Switram kc020 hyd

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A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH”IN THE MANAGEMENT OF SWITRAM (VITILIGO), K.NAMRATA, Department of Kayachikitsa, PG unit Dr.BRKR Govt. Ayurvedic College, HYDERABAD

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Switram kc020 hyd

  1. 1. 1 INTRODUCTION  The aim of medicine is to safeguard and rescue men from the consequences of their vices. Since its inception Ayurveda emphasizes on maintenance of positive health and alleviation of the diseases pestering humankind, among which skin diseases are one. Switra is a dermatological disorder having its references cited in the Vedas. Theterm is derived from “Sweth Varne” meaning white colour. It is basically a diseaserelated to hypopigmentation. Switra is also known as “Sweta Kustam” or “Kilasam”. Switra emerges as a sequel to irregular dietary habits, life style changes, andgenetic predisposition. Constant use of chemicals, cosmetics, plastic, rubbers, andpollution may accelerate the attack of the disease. The disease involves the skin and doesnot cause pain, ulceration or any secretions. Switra inflates an inferiority complex in thepersons affected. Skin is the vital organ involved in this disease. Skin being the largest organ of thebody and on the surface is continually exposed to injury. The colour of the skin plays animportant role as high cosmetic value is attributed to it. Colouring, tattooing, adorningwith jewellery are all part of skin appeal. The general state of the health is reflected in the appearance and condition of theskin and the earliest signs of many systemic diseases may be observed by inspecting it.As the skin is on the surface and it is on display patient with skin diseases are always inpublic eye. The greatest handicap of all is to be unwelcome and isolation by thecommunity. The functions of the skin are impaired in skin diseases making those moreaffected, more vulnerable and less able to reconstitute themselves after damage. 20-30%of skin diseases require serious attention. (Davidson) The disease Switra is one amongthem, as it causes immense mental agony and social embarrassment. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  2. 2. 2 Based on the clinical features of switra, it can be correlated to vitiligo of the thmodern medicine. Vitiligo on the face is ranked 17 by WHO in world’s most Disablingdiseases. Vitiligo is also an ancient malady having references cited in Bible and othercontemporary Texts. It is defined as a common acquired discolouration of the skincharacterized by well circumscribed, ivory or chalky white macules which are flush on tothe surface. Sometimes systemic, Cutaneous, ocular associations may be present. Thehair over the patch may be white or normal. Vitiligo occurs world wide with an overall prevalence of 1%. The higherincidence of the condition has been recorded in India from Asia, followed by Mexico andJapan. The incidence is 6% in Calcutta, 4% in Vellore, 8% in Amaravati, 2.9% in Goa,8.8% in Delhi. The difference of its incidence may be due to higher reporting of vitiligoin a population where an apparent colour contrast and stigma attached to the conditionmay force them to seek early consultation. Both males and females are equally affectedwith no predilection of sex. The age of first onset is below 20 years and the lower limbsare generally the site of first onset. The imperatives of its epidemiology both in rural India and in global arereckoning and have been highlighted. In spite of the latest advancements made in modernmedicine the etiology of vitiligo remains unknown. It is expected to be of autoimmuneorigin as it is associated to some of the autoimmune disorders. Occasionally it may bepossible to identify the triggering factors. An effective panacea for the disease could not be found till date. Generally topicalcorticosteriod therapy, topical PUVA, Oral Psoralen Photo chemotherapy or oral PUVA,Surgical techniques like skingrafting, other techniques like tatooing, camouflage creamsare employed to manage vitiligo. But all the above mentioned methods are associatedwith high risk factors, are expensive, and unsuitable for people living in differentclimatic conditions and the success rate is not commendable. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  3. 3. 3 Ayurveda offers absolution to many diseases among which switra is one.Innumerable yogas have been described to combat the disease. One such comprehensive formula is “Dhatri- Khadira Kwath” from BhaishajyaRatnavali, contemporary text of 19 A.D. A total of 30 patients were taken for this study and all the patients received thetreatment for 45 days. The medicine was administered in kwath form, followed by honeyas anupana. The main aim was to assess the efficacy of the formula in causingpigmentation in the white patches of switra. And three Clinical parameters – colour of thepatch, number of patches and size of the patches were taken into consideration to assessthe result. Present study is divided into five parts. The first part deals with review ofliterature of the disease, second part deals with drug review, third part deals with clinicalstudy – observations and results, fourth part deals with discussion, conclusion, summaryand fifth part deals with references, bibliography and annexure. Thus a humble step has been made to probe into various aspects of switra and itsmanagement with the trial drug. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  4. 4. 4 HISTORICAL REVIEWSwitra is an ancient malady and a historical background will facilitate continuity withcurrent research .Many earliest references of switra dating back to Vedic kala are foundand the contribution of our ancestors in combating the disease is known.For convenience sake time period is divided into:1. PRACHEENA KALA (5000 BC- 7 A.D )2. MADHYAMA KALA ( 8 A.D –15 A.D )3. ADHUNIKA KALA (16 A.D ONWARDS )PRACHEENA KALA (5000 BC- 7 A.D):VEDIC PERIOD: includes description of the disease in Rig, Yajur, Sama &Atharvavedas.RIG VEDA: a) Old looking unmarried princess Ghosa, the daughter of Kaksivana was cured of kusta roga and was made young and beautiful, and was married .1 b) Sujava was cured of kusta and rejuvenated and was married to a good looking 2 girl . 3 c) Diseases like kilasa and Palithya were described . d) Application of Bringraj, Harida , Neelika , Indravaruni in kusta ,palitya rogas .Here Sayanu interprets kusta as Svetha kustam. 4YAJUR VEDA: There is a reference of moon being affected by the disease.5 A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  5. 5. 5ATHARVA VEDA: a) There is a refernce in Atharva Veda that white coloured patches appear in a disease called Sweta kusta, and when it penetrates into deeper dhatus it is called Kilasa kusta .6 In this context “ASIKINI “and “RAJINI” are the drugs used which are veryimportant in the disease.SAMA VEDA : No references found in this veda.Aitheraya Aranyaka: Sage Bharadwaja mentioned twak, mamsa .rakta are derived frommother and in a stage all the three are affectedDuring Uanishad period Asvatayana mentioned maharogas .Narayana interprets Kusta 7as one among them.In Mahabharata (400 B.C) mentioning of many twag doshas are found but no specialreference of Switra is found.Puranas (500 B.C) were influenced by the medical concepts and description of manydiseases are found in them.Padmapurana mentions kusta and Switra as diseases caused due to the imbalance of the 8tridoshas.Markandeya purana mentioned two girls suffered with this disease and were eventuallycured 9It is regarded by this purana that all twag rogas are due to past life sins.Vayu purana regarded kusta and kilasa to have evolved due to faulty practice of yoga 10. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  6. 6. 6 11Vishnu purana mentioned a wide variety of skin diseases in sharirika rogas .Inanatomical chapters a detailed description of embryological development of organs isfound and seven layers of skin have been described in this context.Itihasa purana mentioned switra among several diseases caused due to derangement ofthe doshas .Sins or the papakarmas are considered to play a major role in causing the skindiseases in particular .12.Brahma vaivartha purana mentioned many skin diseases under the heading GALITHA 13VYADHIS among which switra is one.Agni purana mentioned kusta as a broad term to describe all the skin diseases includingswitra.In Yagnavalkya smriti skin or the twacha has been described having six layers and allthe diseases arise from these layers .14Manu smriti (200B.C-200 A.D) has clearly mentioned that a stealer of clothes suffersfrom switram .It is aquainted as hereditary disease and people suffering with this diseaseare not eligible for marriage . 15OTHER LITERATURE DURING VEDIC PERIOD:Other than the Indian literature, earliest references of the condition can be traced back tothe period of Aushooryan (2200 B.C) in the classic TARIKH –E-TIL-IRAN.16Pharaonic medicine in the ebers papyrus (1500B.C) described two types of diseasesaffecting the colour of the skin. a) With tremors probably leprosy b) with colour changeprobably Vitiligo .The latter was said to treatable . 