shunti and Ajamutra. Anemia (Pandu) is commonest complaint. Thus Haridra, Daru Haridra, Shunti andAjamutra are added to supplement the deficiencies in the formation of blood. Discussion and conclusion - Bhutabhishangaja Ojokshaya126
  • 136. Statistical evaluation The clinical evaluation of Ojokalparasayana and Amruta kayakalparasayana wasconducted in 18 cases of Ojokshaya in two different groups due to the HIV infection. Theover all response is significant (P<0.001) in both subjective and parameters. The effect of two groups in all parameters are the same there is a highly significant inHB % when we compared two groups (P < 0.05) and all the after parameters and notsignificant (P>0.05).Recommendations for further study: The following recommendations are made on the basis of the observations made for further studies as well as to observe the limitations. (a) Same yoga can be repeated by taking a large number of samples with randomized control groups. (b) The effect of Ojokalpa Rasayana can be studied along with Shodhana therapy or individually as Bilwadivati and Agnikumara vati. (c) The effect of Ojokalpa Rasayana can be studied on long duration to evaluate its efficacy as antiretroviral therapy along with viral load studies.Limitations of the study: Sample size is small to generalize the result. Samples are selected incidentally. As chosen drug is a compound form it is difficult to specify the action of any individual herb and or to cumulative mode of action. Discussion and conclusion - Bhutabhishangaja Ojokshaya127
  • 137. Conclusion ♦ AIDS is a multi dimensional disease syndrome, affecting physical, mental, social and spiritual facets of the affected person. ♦ The virus HIV hampers the Immune system. At the same time there is no specific treatment available for the AIDS /HIV infection. ♦ Susruta explains about “abhigata” or injury as a cause of Ojokshaya. Very specifically an injury in sexual organs or anus is a high risk factor for transmission of HIV infection. ♦ The Ojokshaya occurred due to general causes apart from infection and that caused due to infection are of two different Samprapti. So in this way pathological events following bhootopaghata correlate with modern understanding of HIV infection. ♦ The prognosis of diseases as explained in Ayurveda and modern science are similar as the early stages of HIV infection can be managed with antiviral and immuno modulators and advanced stage will not improve with any available treatment. ♦ Among 3 major principles of Krimi Chikitsa, the prakriti vighata type suits the present context of HIV infection. ♦ In other words the management is – As antioxident - Amalaki, Shunti and Haritaki Anti tubercular - Pippali, Karanja and Vacha Anti bacterial -Amalaki, vibhitaki, Karanja, Musta, Maricha and Haritaki Anti fungal - Haritaki. Vibhitaki and Karanja Discussion and conclusion - Bhutabhishangaja Ojokshaya128
  • 138. ♦ The normal healthy state of such a body requires normalcy of several factors. This normal strength in the body is called as Sleshma, which has synonym -“Ojas”.♦ Ojas depends upon healthy state of Kapha. Kapha in physiologically represents potential sours of strength and resistance to disease and decay of Bala and Ojas.♦ HIV is transmitted by homosexual and heterosexual contact.♦ Transfusions of whole blood, packed red blood cells, platelets, leukocytes, and plasma are all capable of transmitting HIV infection. It is estimated that 90 to 100% individuals who were transfused with HIV- infected blood became infected.♦ Opportunistic infections are late complications of HIV infection, for the most part occurring in patients with less than 200 CD4+T cells per micro liter. Opportunistic infections are the leading cause of morbidity and mortality in-patients with HIV infection.♦ This infection spectrum is ranging from primary infection with or without acute syndrome are a symptomatic stage and to an advanced disease.♦ The Bhutabhighataja Ojokshaya is a syndrome, which is almost, resembles the disease AIDS.♦ Etiological factors for the Bhutabhighataja Ojokshaya and AIDS are the same.♦ The Ojokapla Rasayana found effective in Bhutabhighataja Ojokshaya i.e. HIV+ve cases. Discussion and conclusion - Bhutabhishangaja Ojokshaya129
