This document summarizes a presentation on statins and their pleiotropic effects. It begins with an overview and introduction on statins. It then discusses cholesterol synthesis and statins' mechanism of action in inhibiting HMG-CoA reductase to lower cholesterol. The document outlines various pleiotropic effects of statins including improving endothelial function, providing plaque stability, anti-inflammatory effects, and effects on other organs. It summarizes several research articles on topics like statins' effect on CRP and the association between statins and vitamin D.
Statin drugs and their harmful side effectsGeorge Mark
With the knowledge about statin drugs becoming clearer now, there is much confusion in the medical community as to their usability for decreasing cholesterol levels
Statin drugs and their harmful side effectsGeorge Mark
With the knowledge about statin drugs becoming clearer now, there is much confusion in the medical community as to their usability for decreasing cholesterol levels
Diabetes mellitus (DM) refers to a group of common metabolic disorders that share the phenotype of hyperglycemia.
Several distinct types of DM are caused by a complex interaction of genetics and environmental factors.
Depending on the etiology of the DM, factors contributing to hyperglycemia include reduced insulin secretion, decreased glucose utilization, and increased glucose production.
The metabolic dysregulation associated with DM causes secondary pathophysiologic changes in multiple organ systems that impose a tremendous burden on the individual with diabetes and on the health care system.
Hypertension pharmacotherapy part 2 pptPranatiChavan
First-line medications used in the treatment of hypertension include diuretics, angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), beta-blockers, and calcium channel blockers (CCBs). Some patients will require 2 or more antihypertensive medications to achieve their BP target. As per special consideration, modified treatment is given in the presentation.
ARBs (Angiotensin receptor blockers) are the most widely used anti hypertensive throughout the world. A solid knowledge related to ARB will make our practice more patients friendly & benefit will be maximum.
Diabetes mellitus (DM) refers to a group of common metabolic disorders that share the phenotype of hyperglycemia.
Several distinct types of DM are caused by a complex interaction of genetics and environmental factors.
Depending on the etiology of the DM, factors contributing to hyperglycemia include reduced insulin secretion, decreased glucose utilization, and increased glucose production.
The metabolic dysregulation associated with DM causes secondary pathophysiologic changes in multiple organ systems that impose a tremendous burden on the individual with diabetes and on the health care system.
Hypertension pharmacotherapy part 2 pptPranatiChavan
First-line medications used in the treatment of hypertension include diuretics, angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), beta-blockers, and calcium channel blockers (CCBs). Some patients will require 2 or more antihypertensive medications to achieve their BP target. As per special consideration, modified treatment is given in the presentation.
ARBs (Angiotensin receptor blockers) are the most widely used anti hypertensive throughout the world. A solid knowledge related to ARB will make our practice more patients friendly & benefit will be maximum.
COMPARATIVE ASSESSMENT OF THE EEFFECT OF ARGINASE INHIBITOR L-NORVALINE AND M...ShubhamBaliyan13
Having metabolic syndrome can induce the risk of developing especially Type 2 Diabetes, insulin resistance , Atherosclerosis, cardiovascular disease, visceral Obesity, Dyslipidemias.
This study aimed at determining the prevalence of metabolic syndrome ( MetS) and its individual components and the most critical predictive risk factors of MetS in Type 2 Diabetes .
Introduction: This review discusses the molecular mechanisms responsible for the normalization of otherwise raised intraocular pressure (IOP) in patients of glaucoma when they are administered statin therapy. Material and Methods: Literature published between 1990 and 2016 on the pathophysiology of glaucoma and the action of statins has been reviewed. Data Synthesis: A decrease in resistance to aqueous humor flow through trabecular meshwork (TM) in the eye tissue results in lessening of the raised intraocular pressure. KATP channels have been discovered in the eye tissue recently. Activation of KATP channels facilitates the flow of aqueous humor through the TM. This presumption is strengthened by the action of statins. Statins activate these KATP channels and, thereby, facilitate the aqueous flow through TM leading to relief in IOP. Statins interfere in the cholesterol biosynthesis pathway leading to decreased cholesterol synthesis. However, a simultaneous decrease in the level of ubiquinone leads to activation of KATP channels. Further, accumulation of LC Acetyl CoAs also activates these KATP channels. Expert Opinion: Statins decrease the elevated intraocular pressure in glaucoma by activating KATP channels. KATP channels are recently discovered therapeutic targets which may be exploited in the treatment of glaucoma.