17In Arabic medicine the terms “BOHAK “BAHAK” ‘BARAS’ are the terms mentioned todenote a similar condition like Vitiligo.18In Bible the term “ZORAAT”denotes Vitiligo.19 A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  7. 7. 7In Japanese literature (1200BC) SHIRABITO is the term used for the condition like likeswitra . 20SAMHITA KALA:Charaka samhita: In this treatise switra is described in the kusta roga chapter .Adetailed description of the disease is found in this text.A special etiology is mentioned forswitram, types and treatment has been vividly described .21 thSushruta samhita: Has also described switra in a detailed fashion.In nidana Stan 5 22chapter description of the disease is found .Bhela samhita; Bhela included switra in eleven kshudra kustas and mentioned it as 23asadya roga .Harita samhita :did not give a detailed description of the disease but mentioned a stealerof clothes and money is prone to get this disease .And arista lakshanas of kusta rogas arementioned and said to be applicable to switra also. 24Kashyapa samhita: included switra in eleven types of kshudra kustas .Five types are 25mentioned but no names and clinical features are found .it is said to be a asadya vyadhi.SANGRAHA KALA;Astang Sangraha: switra as a bahya vikruti and in sutra Stan mentions that using a 26poisonous jalouka for rakta mokshanam shall cause the disease .Astang Hrudayam: describes switra as a separate disease .Etiology, types, clinicalfeatures, prognosis and treatment are clearly mentioned .Vagbatta has considered switrato a medical emergency as delayed medical intervention may lead to completedepigmentation. 27 A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  8. 8. 8MADHYAMA KALA (8 A.D. - 15 A.D):Vangasena: a text book of 10 A.D describes about the etiological factors responsible forthe disease. Specially seven dietary factors are mentioned which cause kusta rogas.The 28etiology of kusta and switra are considered same .Madhava Nidan: a special text on etiology of different diseases describes switra in49thchapter .complete description of the disease is found vividly in this book.29Sharangdhara samhita :( 11-12 A.D) has mentioned the etiology of kusta and switra tobe same and mentioned three types of the disease based on the involvement of thedhatus . 30BhavaPrakash: written by Bhavmisra has given a detailed description about the diseasethe etiology, types ,clinical features ,prognosis and treatment have been in the text.31BUDDHIST LITERATURE:Tripitika literature is the oldest source to have a glimpse of Indian medicine inBuddhist tradition. It is mentioned that kusta, kilasa, ganda, sosa, apasmara, are fiveprevalent abadhas.Vinaya pitam mentioned the disease kilasa i.e spotted deer 32.Sardulakarnavadana: In this book Ayurveda is mentioned along with four vedas.Kushta and kilasa are mentioned seperately33.Lalithavistara: One among the nine important texts deals with the advent of LordBuddha and his teachings. In this context those diseases caused by vata, pitta, sleshmaand sannipata diasease of kushta and kilasa34Saddharmapundarika: Diseases like kusta and kilasa are mentioned seperately35JAIN TRADITION: 16 diseases are enumerated among which leprosy is one. thKalyanakaraka: By Vugraditycharya. 20 chapters are present. From 8 chapter onwardsdiseases are mentioned. Kusta is one among mahamayas. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  9. 9. 9OTHER NON-MEDICAL SOURCES: th ndPanini (7 B.C): Sutras were annotated by patanjali in 2 B.C. Kusta and Kilasa arementioned separately.Kautilya’s Arthasastra: (321-297 B.C) In a chapter on secret means, a number ofdiseases has been mentioned among which kusta is one. In this disease this physician’s 36certificate is honoured.Bana Bhatta (606-648 A.D): In Harsacharitra and Kadambari mentioned the concept ofhealth and described Switra separately. 37Amarakosha (600 A.D): Has mentioned switra separately and terms like “Padasphota”,“Twak pushpi” are mentioned in this context. 38ADHUNIKA KALA (16 A.D ONWARDS):Yogaratnakar: mentioned switra as kilasa and described it in kusta chapter.Bhaishajya Ratnavali: switra is described in kusta roga adhikar. Treatment of switra isdescribed with various formulations . 39RESEARCH WORKS DONE IN VARIOUS INSTITUTIONS :1. Dr.Sheela ratna M.V, Switra roga and its management Mysore 1979.2. Dr.Patil A.K, Survey of Switra in Jamnagar and Vicinity in reference to its nidana and Chikitsa .Jamnagar 1984.3. Dr.Upadhyaya R.K, Therapuetic assessment of some Ayurvedic drugs in treatment of Vitiligo.Varnasi 1985.4. Dr.Shankaran.K, Managament of Switra with special reference to Bakuchi Trivendrum 1986. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  10. 10. 105. Dr.Lahiri P.K, Clinical studies and management of Switra kusta (leucoderma) with Ayurvedic drugs, Calcutta 1987.6. Dr.PrithviRaj, Concept of switra and its management in Ayurveda, varnasi1988.7. Dr.ThakoreS.R, Switra mein Kakodumbara ka Prayogika Adhyayan. Ahmedabad1989.8. Dr.Srikanth Babu, Evolution of Kakodumbaradi yoga in management of Switra. Mysore 1992.9. Dr.Sharada C.L, Clinical study of Switra (leucoderma) and its management with kakodumbara and manahshiladi lepa.Jamnagar 1993.10. Dr.Kambale.S, Switra kustavar nidana parivarjana aushadhi (bavanchi) ani aharacha parinama.Nanded 1996.11. Dr.Prabhakar.Shinde, A Clinical study of the effect of Somarajyadi churnam (int) and Somarajyadi lepa (ext) in Switra .Hyderabad 1996.12. Dr Seeta Devi.P .A clinical study on the effect of lepa in Switra .Mysore 2003.13. Dr.Venugopal CH, A clinical study on the effect of kaseesabadda ras (int) with and without chitraka lepa in Switra (VITILIGO) Hyderabad 2003.14. Dr.Mahantesh P.M, A Comprehensive management of kilasa kusta Vitiligo).Hubli 2006. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  11. 11. 11 NIRUKTIThe term switra is derived from “swith” dhatu meaning white colour. Rak pratyaya isadded and letter “kha” is deleted.It belongs to napunsaka gender. Swith +ra = Switra40 Switra =Sweth varne switraThe term indicates a disease where white coloured patches appear on the skin. Switra is analogous to the disease vitiligo in the contemporary medicine .Theterm Vitiligo is derived from latin word “vitium” meaning defect .41 Documentation of 42the word is present in the book De-Meedicina by the Roman Physician Celsus . A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  12. 12. 12 PARIBHASHAThe definition of Switra is given by all the ancient classics .The acharyas who havedefined switra primarily suggested that this is a disease related to impairment of colour.The term Switra is derived from “sweth varne switra” meaning white colour. 43Amarkosha defined switra as “Swetate twaganena Switram” meaning ‘white colourof the skin’.Shabda kalpa drumam defined it as “Swetate itihi” meaning white colour . 44Kashyapa samhita defined Switram as “Sweta bhavamicchanti switram” meaning 45reflection of white colour .Sushruta defined it as “Twagatam eva aparisravi “one which involves only the skin andhas no oozing tendency.46The essence of all the above mentioned, indicate Switra as a disease in whichhypopigmentation is a cardinal feature.Vitiligo is defined as a dermatological disorder characterized by milky white patchesdevoid of melanocytes .It bears resemblence in having a progressive tendency and 47genetic predisposition. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  13. 13. 13 SHAREERA RACHANAIntroduction: “Twak’ or the “Twacha” are the analogous names to identify the skin inAyurveda. It is one of the largest organs which cover the entire external surface area ofthe body. Twak is aptly defined as “Twach Samvarne” 48 meaning the one which covers. Itcovers the entire external surface of the body protecting the underlying rakta, mamsa, 49medo dhatus . The skin forms a self renewing, self repairing interface between the bodyand the environment.Embryonic Development of Twak:- A perfect combination of healthy sukra and 50sonitha leads to the formation of an healthy embryo . The pancha maha bhutas actaccordingly on the embryo leading to the formation of various anga – pratyangas.Amongst the five, Vayu helps in the division of the cells, and Tejo maha bhuta helps inthe maturation and specialization of the cells forming different layers of cells of differentorgans. Sushruta opined that as the cream is formed over the boiling milk, the variouslayers of the skin are also formed and deposited on the rapidly forming product of thecombination of sukra & sonitha.51 Vagbatta described that during the process of cooling (Processing) of the blood,the layers of twak are formed, and the purity of the skin lies in the purity of blood. 52Sushruta described seven layers of the skin, Charaka 53 and Vagbatta54 described sixlayers of skin. Twak is derived predominantly from vayu and akash mahabhutas and itsadhistana devata is vayu 55. Twak is one of the pancha gnanedriyas56 and its indriyartha isSparsha57, its indriya buddi is Sparshana58. 