  • 139. ♦ The effect of two groups in all parameters are the same there is a highly significant in HB% when we compared two groups (P < 0.05) and all the after parameters and not significant (P>0.05).♦ The Ojokapla Rasayana group is not significant in TLC and CD8 sell count (P>0.05) and after parameters shows highly significant in Amruta Kayakalpa Rasayana group except ratio all the parameters are highly significant (P>0.05).♦ Ojokapla Rasayana group E.S.R. Platelet counts Kornefsky gradings and CD4 are highly significant when compared to Amruta Kayakalpa Rasayana group (P<0.05 and T values).♦ The WBC, Weight and General Health Condition are having same effect in both groups (by comparing P and T values).♦ The parameter HB%, TLC and CD8 cell counts are highly significant Amruta Kayakalpa Rasayana group compared with Ojokapla Rasayana group.♦ Over all there is a more variation in Ojokapla Rasayana group.♦ Amruta Kayakalpa Rasayana group, HB% EWR, TLC, WBC and CD8 are having uniform effect and in Ojokapla Rasayana group platelet count CD4 and weight are having uninformed effect (by comparing co-efficient of variation). Discussion and conclusion - Bhutabhishangaja Ojokshaya130
  • 140. Summary♦ Among them since two decades sudden emerge of new epidemics such as SARS and AIDS/HIV, termed in Ayurveda as Bhootopaghataja Ojokshaya.♦ The etymology of words, Bhoota and Upaghata developed form the word Bhootopaghata is, Bhoota denotes as Krimi or Virus and Upaghata means as infection. So exclusively the word Bhootopaghata indicates as viral infection.♦ In 1983, Human Immuno Deficiency Virus (HIV) was isolated from a patient with lymph- adenopathy.♦ HIV-infected individuals are presenting in increasing numbers to family physicians, obstetricians, gynecologists, pediatricians and surgeons with clinical problems that may be directly or indirectly related to their HIV-infection.♦ When we analyze the basic cause behind the origin of this disease and subsequent transmission, we understand bad conduct of human beings unnatural behavior of man resulted in a disease called HIV infection.♦ As of now an estimated 4-6 million HIV infected cases are present in India.♦ The first case of HIV infection was identified in India in 1986 at Chennai.♦ AIDS is a multi dimensional disease syndrome, affecting physical, mental, social and spiritual facets of the affected person.♦ The virus HIV hampers the Immune system. At the same time there is no specific treatment available for the AIDS /HIV infection.♦ Susruta explains about “abhigata” or injury as a cause of Ojokshaya. Very specifically an injury in sexual organs or anus is a high risk factor for transmission of HIV infection. Summary - Bhootopaghataja Ojokshaya131
  • 141. ♦ Charaka does not explain the signs and symptoms of Ojokshaya, whereas Susruta then explained different stages of Ojokshaya.♦ When we see the modern classification of HIV disease there are 4 stages of HIV infection, which results in death at the end.♦ The first stage is primary infection or acute sero-conversion stage. This particular stage of HIV infection can not be correlated to the stages of Ojokshaya.♦ The Ojokshaya occurred due to general causes apart from infection and that caused due to infection are of two different Samprapti. So in this way pathological events following bhootopaghata correlate with modern understanding of HIV infection.♦ The prognosis of diseases as explained in Ayurveda and modern science are similar as the early stages of HIV infection can be managed with antiviral and immuno modulators and advanced stage will not improve with any available treatment.♦ Among 3 major principles of Krimi Chikitsa, the prakriti vighata type suits the present context of HIV infection.♦ In other words the management is – As antioxident - Amalaki, Shunti and Haritaki Anti tubercular - Pippali, Karanja and Vacha Anti bacterial -Amalaki, vibhitaki, Karanja, Musta, Maricha and Haritaki Anti fungal - Haritaki. Vibhitaki and Karanja♦ Recent advances in medical treatment have given scientists renewed strength in the struggle against HIV-the virus that causes AIDS.♦ AZT inhibits reverse transcription, which is vital for HIV to infect its host. AZT and DDI will stop this from occurring and thus stop the HIV virus from spreading.♦ Those cells include the immune system cells, blood cells, and the nervous system cells. It has been found that HIV only infects cells with CD4. Summary - Bhootopaghataja Ojokshaya132
  • 142. ♦ The vaccine in “Evaluation of an HIV-1 DNA Vaccine Encoding a Modified Gag-Pol in Uninfected Adult Volunteers (Grace Kelly, RN)” trial, VRC 4302, is classified as a genetic vaccine. Genetic vaccines contain the genes (hereditary material) which direct the production of the proteins of the HIV irus. VRC 4302 contains the gene for the Gag and Pol proteins of HIV.♦ Present study is a comparative study to assess two Ayurvedic combinations of immune builders, Immuno-modulators and acts on Ojovikruti by preventing ARC.♦ This dissertation reviews literary review of Ojokshaya and HIV infection in comparison♦ The normal healthy state of such a body requires normalcy of several factors. This normal strength in the body is called as Sleshma, which has synonym -“Ojas”.♦ Ojas depends upon healthy state of Kapha. Kapha in physiologically represents potential sours of strength and resistance to disease and decay of Bala and Ojas.♦ Ojas is the ‘Sara’ i.e. essence of all Dhatus.♦ Ojas is present all over the body and in each cell of the body.♦ It is of two varieties Para Ojas and Apara Ojas.♦ The term Ojas has been stated in Ayurvedic classics represents Kapha, Bala, Shleshma, Rasa and Rakta and it resists disease and decay in further Promotes durability, (preserves the body from decay)♦ Charaka has mentioned that the Ojas is the Ahara for rakshas and if they consume the Ojas, which leads to depletion of Ojas.♦ Specific resistance to the disease is called Immunity.♦ Four different varieties of T cells have been identified: helper / inducer T cells suppressor T cells, cytotoxic T cells (which are also known as effectors T cells or killer cells), and memory T cells. Summary - Bhootopaghataja Ojokshaya133
  • 143. ♦ Antigens can also be processed and presented to T4 cells by various types of cells in the body in addition to macrophages. The other types of antigen presenting cells include the B cells themselves, the Langerahans cells of the skin, and specialized cells called dendritic cells in the lymph nods and spleen.♦ T8 cells mediate cellular immunity. The cytotoxic T cells attack and destroy cells that have antigen, which activated them. To ensure maximal specific T cells response the antigen is linked to molecular components of the HLA system (by B cells, dendritic cells and macrophages) and presented to T cell.♦ Cytotoxic T cells cause antigen-specific lyses by direct cell-to-cell contact.♦ Any HIV-infected individual with CD4+T cell count of<200/microliter had AIDS by definition, regardless of the presence of symptoms or opportunistic diseases.