59 The entire body is a combination of three doshas, Sapta dhatus and three malas .Skin also being a part of this body is composed of vata, pitta and kapha. It is an upadhatuof mamsa dhatu. Sweda is excreted through the skin. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  14. 14. 14 The tridoshas have their respective role to play in the twak. The skin being the 60 51.seat of vata it does the sparsha grahana, pitta helps in imparting the colour and lusterKapha gives the mrudutwa and snigdatwa to the skin.62 In the process of formation of various dhatus, the mamsa dhatu is derived from 63 64rakta dhatu. The prasada bhagha of mamsa dhatu is subdivided into vasa & twak.These two are nourished by the mamsa dhatu. Apart from receiving nourishment from itsparent dhatu, twak is also nourished by numerous rasavahinis. Sometimes the rasa andtwak become analogous, twak Sara person is considered as rasa Sara also65. Twak is considered to be a rasaja bhava by the virtue of its property to reflect the 66varna.LAYERS OF THE SKIN: st 671 Layer: is named as “udakadhara” by charaka and is believed to contain waterysubstance such as rasa or lasika (body lymph). Sushruta named it as ‘avabhasini’ whichmeasures 1/18vreehi; this layer reflects the colour and complexion of the skin 68.Vagbhatta named it as “bhasini”. It is the site for manifestation of sidma andpadmakantakam. nd2 Layer: is named as ‘asrgdhara’ by charaka as it contains blood capillaries. Sushrutanamed it as “Lohita”. It measures 1/16 vreehi. Vagbhatta named it as “Lohini”.Cutaneous infections like Tilakalaka, Nyaccha, and Vyanga are manifested here. rd3 Layer: Unnamed by charaka, Sushruta named it as “sweta” it measures 1/12 vreehi.It is the site for manifestation of Charmadala, Ajagillika, and Mashaka.Charaka describedthis layer to be the seat for Sidma & Kilasa.4th Layer: Not named by charaka & Vagbhatta but explained it to be the site for all thvarieties of kusta and dadru. Sushruta named it as ‘Tamra’ measuring about 1/8 vreehiand seat for various types of kusta and kilasa. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  15. 15. 15 th5 Layer: Not named by Charaka and Vagbatta but explained diseases like alaji, and thvidradhi being manifested here. Sushruta named this layer “vedini” measuring about 1/6of vreehi. And diseases like kusta and visarpa are explained here.6th Layer: Not named by Charaka but Vagbhatta named it as “pranadhara” the supporterof life and seat for diseases like arumshi. Excision of which leads to tremors and enteringto darkness. Any manifestations are deep rooted here and difficult to treat. Sushrutanamed this layer as ‘Rohini’ which measures 1 vreehi. Grandhi, arbudas, apache, slipada,galaganda are manifested here. All muscular outgrowths are noted here. th7 Layer: Named by sushruta as “Mamsadhara”. The deepest layer, thickness is doublethe vreehi, and diseases like Bhagandara, Vidradhi are manifested here. All the diseasesinvolving mamsa and rakta dhathu are explained here. 69According to Charaka :Table -1S.No. Name of the Layer Function Diseases 1. Udaka dhara Protects the loss of body fluids - 2. Asragdhara Reservoir of blood - 3. Tritiya - Sidma, kilasa 4. Chaturtha - Dadru, Kusta 5. Panchami - Alaji, Vidradi 6. Shasti - Tremors and darkness before eyes. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  16. 16. 16According to Sushruta70:Table -2 S.No. Name of Thickness Function Diseases the layer1. Avabhasini 1/18 Vreehi Reflection of Sidma, Padma Kantakam colour & complexion2. Lohita 1/16 Vreehi - Tilakalaka, Nyaccha, Vyanga3. Swetha 1/12 Vreehi - Charmadala, Ajagallika, Mashaka4. Tamra 1/8 Vreehi - Kilasa & Kusta5. Vedini 1/6 Vreehi - Kusta & visarpa6. Rohini 1 Vreehi - Granthi, Apacchi, Arbuda, Galaganda, Sleepada7. Mamsadara 2 Vreehi - Bhagandara, Vidradi, ArsasAccording to Astangahrudaya 71:Table -3S.No. Name Function Diseases of the layer 1. Bhasini Expresses Colour and five - shades of complexion 2. Lohini - - 3. Swetha - - 4. Tamra - - 5. Vedini - - 6. Rohini - - 7. Mamsadhara - - A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  17. 17. 17 ANATOMY OF THE SKIN Among the three primary germ layers of the embryo, the epidermis is derivedfrom the ectoderm-the outer most primary germ layers. At the beginning of the secondmonth the ectoderm consists of simple cuboidal epithelium. These cells flatten and areknown as Periderm. By the end of fourth month, all layers of the epidermis are formed and each layerassumes its characteristic structure. The dermis is derived from wandering mesodermal cells. The mesenchymebecomes arranged in a zone beneath the ectoderm and there undergoes changes in theconnective tissues that form the dermis. Nails develop during third month from ectoderm. Hairfollicles develop betweenthird & fourth month from the ectoderm. By the fifth and sixth month follicles producedelicate hair called lanugo which usually shed before birth. The secretory portions of sebaceous and sudoriferous glands are derived fromectoderm. The connecting tissues and blood vessels associated with the glands developfrom mesoderm.Microstructure of the Skin:Epidermis: is a compound tissue consisting mainly of continuously self replacingstratified keratinized squamous epithelium. The principle cells of which are calledKeratinocytes. Other Cellular elements of different developmental orgin within themature epidermis includes melanocytes or the pigment forming cells from embryonicneural crest. Langercells are immunocompetent antigen presenting cells derived frombone marrow. Other cells are Lymphocytes. These disparate cells are collectivelyknown as non-keratinocytes or epidermal immigrants. Neurally associated Merkel cellsare now thought to be modified Keratinocytes. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  18. 18. 18 Sensory nerve endings are also sparsely present within the epidermis. Eachcomponent has an individual primary function, but the fact of there intimate spatialassociations and of functional interactions has led to the concept of epidermal symbionts. The population of keratinocytes undergoes continuous renewal through out thelife a mitotic layer of cells at the base replacing those shed at the surface. As they moveaway from the base of the epidermis, the keratinocytes undergo progressive changes inshape and content full of protein keratin, a process known as keratinisation. It is usual to divide the epidermis into number of strata from deep to superficial asfollows, S.basale, S.spinosum, S.granulosum, S.lucidum and S.corneum. The first threeof these layers are metabolically active and often grouped together as the stratummalpighi. The more superficial strata of cells achieving terminal keratinazationconstitute the cornified zone.1. Stratum basale: This includes the deepest layer of cells adjacent to the dermis andappears to rest upon a continuous narrow ‘basement membrane’ which includes the basalplasma membrane of the cell, a basal lamina consisting of lamina lucida and laminadensa, and a dermal reticular lamina. This area is also known as epidermal – dermaljunction. The cytoplasm contains the common cellular organelles, melanosomes andmany cytoskeletal intermediate filaments. The plasma membranes of the opposed cellsare connected by desmosomes and the basal plasma membrane has hemidesmosomes.Melanocytes, Langerhans cells and Merkelcells are interspread among the basalkeratinocytes.2. Stratum spinosum (Prickle Cell Layer): This contains several layers of maturekeratinocytes packed closely and inter digitating by means of numerous projections andindentations of the cell membrane which are linked by many desmosomes giving thenspiny appearance, hence also called as Prickle cell layer. The cytoplasm contains thecommon organelles including some lysosomes and melanosomes. Langerhans cells and A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  19. 19. 