♦ It is important to distinguish between being infected with HIV and having AIDS. People infected with HIV may take 5-7years or more to develop as AIDS.♦ The four recognized human retroviruses belong to two distinct groups, i.e.HIV-1 and HIV-2.♦ The most common cause of HIV disease throughout the world is HIV-1 comprises several subtypes with different geographic distribution.♦ HIV is free from live, when it is out side the body. HIV has a number of mechanisms to evade elimination by the immune system.♦ HIV-1 and HIV-2 are both viruses that belong to the same family, but vary in genetic make up. Both HIV-1 and HIV-2 have been detected in India and both leads to AIDS.♦ However studies of lymphoid tissue using PCR analysis for HIV RNA and in site hybridization for individual virus expressing cells clearly demonstrated that HIV replication occurs throughout the course of HIV infection, even during clinical latency. Summary - Bhootopaghataja Ojokshaya134
  • 144. The availability of sensitive PCR techniques leads to the demonstration that viremia present at all stages of HIV disease.♦ HIV is transmitted by homosexual and heterosexual contact.♦ Transfusions of whole blood, packed red blood cells, platelets, leukocytes, and plasma are all capable of transmitting HIV infection. It is estimated that 90 to 100% individuals who were transfused with HIV-infected blood became infected.♦ HIV has been demonstrated in seminal fluid both within infected mononuclear cells and in the cell free state. There is a strong association of transmission of HIV with receptive intercourse.♦ HIV infection can be transmitted from an infected mother to her fetus during pregnancy or during delivery.♦ HIV is an RNA virus whose hallmark is the reverse transcription of its genomic RNA to DNA by the enzyme reverse transcriptase. Life cycle of HIV infection♦ Opportunistic infections are late complications of HIV infection, for the most part occurring in patients with less than 200 CD4+T cells per micro liter. Opportunistic infections are the leading cause of morbidity and mortality in-patients with HIV infection.♦ Approximately 80% of AIDS patients die as direct result of an infection other than HIV, with bacterial infections heading the list.♦ Tuberculosis is a particularly important problem with HIV infection. Tuberculosis may be the earliest clinical sign of HIV infection. Disseminated disease is more common with low CD4+T cell counts.♦ The diagnosis of HIV infection depends on the demonstration of antibodies to HIV and or the direct detection of HIV or one of its components. The standard screening test for HIV is the enzyme linked immuno sorbent assay (ELISA). Summary - Bhootopaghataja Ojokshaya135
  • 145. ♦ Patients with CD4+T cell counts below 200/ul are at high risk of infection with preumocytis carini, while patients with CD4+T cell counts below 100/microliter are at high risk of infection with cytomegalovirus and mycobacterium avium-intracellular complex.♦ The cornerstone of medical management of HIV infection is antiretroviral therapy. Suppression of HIV replication is an important component in prolonging life.♦ Accelerated weight loss in an HIV infected patient is sign of disease progression.♦ Prevention of STDs would also reduce the risk of HIV transmission.♦ By running public awareness campaigns for HIV♦ T. Chelaula inhibited HIV-1 proteas activity at a concentration of 25 microg/ml in the flurogenic assay.♦ The HIV-1 protease (PR) inhibitory activity was determined by using the fruit peal methanol extract of Vibhitaki.♦ Objectives of the study♦ To evaluate the efficacy of Ojokalpa Rasayana and Amrut Kayakalpa Rasayana in improving the clinical status of Ojokshaya with special reference to HIV infection♦ To assess the role Ojokalpa Rasayana and Amrut Kayakalpa Rasayana on CD4 cell count, which is a marker of stages of the HIV infection along with viral load.♦ Drug: Ojokalpa Rasayana♦ General health condition (Grade), Karnofsky performance score, Body weight, Total WBC count, Total count platelets, Total count lymphocytes, Erythrocytes sedimentation rate, CD4 cell count, CD8 cell count and CD4: CD8 ratio are elicited in the patients before and after the treatment.♦ This infection spectrum is ranging from primary infection with or without acute syndrome are a symptomatic stage and to an advanced disease. Summary - Bhootopaghataja Ojokshaya136
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  • 152. 203. Thatte, U.M. Dahanukar, S.A. Comparative study of immunomodualting activity of Indian medicinal plants, Lithium carbonate and Glucan, 1988, October, (10) 639-44204. A survey of some Indian medicinal plants for anti human immuno deficiency virus (HIV) activity, M. Premanathan et.al. The Indian journal of medicinal research, vol 112-9205. Ayurmedline, Vol-2, pp 556206. Astanga Hridaya sutra 11/37207. Susruta Samhita Sutra, 15/23-27, Edited by Vd. Jadavaji Trikamji Acharya, published by Chaukhambha Orientalia, Varanasi, 1980208. Charaka Samhita Shareera 2/10, Edited by Vd. Jadavaji Trikamji Acharya, published by Chaukhambha Sanskrit Samstan, Varanasi, 1984209. Sahasra yoga gutika prakarana210. Ibid, 189211. Indian materia medica, pp 45212. Ibid 856213. Ibid 1001214. Ibid 1260215. Ibid 295216. Ibid 414217. Ibid 187218. Bhavaprakasha poorva khanda haritakyadi varga 42219. Ibid 60-61220. Indian materia medica, pp 478221. Sahasrayoga Gutika prakarana222. Product index – Amruta Drugs223. (a) Choi S, Lagakos SW, Schooley RT, Volberding PA. CD4+ lymphocytes are an incomplete surrogate marker for clinical progression in persons with asymptomatic HIV infection taking zidovudine. Ann Intern Med. 1993;118:674-680 (b) Volberding PA, Lagakos SW, Grimes JM, et al. A comparison of immediate withdeferred zidovudine therapy for asymptomatic HIV-infected adults with CD4 cell countsof 500 or more per cubic millimeter. N Engl J Med. 1995;333:401-407 (c)Stein DS, Korvick JA, Vermund SH. CD4+ lymphocyte cell enumeration forprediction of clinical course of human immunodeficiency virus disease: a review. J InfectDis. 1992;165:352-363224. Predictive value of viral load measurements in asymptomatic untreated HIV-1 infection, John.P.A, et.al. in AIDS 10 (3) pp 255-262, 1996 VII Reference –Bhutabhishanga Ojokshaya
  • 153. 225. BMJ Nov. 2001226. Rajgopal K. Clinical evaluation of the efficacy of the an ayurvedic drug formulation against HIV and AIDS in proceedings of seminar on Ayurvedic management of AIDS and Cancer, Jamnagar, 1999.227. Evaluation of immuno potenntiating activity of a herbo mineral formulation PV- 150986 in HIV infection 1998,228. Susruta Samhita sutra 15/24229. Charaka Samhita Nidana 4/37230. Charaka Samhita Chikitsa 16/4-6231. Charaka Samhita Chikitsa 8/40-41232. Susruta Samhita Uttara 39/43-45233. Charaka Samhita Chikitsa 23/15234. Charaka Samhita Chikitsa 8/40-41235. Susruta Samhita sutra 15/28 Dalhana on it236. Ibid237. BMJ Nov. 2001238. Philips AN, Lee CA, Elford J, et al. Serial CD4 lymphocyte counts and development of AIDS.lancet.1991: 337:389-392 VIII Reference –Bhutabhishanga Ojokshaya