19the occasional associated lymphocytes are the only non -keratinocytes present in thestratum spinosum.3. Stratum granulosum: In this stratum three to four layers of flattened cells withextensive changes in Keratinocyte structure occurs . The nuclei become pycnotic andbegan to disintegrate, the membraneous organelles such as mitocondria, golgi membranesand ribosomes degenerate, and keratin filament bundles become more compact andassociated with Keratohyalin granules. Small round granules with a lamellar internalstructure also appear in the cytoplasm. The lamellar granules are concentrated deep to theplasma membrane of the granular cell with which they fuse liberating their predominantlylipid content in to the intercellular space not only of this stratum, but also into the spacebetween it and the stratum corneum. They form an important component of thepermeability barrier of the epidermis, langerhans cells may occasionally be seen at lowerlevels of stratum granulosum.4. Stratum lucidum: Only found in thick glabrous palmo-plantar skin, this layerrepresents poorly understood stage in Keratinocyte differentiation. Ultrastructurallyresembles the transitional cell, an incompletely keratinized cell occasionally seen in theinnermost layer of the statum corneum of non-glabrous skin.5. Stratum corneum: This stratum is the final product of epidermal differentiation orKeratinazation. It consists of closely packed layers of flattened Polyhedral Corneocytes.These cells overlap at their lateral margins and interlock with cells of opposed layers byridges, grooves and microvilli. In this skin the statum may be only a few cells deep, but inthick skin it may be more than 50 cells deep. The interior of this corneocyte is devoid ofnucleus and membraneous organelles, consisting solely of a dense array of keratinfilaments embedded in an interfilmentous matrix partly composed of filaggrin derivedfrom keratohyalin granules. Desquamation of the outer layers of the stratum corneum involves a poorlyunderstood loosening of attachments (desmosomes and inter cellular substances) betweenthe cells, probably involving enzyme action and is normally imperceptible, when A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  20. 20. 20execessive, it appears in hairy regions as dandruff and more massively in certain diseasesas peeling, scaling, and exfoliation. Langerhans cells are not present in the stratumcorneum and therefore are not desquamated.Melanophages are macrophages which have ingested performed melanin andmelanphores or dermal melanocytes, within which melanin can be rapidly aggregated ordispersed to change body colour in adaptation to environmental backgrounds. Embryonic precursors of melanocytes migrate from the neural crest to enter theepidermis as melanocytes from about eight gestational weeks. It is estimated that a singlemelanocyte may be in functional intact via its dendrites with up to 30 Keratinocytes toform an entity called the epidermal melanin unit. Melanocytes decrease significantlyin number in old age and are absent from grey hair. EPIDERMAL MELANOCYTES AND SKIN PIGMENTATION Melanocytes are melanin pigment forming cells derived from the neural crest andwidely distributed throughout the body in vertebrates. In humans they are present in theepidermis and its appendages, in oral epithelium, some mucous membranes, the uvealtract of the eyeball, parts of the middle and internal ear and in the leptomeninges at thebase of the brain. The cells of the retinal pigment epithelium, developed from the outerwall of the optic cup, also produce melanin, and neurons in different locations within thebrain stem synthesize a variety of melanin called neuromelanin. True melanins are complicated,high molecular weight polymers attached to astructural protein (to form melanoproteins) and in humans there are two classes, thebrown black eumelanin and redyellow Phaeomelanin both derived from tyrosinecatalysed by the enzyme tyrozinase . The dermis is for the survival of the epidermis andimportant morphogenetic signals are exchanged at the interface between the epidermal-dermal junction during development and postnatally. The dermis can be divided intosuperficial papillary layer, and a deeper reticular layer. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  21. 21. 21Dermis: The dermis is an irregular, moderately soft connective tissue, with a matrixcomposed of an inter woven collageneous and elastic network in an amorphous groundsubstance of glycosamino glycans, glycoproteins and bound water, which accommodatesnerves, blood vessels, lymphatics, epidermal appendages and a changing population ofcells. The dermis provides considerable strength to skin by virtue of the number andarrangement of its collagen fibres, which give it tensile strength and it has elastic recoil,because of its elastic fibres.Layers of dermis:1. Papillary Layer:- This is immediately deep to the epidermis and is specialized to provide mechanical anchorage, metabolic support and trophic maintainance to the overlying tissue as well as housing rich networks of sensory nerve endings and blood vessels. Its superficial surface is marked by numerous papillae which interdigitae with recesses in the base of the epidermis and form the dermal- epidermal junction at the interface. The papillae have round or blunt apices which may be divided into several cusps. In skin especially in regions with little mechanical stress and minimal sensitivity, papillae are few and very small, while in thick skin of the palm and sole of the foot, they are much larger, closely integrated, and arranged in curved parallel lines following the pattern of ridges and grooves typical of these surfaces. Lying under each epidermal ridge are two longitudinal rows of papillae or either side of epidermal retepegs through which the sweat ducts pass on the way to the surface. Each papilla contains dense collagen fibres, elastic fibrils, microfibrils, attached to the basal lamina. Also present in thick hairless skin meissner’s corpuscular nerve endings.2. Reticular Layer: This merges with the deep aspect of the papillary layer. Its bundles of collagen fibres are thick than those in the papillary layer and interlace with them and with each other form a strong yet deformable three dimensional lattice in which many fibres are parallel to each other and within which lies a variable number of elastic fibres. The Orientation of the collagenfibres may be related to the direction of action of the mechanical forces to which the dermis is subjected and may be involved in the development of the skin surface lines. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  22. 22. 22ULTRASTRUCTURE OF MELANOGENESIS: Melanocyte is a dendrite non-keratinocyte, lacking desmosomal contacts withapposed keratinocytes. The nucleus is large round and euchromatic. In the cytoplasm are intermediate filaments, a prominent golgi complex andvesicles, associated granular endoplasmic reticulum, mitochondria and coated vesiclestogether with a characteristic marker organelle, the melanosome. The melanosome is a membrane bound structure which undergoes a sequence offour developmental stages during which melanin is synthesized and deposited within it bythe tyrosine – tyrosinase reaction. Stage –I Stage I melanosome is spherical vacuole, derived probably from the rough endoplasmic reticulum, and containing filamento - amorphous structural protein and vesiculo globular bodies. Stage-II Stage II Eumelanosomes become spherical or ellipsoid and the inner matrix becomes organized into filamentous sheets exhibiting a 9nm periodicity. Stage-III At Stage III melanin begins to be deposited on the innersheets, gradually observing their arrangement, until densely pigmented. Stage-IV is reached, exhibiting no other internal structures apart from non- melanized vesiculo globular bodies. Phaeomelanosomes retain their spherical shape throughout all stages. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  23. 23. 23 In most active melanocytes, melanosomes of the four stages are present. Whenmature, stage IV melanosomes move into the dendrites along the surfaces ofmicrotubules and are transferred to keratinocytes by a special type of phagocytosis, withsubsequent liberation of melanosomes into the keratinocytes cytoplasm. Hence colour of the skin plays a vital role in protecting the humans from variousphysical, chemical agents and harmful effect of sunlight.APPENDAGES OF THE SKIN: Organs that develop from the embryonic epidermis – hair, sweat glands,sebaceous glands, nails ceruminous glands, have a host of important functions toperform. Hair and nails protect the body. The sweat glands help regulate bodytemperature. The sebaceous glands produce an oily substance the sebum and ceruminousglands provide waxy secretion in the ear canal. Skin along with its appendages forms theintegumentary system72-73. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  24. 24. 24 SHAREERA KRIYA Ayurveda defines “Shareera” as “Sheeryate iti Shareeram” means the one whichconstantly undergoes wear and tear. This applies to all the organs which constitute theshareera, particularly the skin. As defined by Shabdakalpadrumam. “Twachati Samvrunoti medo shonithadikamiti”74 Twak covers the underlying rakta, mamsa, medo dhatus. Twak not only covers theentire body area but also forms a strong physical barrier against microbial invasion. Itprotects the body against mechanical, chemical, thermal, osmotic and photo damage. It ismajor site of inter communication between the body and environment. Second vital function of the twak is to impart Varna or the colour to the body andits structures. It reflects the luster and brilliance present in it. The Varna of an individual is determined in the embryonic stage of life. It is arasaja bhava75. The tejomahabhuta is the main factor in determining the varna76. The kindof food taken during pregnancy also determines the colour. The four prakrut varnasformed by the combination of different mahabhutas.  Tejo+Jala = Gouravarna  Tejo+Prithvi = Krishna varna  Prithvi + Akash = Krishna – Shyama  Jala + Akash = Goura – Shyam Charaka has attributed the Varna aspect to the udana vata (one among 77panchavidha vatas). The vital functions of Pitta are mentioned as production of normaland abnormal temperature in the body as well as normal or abnormal colour of the 78.Skin Among the five types of Pitta, imparting colour to the skin is a specializedfunction of the Bhrajakapitta 79. As pitta is involved in the above said function, kaphabuilds the texture of the skin making it supple, shiny and strong.80 A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  25. 25. 25 There are two major aspects of varna-(i) Prabha (brilliance of the skin) (ii) Chaya(Substratum of the colour) Prabha is of 7 types- rakta, Peeta, Sita, Syava, Harita,Pandura, Asita. Prabha specifies the colour of an individual. Chaya is of 5 types, 81according to the panchamahabutas . Nabhasi, Vayavi, Agneeyi, Ambasi, Parthivi and isthe substratum of the colour. Prabha is reflected to farther distance but chaya can beappreciated only from a close view. Prabha and chaya are inseparable aspects of Varnaand their reflection is the vital function of Prakrit pitta. In a deranged state, pitta exhibitsabnormal colours. Amongst the dhatus, twak is closely related to rasadhatu. It derives nutrition fromthe rasadhatu through its channels. The texture of the skin is depended on the quality of 82nutrition provided Sweda, which is a mala of medodhatu, is expelled out through skin. But in normalstate it acts like a dhatu. It is held in the skin, thereby moisturizing it83. Tridoshas have their own specific properties by the virtue of which they perform 84various functions. “Ushma” is the inherent property of pitta, which enables it performthermoregulation and helps in eliciting the lustre of the skin 85Applied aspect: 86 In ksheena avastha of pitta “Prabhahani” is noticed If pitta prahopakara diet is consumed it vitiates pitta causing digestion of the cells 87 producing colour to the hair leading to a condition called “Palityam” In a vitiated state vata, pitta and kapha exhibit black, yellow and white colour respectively. 88 A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  26. 26. 26BHARAJAKA PITTA & ITS FUNCTIONS: It has been specified by sushruta that production of colour, exhibition of luster ofskin are the functions of Bhrajakapitta 89 The word Bhrajaka is derived from “Bhraj Dhatu meaning “Deepti” or “Kanti”‘Sushruta’ mentioned that Bhrajaka pitta resides in the skin. ‘Dalhana’ Commented that 90Bhrajakapitta resides in the bahyatwak i.e. avabhasini. Hence it is mentioned in thereference of avabhasini that its main function is reflection of colour & luster. Vagbatta also stated that Bhrajaka pitta is located in the skin and reflects the 91radiance of the skin. Arunadutta commented that Bhrajaka pitta performs functions like 92“deepana” “Pachana” of the substances used for abhyanga, lepa, Parisheka Chakrapani mentioned that variations in the body temperature and colour are the 93functions of bhrajaka pitta . Dalhana stated absorption and digestion of the substances used together with oilsand decoctions used for sprinkling over the body is also done by the Bhrajakapitta. Bhela Samhita has also described the function of Bhrajakapitta as providingushma and Prabha to the body94 .Hence it can be concluded that Bhrajaka pitta resides inthe avabhasini the first layer of twak and performs vital function like. Providing luster and brilliance to the skin. Helps in thermoregulation of the body. Capable fo presystemic metabolism of drugs and other substances applied topically through the process of “abhyanga” “parisheka” “avagahana” & “lepa”.Applied aspect: Any derangement in the Bhrajakapitta functions leads to alteration ofskin colour and impaired thermo regulation. In the present disease switram, pathology isnoted due to the impairment of this pitta. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  27. 27. 27 The third vital function of twak is thermo regulation. By the virtue of pitta(Bhrajaka) located in the skin this function is performed. “The Ushma” property of pittaaides in this function. Any derangement of pitta leads to “mandoanala” condition and“Sheetam” 95 abnormal cold sensation to the body. The fourth important function of twak is being a sensory organ. Twak is one 97 97among the pancha gyanendriyas . It is seat for the vata . And “Sparsha” or the tactilesensation is the inherent property of vata98 among the panchavidha vatas; the Pranavatacontrols all the indriyas99. All kinds of sensations like touch, temperature, pain, pleasureare perceived by the skin. The fifth function of the skin is excretion. It is the channel for the excretion ofsweda which is considered as a mala of the body. If sweda is not generated sufficiently itleads to bad odour, Cracks in the skin and hairfall. 100 Sixth function of the twak is to act like channel or marga. Twak is categorized 101under shakha along with other dhatus and shakha is classified under bahyarogamarga102 .This rogamarga help in manifestation of the diseases and prognosis can beknown. Certain shodhana procedures are done to transfer the dhoshas from shaka tokosta. Hence skin or twak also acts as a channel. It also lodges the nakha and smashruwhich are the malas of asthi. Hence, it can be said that the twak is a tridoshaja bhava in which vata acts as ainitiative principle pitta acts a metabolic principle and kapha is a preservative principle. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  28. 28. 28 PHYSIOLOGY OF THE SKIN The skin is the largest organ of the body, being on the surface and continuallyexposed to injury. It has to be both strong and supple to resist the wear and tear. It formsthe integumentary system along with its derivatives like hair, nails, sweat and sebaceousglands. It forms about 8% of the total body mass and its surface area varies with heightand weight.Functions of the skin:1. Protection: The skin covers the entire body. It forms self renewing and self repairing interface between the body and its environment it is major site of inter communication in both directions between the two. Within limits it forms an effective barrier against microbial invasion, and has properties which can protect against mechanical, chemical, osmotic, thermal and photo damage.2. Thermoregulation:- In response to high environmental temperature of strenuous exercise, the evaporation of the sweat from the skin surface lowers an elevated body temperature to normal. In response to low environmental temperature production of sweat is decreased, which helps to conserve heat. Apart from this, changes in the blood flow also regulate body temperature. The rich vasculature of the skin has a generous rescue to meet the requirements of wounding and repair, so common on surface. Dilatation can increase the flood flow 100 fold, assisting the thermo regulation.3. Sensation: Skin is a major sense organ, richly supplied by nerve terminals and specialized receptors for touch, temperature, pain, pleasure stimuli.4. Excretion: Besides removing heat and some water from the body, sweat is also a vehicle for excretion of small amounts of salts and several organic compounds. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  29. 29. 295. Synthesis of Vitamin D: It can be regarded as endocrine organ as it carries out many biochemical synthetic processes (Boyce 1994) including formation of vitamin D. It can synthesize vitamin D from calciferol in the presence of sunlight. Apart from synthesizing vitamin D it also helps in the synthesis of cytokines and growth factors. Cytokines include inter leukins, interferons.6. Immunity: It is an important site of immuno-surveillance against the entry of antigens and initiation of primary immune response.7. Frictional property: Skin has good frictional properties, assisting in locomotion and manipulation by its texture. It is elastic, and can be stretched and compressed within limits. It is capable of absorption and excretion and selectively and regionally permeable to a variety of chemical substances.8. Skin Colour: The colour of human skin derives from and varies with the amount of blood (and its degree of oxygenation) in the cutaneous circulation, the thickness of the stratum corneum and the certainty of specialized cells producing the pigment melanin. Melanin has protective role against ultraviolet radiation, and acts as a scavenger of harmful free radicals produced under this and other circumstances. Racial variations in the colour are mainly due to the differences in the amount, type, distribution of melanin and are genetically determined. The anterior pituitary gland or the adeno hypophysis secretes hormones thatregulate a wide range of bodily activities including skin pigmentation. Some cortiotrophsof remnants of pars intermedia secrete MSH – melanocytes stimulating hormone whicheffects the skin pigmentation. MSH increases skin pigmentation by stimulating thedispersion of melanin granules in melanocytes in amphibians. Its exact role in humans isunknown. Three pigments, melanin, carotene and haemoglobin give colour to the skin.Melanin is located mostly in the epidermis, carotene in dermis and haemoglobin in thered blood corpuscles. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  30. 30. 30 The amount of melanin varies the skin colour. Melanocytes are most plentiful inthe nucous membrane, penis, nipple of the breast, areola, face and he extremities. Thenumbers of melanocytes are same in all the races but the amount of melanin produceddecides the colour. Melanocytes synthesize melanin from the amino acid tyrosine, in the presence ofan enzyme tyrosinase in an organelle melanosome. Exposure to ultraviolet radiationincreases the enzymatic activity leading to the darkness of the skin which further protectsthe body from ultraviolet radiation. In this condition called VITILIGO there is partial or complete loss of melanocytesfrom patches of skin thereby producing hypopigmented spots. The colour of the hair isalso due to the substance melanin, absence of which causes white colour of the hair. Thecells melanocytes are scattered in the matrix of the bulb of the hair.TYROSINASE, AND SYNTHESIS OF MELANINS: Tyrosinase is a copper containing metallo enzyme, present in the form of several isozymes, which catalyses initial stages of the synthesis of tyrosine – melanin. It is formed by ribosomes on the granular endoplasmic reticulum, conveyed to the golgi complex, glycosylated and incorporated into coated vesicles which attach to the limiting membrane of the stage I melanosome, liberating active enzyme. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  31. 31. 31ILLUSTRATION-1: The first two steps include oxidation of tyrosine to DOPA OXIDATION TYROSINE DOPA TYROSINASE Oxidation of DOPA to Dopaquinone OXIDATION DOPA DOPAQUINONE TYROSINASE In eumelanin synthesis, dopachrome is formed converted into dihydroxyindoles and 5-6 dihydroxy indoles, 2-dicarboxylic acid. Dopaquinone Dopachrome Dopachrome Oxido Dopachrome tautomerase reductase 5-6 dihydroxy indoles and dihydroxyindole 2-dicarboxylic acid s The final stages in the pathway to melanin essentially involves complex polymerizations in which tyrosinase may again be involved. In phaeo melanin synthesis, the amino acid cysteine is added to dopaquinone to form 5-S cysteinyldopa. Most natural melanins are mixture of eumelanins and phaeomelanin A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  32. 32. 32FUNCTIONS OF MELANINS: Melanin has biophysical and biochemical properties related to its functions in the skin. It protects against the damaging effects of the ultra violet radiation on DNA through its special absorptive electron-photon coupling and amorphous semiconductor properties, whereby it can absorb any different types of energy and dissipate them in the form of vibrational modes or heat. Its redox capacity makes it an efficient scavenger of damaging free radicals, however generated, and its ability to bind to a variety of metal ions and drugs suffest it can act as an anti toxic agent. However, if the energy input is too great, these properties can be expressed in the output of toxins activated, chemical species which can be damaging. Another disadvantage is that a high concentration of melanin in relation to incident solar UV may adversely affect synthesis of vitamin D.DETERMINATION AND CONTROL OF MELANIN PIGMENTATION: Melanin Pigmentation of human skin can be analysed in two bases (1) Constitutive (2) facultative Constitutive pigmentation is the intrinsic level, genetically determined. Facultative pigmentation comprises reversible changes induced by environmental agents eg: UV and X-radiation, chemicals and hormonal influences. Genetics: Specific genes can influence differentiation of neural crest cells into melanoblasts, and also melano blast migration to the skin, their differentiation with melanocytes and morphological features of these such as shape, size, and A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  33. 33. 33 length of dendrites, which in turn determine the size of the pool of keratinocytes to which each cell transfers its melanosomes. Other genes acting primarily within the melanocyte control the synthesis of tyrosinase, its type and activity, the type of melanin synthesized the size, shape, protein structure and number of melanosomes, their degree of melanization and their rate of transfer to keratinocytes. Constitutive melanin pigmentation in man is probably under similar precise genetic control. Racial variations in pigmentation are due to differences in melanocyte morphology and activity of melanocytes than to numerical differences. In heavily pigmented skins the cells tend to be larger, more dendritic and to contain more and larger Stage III and IV melanosomes than melanocytes. Ultraviolet radiation: The response of the melanin pigmentary system to ultraviolet varies with genetic and constitutional factors. It includes immediate tanning, or pigment darkening, which can occur within few minutes due to photo oxidation of preexisting melanin. Delayed tanning occurs after about 48hrs and involves stimulation of new melanogenesis within the melanocytes, and transfer of additional melanosomes to keratinocytes. There may also be some increase in size of active melanocytes and their numbers. Lower frequency UV band induces synthesis of keratinocytes of b-FGF, as well as inter leukin I which induces them to produce  melanocyte stimulating  hormone a known stimulant of melanogenesis. Hormonal Influences: In amphibians MSH from the anterior lobe of the hypophysis and melatonin, a skin lightening hormone secreted by the pineal, are involved in pigmentary alterations. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  34. 34. 34 Their importance as normal regulatory factors in man is unclear. In pregnancy, higher levels of circulating Oestrogens and progesterone are responsible for the increased melanization of the face, abdominal and genital skin and the nipple and areola. A number of other factors operating within the epidermis such as interleukins, arachidonic acid, prostaglandins and various cytokines, also affect melanogenesis. Level of pigmentation at anytime represents a balance between a large number of competing influences between constitutive and facultative, and these must be taken into account in the analysis and diagnosis of hypo and hyperpigmentary disorders103. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  35. 35. 35 NIDANA Nidana is defined as the etiological factors responsible for causing the disease104All the diseases affecting the skin in particular are described under one heading “kustarogas”. As switra also affects the skin it is described in this chapter. All the acharyas have mentioned a common nidana for kusta and switra. 105Acharya charaka has mentioned a vishesha nidana for switra.106 The etiological factor can be sub divided intoa. Aharaja nidanab. Viharaja nidanc. Chikista sambandhid. Anyajaa. Aharaja nidan: Vagbatta mentioned, a pregnant women consuming excessive kaphakara ahara, the baby shall be affected with switra.107 Viruddha ahara Mithyahara Asatmya bhojana Ahita bhojana Adhika matra Bhojana Ajeerna anantara bhojanam Vidhi viruddha ahara sevanam Kuvidhi of langhana Sheetala – ushna ahara sevanam Drava, snigdha, guru padarthas Gramya, anupa, jaleeyamamsa sevanam, anantharam dugda sevanam Navanna, dadhi, matsya, lavana, amla, masha, mulaka, pisti, tila, ksheera, Guda sevanam A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  36. 36. 36 Tila, guda, dudga sevanam 108. Chilachima variety of fish 109Seven dietery factors (7) specially mentioned by vangasenaTila, Taila, Kulatthi, Valmika roga, Lingaroga, Mahisha dadhi, Vruntakam.b. Viharaja Nidan Chardi, Mala-mutradi vegadharana Ati vyayamam Ati Santapasevanam Vyayamam in ajeernaavastha Mithya vihara Diva swapnam Garma srama, Bhayarthanam sheethambu sevanam.c. Chikista sambandhi Nidana: Vagbatta mentioned usage of savisha jalouka in rakta mokshana leads to switra at 110 that site 111 Snehapana anantaram doing vyayamama,or vyavayam leads to skin diseases Suppression of vamana vegas or doing vyayamam or maithuna after vamana leads 112 to skin diseases . Panchakarma apacharas specifically produces skin diseases 113 Taking apakwa Vajra, Vaikrantha, Nag, Loha, Hingula, Rasakarpur, Tutha leads to skin diseases 114. Apakwa Hartal bhasma and Vanga bhasma leads to switra specifically. 115Vaidya Nimittija: Snehapan after attaining samyak snigdha lakshnas causes sneha vyapat which 116 leads to kustarogas . 117 Doing dushita rakta stambana leads to kilasa and kusta A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  37. 37. 