  • 154. Bibliography 1. Charaka samhita Poorvardha and Uttarardha, vidyotini Hindicomentary, by Pt. Kashinath shashtri and Dr. Gorakhanatha Chaturvedhi, Published by Chaukhambha Bharati Academy Varanasi. 2. Sushruta samhita Poorvardha and Uttarardha with nibhandha sangraha comentory by Vaidya Yadavaji Trikamaji Acarya, published by Krishnadas Academy Varanasi printed at 1998. 3. Astanga hridayam 1-2 by prof. K.R. Srikantha murthy 2nd edition 1995, published by Krishnadasa academy. 4. Astanga Sangraha 1-2 by prof. K.R. Srikantha Murthy 1st edition 1996 , published by Chaukhambha orientalia, Varanasi. 5. Madhava nidana part I and II by Sri Madavakar with Madhukosha comentory by Shri Vijayaraksheeta and Shreekanthadatta, with vidyothini hindi comentory by shri Sudarshana Shastri, published by Chaukhambha Samskruta Bhavana Varanasi. 32nd edition 2002. 6. Dravya Guna Vignanan II part by prof. P.V. Sharma, 16th edition 1994, published by Chaukhambha Bharati academay Varanasi. 7. Dravya Guna Vignanan II part by Dr. JLN Shashtri Ist edition 2004, published by Chaukhambha orientalia Varanasi. 8. Vaidhyaka shabdha sindu by Kaviraj Nagendranatha sen 3rd edition 1983, published by Chaukumbha orientalia Varanasi. 9. A Sanskrit - English dictionary by Shri Monier Monier Williams 1st edition 1993, published by Motilal Banarasidas, publishers pvt. Ltd. Delhi. 10. Dhanvantari Nighantu by prof. Priyavruta Sharma, 1st edition 1982, published by Chaukhambha orientalia Varanasi. Bibliography- Bhutabhishanga Ojokshaya i
  • 155. 11. Madanapalana Nighantu12. Raj Nighantu by Dr. Indradeo, tripati, 2nd edition 1998, published by krishnadasa academy Varanasi.13. Indian medicinal plants by K.R. Kirtikar and B.D. Basu 2nd edition published by Lalitamohana Basu Allahabad.14. Kaiyadeva Nighantu pattya pattya vibhodhaka by Dr. Guruprasad Sharma 1st edition 1979 published by Chaukhambha orientalia Varanasi.15. Nighantu adarsha by Bapulal G. Vaidya 1st edition 1968, published by Chakhamba Vidyabhavana Varanasi.16. Bhavaprakasha of Shri Bhavamishra vidhyotini hindi commentary by Bhaishajyaratna Pt. Shri Bramha Shankar Mishra. 5th edition 1988, published chaukhumba Sanskrit Samsthana Varanasi.17. Kashyapa samhita Ayurveda linear shri. Satyapala Bhishagacharya, published by Chaukhamba Sankrit Samsthana, Varanasi.18. Vedome Ayurveda by Vaidya Pt. Ramagopala Shashtri 1656 published by La madana mohanalalal Ayurvedic Anusandhan Trust, Delhi.19. Sharangadhara Samhita by Pt. Parusharama Shastri Vidyasagar 3rd edition 1983, published by Chaukhambha Orientalia, Varanasi.20. Agnipuranaki Ayurvediya Anusandhana Samiksha By Vivekananda Pandeya 1st edition 1997, published by Shri Satguru publications Delhi.21. Essentials of Basic Ayurveda concepts by prof. V.V.S. Shashtri 1st edition 1999, published by Principal D.G.M.A.M.C. Gadag.22. Shareer kriya vignana by Dr. P.V. Sharma 4th edition 1982, published by Chaukhambha Bharati Academy. Bibliography- Bhutabhishanga Ojokshaya ii
  • 156. 23. Shabdha kalpa druma by Raja Radha Kanthadeva 1-5 Vol 3rd edition 1967, published by Chaukhambha Bhavan Varanasi.24. Devidson’s principles and practice of medicine 17th edition by CRW Edwards, IAD Bouchier, C Haslett, 1996, published by Great Britten by BPC Paulton Books Ltd.25. Huchison’s Clinical methods by Michelswsh published by W,B, Saunders 21st edition 2002.26. Pharmocology and Pharmocotherapetic by R.S. Satuskar and S.D. Bhandarkar, S.S. Ainapure 17th edition 2001 published by Popular prakashan Pvt. Ltd. Mumbai.27. Taber’s cyclopadic medical dictonery by Clyaton L. Thomus 17th edition 1993 published by Jeetendra P Vij for Jay Pee brothers medical publications pvt. Ltd. New Delhi.28. Herrison’s principles and internal medicinal by fauci, Braunwald and others.1-2 14th edition 1998 published by Mc-Graw-Hill Book company Singapore.29. Text book of Medical Physicology by Arthur C Guyton and John Hall 10th edition 2000, published by Harcourt. Asia pvt. Ltd.30. Gray’s anatomy by lawpence H Bennister and others, 38th edition 2000, published by Charchil living stone, Edern Burgh London. Harcourt publishers.31. API textbook of medicine 6th edition 1999 by Gurumukha Sainani, published by Association of physicians of India, Mumbai.32. Boyd’s textbook of pathology by AC Ratehie 9th edition 1-2 1990, published by Lea and Sebrigy USA.33. Methods in Biostatics by B.K. Mahajan 6th edition 1997 published by Jay Pee brothers medical publications pvt. Ltd. New Delhi. Bibliography- Bhutabhishanga Ojokshaya iii