37d. Anya nidana: In adibala pravrutti Sukra – shonitha beeja doshas leads to kusta rogas in the progeny118 Manasika causes like bhaya, krodha leads to skin diseases 119 Dadga and kshatas produce switra 120 Bhoja mentioned vrana and parasparsha to be the cause for switra121 Manu smriti described stealing of clothes and wealth leads to switra 122 Harita samhita mentioned stealing of silver leads to switra123 Kashyapa mentions abstinence from yagnas, yagas, Homas, Bali, Improper athidi sevana leads to switra.124 Papakarmas of previous births Brahmana, Stri, Sajjana, go hatya Disrespecting parents, insulting Gods Having died of skin disease in the previous birth 125Vishesha Nidana specially mentioned by charaka 126 Viruddha annapana sevana Vacham asatyam Papakarmas Krutagna bhavas Ninda suranam Guru garshanam Poorva kruta karmas A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  38. 38. 38Aharaja Nidana:Table – 4S.No. Nidana C.S. S.S A.H M.Ni B.P Va.S 1. Garbhini consuming excessive - - + - - - kaphakara ahara 2. Virudha ahara + + + + + + 3. Mithyahara - + + - - + 4. Asatmya Bhojan - + - - - - 5. Ahita Bhojan - + - - - - 6. Adhika matra Bhojan - - - + - + 7. Ajeernam anantara Bhojanam - + - + + + 8. Vidhi virudha ahara sevana - - - - + - 9. Kuvidhi of Langana - - - - - + 10. Sheetala – Ushna Ahara Sevanam - - - + + + 11. Drava – Snigdha – Guru padartha - + - + + + 12. Tila guda – dugda sevanam - - - + + + 13. Chilachima variety of fish + - - - - - 14. Gramya, anupa, jaleeyamamsa - + - - - - sevanam, Anantaram dugda sevanam 15. Navanna, dadhi, Matsya Lavana, Amla, - - - + + + Masha, Mulaka, Pisti, tila, Ksheera, Gud sevanam.Viharaja Nidana:Table - 5S.No. Nidana C.S. S.S A.H M.Ni B.P Va.S 1. Chardi, Mala-mutradi vegadharana - + - + + + 2. Ati vyayayam - - - - - + 3. Ati santapasevanam - - - + + + 4. Vyavayam in ajeernavastha - - - - + + 5. Mithya vihara - - + - - - 6. Diva swapnam - - - + + + 7. Garma, Srama, Bhayarthanam - + - + + + sheethambu sevanam A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  39. 39. 39Chikitsa Sambandhi Nidan:Table - 6S.No. Nidana C.S. S.S A.H M.Ni B.P Va.S 1. Savisha Jalouka Prayog - - + + - - 2. Snehapana anantaravyayamam or - + - - - - maithun 3. Suppression of vamanadi vegas - - - + - + 4. Doing vyayama or maithun after - + - - - - vamana 5. Panchakarma apacharas - - - + + - 6. Snehapana after attaining samyak + - - - - - snigdha lakshanas 7. Dushitha raktha stambhana + - - - - -Anya Nidan:Table - 7S.No. Nidana C.S. S.S A.H M.N B.P Va.S M.S B.J Ka 1. Sukra shonitha beeja - + - - - - - - - doshas 2. Bhaya, Krodha - - - + + - - - - 3. Kshata, Dagda - - + - - - - - - 4. Vranas - - - - - - - + - 5. Para sparsha - - - - - - - + - 6. Stealing of clothes & - - - - - - + - - Wealth 7. Abstinence from - - - - - - - - + yagna, homa, bali 8. Papakarmas of + + + - - - - - - previous births 9. Brahmana, Stri, - + + + - - - - - Sajjana go Hatya 10. Vipra guru garshana + - - - + + - - - 11. Vacham asatyam + - - - - - - - - 12. Ninda suranam + - + - - - - - - 13. Having died of skin - + - - - - - - - diseases in previous birth A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  40. 40. 40 ETIOLOGY The etiology of vitiligo is unknown but triggering / precipitating factors areidentified.Triggering / Precipitating factors: It is difficult to precisely define the triggering factors for vitiligo. Neverthless itis essential to elicit the details of history of emotional stress, drug intake, infections, 127trauma / injury (Koebner’s phenomenon) existant prior to the development of vitiligolesions .128-130 It is believed that major oxidative stress occurs in vitiligo skin, which is 131-132evidenced by low catalase levels and cellular vacuolization in the epidermis .several factors may contribute to the oxidative stress, thus leading to the accumulation ofepidermal hydrogen peroxide. The presence of the hydrogen peroxide can bedemonstrated invivo by using non-invasive Fourier transform Raman Spectro 133-134ScopyILLUSTRATION-2: VITILIGO TRIGGERING / PRECIPITATING FACTORS , THEIR ROLE IN PATHOGENESIS135-138Triggering Molecular level Genetic factors Factors Changes1. Nutritional Deficiency2. Emotional stress Biochemical changes Normal Skin3. Drugs4. Infections Enzymatic Disturbances Previtiligo5. Focal sepsis and toxins Auto Immunity and Vitiligo Immune dysfunction6. Exposure to chemical7. Oxidative stress Epidermal hydrogen peroxide VITILIGO accumulation A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  41. 41. 41 POORVARUPAS Poorvarupas are defined as the prodromal symptoms of a disease to bemanifested. Madhukosh commentary defined poorvarupas as Bhavi Vyadhi Prabodhakas 139Generally the poorvarupas are only indicators of a particular disease to be manifested. Some times they are avyaktam not present at all and at times they are minimally 140exhibited. . The disease switram does not exhibit any poorvarupas, but as it has thesame causative factors like that of kusta 141, the poorva rupas exhibited by kusta rogas canbe considered for switram occasionally.Kusta Poorvarupas: 142 Sparsha Agnanam Atiswedam Aswedam Vivarnyam Loma harsha Kharatwam Kandu Toda Srama143 Klama Shula in vrana Sheegrautpatti Chira Stithiti Daha Suptata Ruksham Pipasa A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  42. 42. 42 Gouravam Doubalyam Vepathu Pidaka Arunshi Ativedana Kota utpatti Ati bhrama Ati kopanam 144 Asruja Karshanyam A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  43. 43. 43 RUPA Rupa can be defined as the clinical features of the manifested disease. They arethe subjective evidences of a disease. They are exhibited only after the completemanifestation of a disease. In the Shatkriyakalas the rupas are exhibited in the 145vyaktavasta . Dalhana commented that the rupas are exhibited after the completion ofDosha – dushya samurchana and the pratyatmaka lingam or the cardinal symptom is firstexhibited. 146 Eswarasena’s commentary on Madhava nidan defined rupam “Vyadhi hi Swarupam……. Tad Vyaktam Tadrupam. Madhukosh defined rupam as 147 “Utpanna vyadhi bodhakameva lingam rupam” 148 In switram, according to definition of kashyapa expressions of white colourpatches on the body is the Pratyatmaka linga of switram. Sushruta defined the rupas as “Twagtam eva aparisravi” 149. The patch involvesthe skin and has no oozing tendencyVishista dosha lakshanas: According to classical texts the vataja, pittaja, sleshmaja types of switram havebeen mentioned. The tridoshas invade rakta, mamsa, and medodhatus respectively andproduce lakshanas accordingly. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  44. 44. 44Vataja: Mandala Aruna varnam or rakta varnam Ruksham Sparsha katinatvam Parusham Keshanashanam Paridwamsi (Romapatrari)Pittaja Tamra Varnam Kamala Patravat Daham Roma VidwamsamSleshmaja Swetavarnam Snigdam Stulam Kandu yuktam Guru GhanamCharaka mentioned three varieties of the disease by the virtue of involvement of 150dhatus . 151 Daruna: When rakta dhatu is invaded by vata dosha it exhibits raktavarna Aruna: Mamsadhatu invaded by Pitta dosha it exhibits tamravarna Switra: Medodhatu invaded by kapha dosha it exhibits swethavarna A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  45. 45. 45Rupas:Table -8 S.No. Lakshanas C.S S.S152 A.H 153 M.Ni154 Sha.Sha B.PVataja 1. Mandalam - + - + - - 2. Arunavarnam - + + + - - 3. Raktavarnam + - - - - + 4. Rooksham - - + - - + 5. Sparsha katinatvam - + - + - - 6. Parusham - + - + - - 7. Keshanashanam - + - + - - 8. Paridwamsi - + - + - -Pittaja 1. Tamravarnam + - + - - + 2. Kamalapatravat - + + + - + 3. Daham - + + + - + 4. Romavidvamsam - - + - - +Sleshmaja 1. Swetavarnam + + + + - + 2. Snigdam - + - + - - 3. Stulam - + - + - - 4. Kandu yuktam - + + + - + 5. Guru - - + - - + 6. Ghanam - - + - - + A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  46. 46. 46 CLINICAL FEATURESEPIDEMIOLOGY: Vitiligo occurs world wide with an overall prevalence of 1%. However, its 155-161incidence ranges from 0.1 >to 8.8% . The highest incidence of the condition hasbeen recorded in India followed by Mexico & Japan. Behl et.al 162-163 had organized camps in rural areas and industrial pockets in Indiato evaluate the status of vitiligo. Its incidence was found to be higher in villagers livingnear dyeing, printing, carpet industries. A higher incidence of vitiligo in such areas maybe due to inclusion of cases with chemically induced depigmentation by industrialphenols, quinone’s which might have a completely different pathomechanism. Itsincidence however was relatively low amongst those residing adjoining copper mines.SEX INCIDENCE: Adults and children of both sexes are equally affected although the greaternumber of reports among females is probably due to the greater social consequences to 164-171women and girls affected by this conditionAGE INCIDENCE: Almost half the patients present before the age of 20 years and nearly 70-80% 172-176before the age of 30 years.FAMILY HISTORY: The proportion of patients with positive family history varies from one part of theworld to another. In India, in particular, it ranges from 6.25-18%. In some studies it is ashigh as 40%. The mode of transmission of vitiligo is quite complex. It is probablypolygenic with a variable penetrance177-181 A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  47. 47. 