  • 157. 34. Medical micro biology and immunology by Warren of Levingson and Erneast Jawetz 3rd edition 1992 published by Prentice Hall International INC. Bibliography- Bhutabhishanga Ojokshaya iv
  • 158. Special case sheet for Bhutabhishangaja Ojokshaya (HIV Infection) PGCRC ,(KA YACH IK ITSA) , SHRI. D .G.M.AYUR VED IC MED ICA L COLLEGE, GADA GG u id e: D r . Siva r ama Pras ad Ke tha makk a Schola r:C o - g u ide s: D r . A sh ok K u m ar Pan da C .S.Ha nama nta go ud ar1. Name of the Patient Sl.No.2. Sex - M F OPD No3. Age - Years IPD No Birth data: Place of Birth District State AM Date Month Year Time Hours Minutes PM4. Religion Hindu Muslim Christian Other5. Occupation - Sex worker Driver Business Service Student Household6. Economical status Poor Middle class Higher middle Higher class7. Marital Status - Married Single Divorced Widow/er 2/3 M a r r i a g e s8. Address Phone: Pin Schedule initiation9. Selection Included Excluded Schedule completion10. Group A) Ojokalpa Rasayana B) AKK Rasayana11. Result Responded Not responded Discontinued INFORMED CONSENT I Son/Daughter/Wife of amexercising my free will, to participate in above study as a subject. I have beeninformed to my satisfaction, by the attending physician the purpose of the clinicalevaluation and nature of the drug treatment. I am also aware of my right to quit thetreatment, at any time during the course. Patients Signature
  • 159. 1. CHIEF COMPLAINTS WITH DURATIONSl. Duration ComplaintsNo Less than 1 yr 1 to 2 years Above 2 years1 Loss of weight2 General weakness (Glani)3 Loss of appetite (Aruchi)4 Fever (Jwara)5 Internees of Body (Stabdhagatrata)6 Loss of complexion (Vyadhitendriya)7 Emaciation (Mamsa Kshaya)8 Looseness of Joints (Sandhi Vislesha)9 Somnolence (Anidra)10 Delirium / Convulsions (Pralapa)2. ASSOCIATED COMPLAINTS Annavaha Srotas Rasavaha Srotas1 Oral thrush/ Nausea/ Vomiting 1 Giddiness2 Bleeding gums 2 Palpitation3 Pain Abdomen / distention Mutravaha Srotas4 Dysphagia / soar throat 1 Burning micturition5 White tongue (Candidiasis) 2 Urethral discharge6 Hairy tongue (leucoplakia) Pureeshavaha Srotas Pranavaha Srotas 1 Diarrhea1 Cough 2 Anal itching (Candidiasis)2 Blood with sputum Prajanana Samstana3 Breathlessness 1 Genital ulcers4 Chest pain 2 Genital warts5 Headache 3 Vaginal Candidiasis Raktavaha Srotas Others1 Skin eruptions 1 Drowsiness2 Molluscum 2 Lymphdenitis3 Warts 3 Acne Vulgaris4 Herpes zoster 4 2
  • 160. 3. HISTORY OF PRESENT ILLNESS(a) How it was diagnosed? Intentional / Accidental(b) Mode of onset -1) Source of infection Sexual exposure Blood transfusion Injections2) Early symptoms3) Later symptoms(c) Mode of progress Typical Rapid Longtime non progressive(d) Suffering from any systemic disease? Tuberculosis Diabetes Mellitus Hypertension Cancer Venereal diseases Cardiac disease4. HISTORY OF PAST ILLNESS5. TREATMENT HISTORY6. FAMILY HISTORY 3
  • 161. 7. PERSONAL HISTORY a) Food habits Vegetarian Mixed diet Taste Sweet Sour Salty preferred Pungent Bitter Astringent b) Sleep Day Night Sound Disturbed c) Hygiene Good Unhygienic d) Addictions Tobacco Alcohol Drugs e) Sexual behaviors Heterosexual Homosexual Marital Extra marital Single multiple f) Blood transfusion Donor Recipient Frequency g) Bowel habits Normal Loose Constipated h) Menstrual History Regular Irregular Amenorrhea Menopause8. EXAMINATIONa) Vitals Temperature ºF Pulse Blood pressure / Respiratory rate Weight Height Body-Mass Indexb) General Built & Nutrition well Moderate Poor Oral Cavity Ulcers Hairy Leucoplakia Coated Lymph nodes enlargement Epitroclear Cervical Supra clavicular Axillary Inguinal Any other 4
  • 162. c) Ayurvedic assessment1. Hetu Ahara Vihara Anya B A B A B AAnashana Vatatapa sevana Koapam - AngerAlpashana Ati Vyayama Soka Ati Vyavaya Chinta Sonita a t i v a r t a n a Bhaya Prajagara Bhootopaghgta2. Dosha Vata Vriddhi Pitta Vriddhi Kapha Vriddhi B A B A B AKarshya Peetamootra AgnisadanaKarshnya Peetanetra PrasekaUshnakamitwa Peetavit AlasyaKampa Peeta twak GowravaAnaha Atikshudha SwetangataShakritgraha Atidaha SheetangataBalabhramsha ShlathangataNidrabhramsha SwasaPralapa KasaBhrama Atinidra Vata Kshaya Pitta Kshaya Kapha Kshaya B A B A B AAngasada Mandagni BhramaAlpabhshite Shareera Urah shoonyataAhitam sh ee ta tw amChesta heenata Prabhahani Shira shoonyataVyamoha HriddravaSleshma vriddhi Sandhi saithilya3. Lakshana Ojo Vishramsha Ojo Vyapat B A B AGatra sadanam Stabdha gatrataDosha chyavanam Guru gatrataSandhi vislesha Vata shophaKriya sannirodha Varna hani Glani Tandra Nidra Ojo KshayaBhaya DowrbalyaChinta VyathitendriyaDuschaaya DurmanaRooksha KshamaMoorcha Mamsa kshayaMoha Pralapa 5
  • 163. d) Systemic 1) Respiratory system Shape of chest Normal Deformed Trachea Normal Right Shift Left Shift Movements Normal Restricted Auscultatory findings Breath Sounds Vesicular Bronchial Added sounds Ronchi Crepitation Rub (Advise X-ray chest / Sputum examination if required) Report: - 2) Gastrointestinal tract Tenderness Mild Moderate Severe Organomegaly Liver Mild Moderate Severe Spleen Mild Moderate Severe Fluid Thrill Present Absent Shifting dullness Present Absent Abdominal Lump Present Absent (Advise U.S.G if required) Report: - 3) Cardiovascular system S1 S2 Murmur (Advise E.C.G. if required) 6
  • 164. 4) Central Nervous System Any neurological deficit, if so specify.5) Genito-Urinary system6) Any other (if any)9. LABORATORY INVESTIGATIONS HAEMATOLOGICAL DIFFERENTIAL COUNT Hb% gm/dl Lymphocytes Total Count Lymphocytes /µl Neutrophils Total Count Platelets /µl Eosinophils Total Count Leucocyte /µl Basophils st E.S.R mm/1 Hour Monocytes Random Blood Sugar mg/dl SPECIAL INVESTIGATIONS Elisa HIV- I & II Rapid (Tridot) Western Blot CD4 cell count /mm 3 CD8 cell count /mm 3 CD4 : CD8 Ratio10. DIAGNOSIS STAGE11. ASSESSMENT CRITERIA SUBJECTIVEParameter Before After Parameter Before AfterGeneral health Karnofskycondition (Grade) performance score OBJECTIVETotal W.B.C Count Total Count PlateletsCD4 cell count Total Count LymphocytesCD8 cell count E.S.R.CD4 : CD8 ratio Body weight 7
  • 165. PERIODICAL ASSESSMENT stDate Baseline 1 2nd 3rd Final Follow up Follow up Data Assessment Assessment Assessment Assessment Assessment-1 Assessment-2 0 days 30 days 60 days 90 days 120 days 150 days 180 days DateGH Sc or eK P Sco rePulse RateB lo od P res su reT e mpe ra t ur eRe sp irat ory R a tew eightT LCCD4CD8CD4:CD8 FINAL ASSESSMENTS L .NO ASSESSMENT CATEGORY NOTES 1 Patients impression 2 Side effects 3 Investigators note 8
  • 166. Guidelines for gradations in HIV positive casesKARNOFSKY PERFORMANCE SCORES.No Karnofsky performance score Score1 Normal - no evidence of disease 1002 Able to carry on normal activity 903 Normal activity with effort with some symptoms and 80 signs of disease4 Cares for self, unable to carry on normal activity 705 Requires occasional assistance and medical care 606 Requires considerable assistance and frequent 50 medical care7 Disable, requires special care and assistance 408 Severely disabled, hospitalization indicated 309 Very sick, active supportive treatment required 2010 Morbid, fatal processes are progressing rapidly 1011 Dead 00IMPROVEMENT IN GENERAL HEALTH Grade Parameter for grading 0 Static / worsen 1 Mildly better 2 Moderately better 3 Much better 9