47PERCENTAGE OF INCIDENCE: 1947 - Calcutta / India - 6% 1958 - Vellore / India - 4% 1969 - Amaravati/ India - 8% 1972 - Delhi / India - 8.8% 1974 - Goa / India - 2.9% 1988 - Delhi / India - 1.25%The difference in its incidence may be due to higher reporting of vitiligo in populationwhere apparent colour contrast may force them to seek an early consultation.CLINICAL FEATURES: Vitiligo is characterized by the appearance of patchy discolouration evident in theform of typical chalky – white or milky white macules. The macules are round and oval in shape with scalloped margins 182-183 The size of the macules may vary from few mm to several cms with the lesionsaffecting the skin and or mucous membrances. The lesions are asymptomatic although itching, burning may precede or 184-185accompany the onset of lesions in few patients . Vitiligo is a slow and progressive disease and may have remissions andexacerbations correlating with trigerring events 186-187 Occassionally the lesions of vitiligo may begin to form around a pigmentednaevus 188(Sutton’s nevus, Leucoderma aquisitum centrifugum) and then go on to affect 189distant regions . A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  48. 48. 48 Although any part of the skin or mucous membrane is amenable to developvitiligo, the disease has a predilection for normal hyperpigmented regions such as theface, groin, axillae, areola, and genitalia. Furthermore lesions may develop in areas like, ankles, elbows, knees, which aresubjected to repeated trauma / friction, an outcome of koebner’s phenomenon 190. 191-193 In the event of extensive disease the lesions are symmetrically distributedwith an exclusive dermatomal distribution or mucous membrane involvement 194-196 Lip-tip syndrome, another variant of vitiligo is characterized by depigmentationfo the terminal phalanges and the lips.CLINICAL VARIANTS:1. Trichrome Vitiligo: Recognized by the presence of a narrow to broad intermediate colour zone between vitiligo macule and normal pigmented surrounding skin. It is a variant of unstable vitiligo 197.2. Quadrichrome Vitiligo: It is well documented fourth colour in vitiligo lesions, usually seen in darker skin types. A macular perifollicular or marginal hyper pigmentation is its salient feature and denotes a repigmentating disease.3. Penta chrome vitiligo: Infrequently encountered variant in which there is a sequential display of white, tan, brown, blue-gray hyperpigmentation and normal 198 skin. Black Skinned individual are predisposed to have this disorder4. Blue vitiligo: It usually corresponds to vitiligo macules occurring at the site of post inflammatory hypermelanosis 199.5. Inflammatory Vitiligo: It is an entity which may reveal an erythematous, raised border in a vitiligo macule with frequent itching / oozing. These can be induced by aggressive therapy200-202. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  49. 49. 49CLINICAL FEATURES OF VARIOUS TYPES OF VITILIGO:1. Localized: Focal: One or more macules in one area, but not clearly as in segmental or Zosteriform distribution. Segmental: One or more macules in quasidermatomal pattern. Mucosal: Involvement of mucosal membranes alone.2. Generalized Acrofacial: Involvement of distal extremities and face. Vulgaris: Scattered macules over the body. Mixed: Acrofacial and vulgaris involvement or segmental and acrofacial.3. Universal: Complete or nearly complete depigmentation.According to progression and prognosisSegmental: Has an early onset in life, spreads rapidly in affected area. The cause may arrest and depigmented patches can persist unchanged for the life. Vitiligo Zosteriformis: Macules distributed along a dermatome or lines of body cleavage.Non Segmental:Shows poor prognosis. Includes all types of vitiligo, except segmental type. Vitiligo _areata: 1 or 2 macules (Focal, Localized or partial). Vitiligo acrofacialis : Macules affecting face and tips of hands and feet. Vitiligo vulgaris: Scattered macules over the body. Vitiligo mucosal: Involvement of mucosal membranes alone. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  50. 50. 50According to clinical stages: Progressive Vitiligo: Developing new lesions . Increasing old lesions Ill defined border of lesion Quiescent stage: No appearance of new lesions Stationary old lesions Well defined, hyperpigmented bordersASSOCIATIONS OF VITILIGO: 203-210Cutaneous associations Premature graying of hair Leucotricha Halo nevus Lichen planus Alopecia areata Occasionally other skin disorders like Dermatitis herpetiformis, Giant congenitalmelanocytic nevus, Chronic urticaria, Malignant melanoma have been seen in associationwith vitiligo. Other interesting autoimmune associations include Morphea, and Hashimoto’s 211thyrioditis . While presenting strong direct and indirect evidence of auto immune etiology of 212alopecia areata, Hordinsky and Ericson stressed its association with vitiligo in manypatients. A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  51. 51. 51Occular associations: Vogt-Koyanagi-Harada syndrome213-218 refers to full constellation of vitiligo,Poliosis and Alopecia with pan uvetis and auditory and neurological manifestations. However iris, retinal pigmentary abnormalities may be present as isolated 219-221findings in vitiligo patients. Choroidal abnormalities and irites may also be presentSystemic associations: Hypo / hyper thyroidism, Diabetes mellitus, Addisions disease, Perniciousanaemia, Lymphoma, Leukemia, HIV, Autoimmune poly endocrinopathy ,Candidiasis,Ectodermal dystrophy.CHILDHOOD VITILIGO: Morphological characteristics in childhood vitiligo are more or less identical tothose of adult onset vitiligo. Interestingly there has been steady increase in the evidenceof child hood vitiligo during past two decades222.CONTACT VITILIGO: Contact vitiligo is an acquired leucoderma as a result of repeated topical orsystemic exposure to variety of chemicals223. These chemicals are mainly alley phenols,catechols used in manufacturing plastics, resins, synthetics, rubber, paints, petroleum,deodorants, germicides, insectides, photographic chemicals, varnishes etc., Thesechemicals are also present in certain objects like footware, plastic watch strap andbindis.224-225 A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  52. 52. 52 SAMPRAPTI Samprapti is defined as the phenomenon of dosha-dushya samurcchana226. Thecomplete process of manifestation of a disease is explained in this context. 227 The nidana and samprapti for kusta and switra are similar . The whole process 228of samprapti can be understood through shatkriyakalas Sanchaya Prakopa Dosha Prakopa avastha Prasara Stanasamshryam Dosha – dusya samurcchana Vyakti Vyadhi utpatti avastha Bheda The knowledge of samprapti is essential to break the chain of pathogenesis toprevent further progression of the disease and to implement specific treatment at differentstages of pathogenesis 229. 2301. SANCHAYAM: is the accumulation of vitiated doshas in their respective places .The doshas remain in equilibrium, unless disturbed by external causes. Viruddha ahara-vihara, Manasika karanas like Bhaya, krodha, papakarnas, sadvrut apacharas are the endogenous causes. Kshata, dagda, vranas, Savishajaloukaprayoga are the exogenous causes. The exogenous and endogenous causes are responsible for the vitiation of doshas. Viruddha ahara produces amavisha which is antagonistic to the dhatus, there by 231 leads to various disease. Adhika amla, lavana, ushna, teekshana dravyas cause pitta prakopa leading to rakta dusti 232 A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)
  53. 53. 53 233 Virudha vihara, diwaswapnam, atisantapasevanam causes pitta prakopa Suppression of natural urges causes vitiation of apanavata and it travels in pratilomagati disturbs samanavata which in turn disturbs udana vata (responsible for Varna). Bhaya, kroda increase rajogunam in the body, which in turn causes vata-pitta prakopa Papakarmas, sadvrut apacharas leads to psycho-somatic disturbances, leads to vitiation of vata pitta doshas 234. In agantuja karanas, directly twakdusti occurs and lakshanas are exhibited, later 235 on the doshas are vitiated.2. PRAKOPA: Prakopa the next stage of sanchaya. The accumulation of vitiated doshascontinues and the doshas are ready to rise above their respective stanas236. Nidana Factors Sanchaya Prakopa Are continued3. PRASARA: This is the stage where the vitiated doshas get dislodged from theirrespective places and start spreading all over the body through siras or channels. Inswitra, the vitiated vata, pitta, kapha spread in the body through “Tiryagata Siras” 237 238which implies urdwa, adho, tiryak Siras. The doshas spread in all the directions .4. STANA SAMSHRAYAM: The most important phase of shatkriyakalas where themajor event “Samprapti” occurs239. Dosha – dushya samurcchana and vyadhi purvarupasare exhibited in this stage A CLINICAL STUDY ON THE EFFECT OF “DHATRI - KHADIRA KWATH” IN THE MANAGEMENT OF SWITRAM (VITILIGO)

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