this presentation deals with drug price control in India. it has also updated information on drug price regulation. any suggestion regarding this topic is most welcomed.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
1. STATINS AND ITS
PLEIOTROPIC EFFECTS
PRESENTED BY-
DR.AAKANKSHA PRIYA
PGY 1
AIIMS PATNA
MODULATOR – DR.P.P GUPTA
PROFESSOR AND HEAD OF DEPARTMENT
DEPT.OF PHARMACOLOGY
AIIMS PATNA
2. OVERVIEW
1. Introduction
2. Cholesterol and its synthesis
3. Statins and its mechanism of action
4. Pleiotropic effects of statins
5. Research article on statin safety and vitamin D.
6. Bibliography
3. INTRODUCTION
Cardiovascular diseases (coronary heart disease) principal cause of
morbidity and mortality in developing as well as developed countries.
Atherosclerosis is the main underlying cause of disorders in CVDs.
An association has been established between Elevated levels of plasma
Cholesterol and increased atherosclerotic diseases.
Several landmark clinical trials Eg: Scandinavian simvastatin survival study,
cholesterol and Recurrent Events, Heart Protection study etc have
demonstrated the benefit of lipid lowering with 3-hydroxy-3-
methylglutaryl coenzyme A[HMG CoA] reductase enzyme inhibitors
/statins for primary and secondary of CHDs.
Statins also exerts many pleiotropic effects too.
4. CHOLESTEROL
Cholesterol and its derivatives are important
components of cell membrane, immediate
precursors of steroid hormones, bile acids and
Vitamin D synthesis.
5. CONT…
Cholesterol in excessive amounts, becomes an important risk
factors for CVDs.
Demonstrated in clinical trials from “FRAMINGHAM HEART
SOCIETY” and “MULTIPLE RISK FACTOR INTERVENTION
TRIAL.”
>2/3 body cholesterol is synthesized in Liver.
Therefore, inhibition of hepatic biosynthesis is target of
choice for reducing Serum cholesterol.
7. DISCOVERY OF STATINS
Statins(similar to HMG CoA Reductase) were first isolated
from a mold, Penicillium citrinum in 1976 by Endo et al.
First statin was studied in Rats is Compactin,( Mevastatins)
but was withdrawn due to its hepatocellular toxicity.
Lovastatin become the first statin approved to be used in
humans was isolated from aspergillus terreus by Hoffman et
al. in 1979.
8. MECHANISM OF ACTION OF
STATINS
Competitive inhibitors of HMG CoA Reductase
Statins occupies a portion of binding site of HMG CoA
Reductase, thus blocking access of substrate to the active site
on the enzyme
There by reducing the conversion of HMG CoA to
Mevalonate(Rate – Limiting step)
9. CONT…
Statins inhibits hepatic cholesterol
synthesis
Increase expression of LDL-C
receptor gene
Increased receptors leads to
increased removal of LDL from blood
11. UNDERSTANDING OF PLEIOTROPIC
EFFECTS
Pleiotropic effects are those effects which are
independent of direct reduction in Low density
lipoproteins cholesterol(LDL-C).
Plays an important role in reducing cardiovascular
morbidity and mortality.
12. TYPES PLEIOTROPIC EFFECTS OF
STATINS
Improves Endothelial Function.
Provides stability to the Plaques.
Acts as an Anti Inflammatory agents.
Provides Oxidative modification of LDL
Acts as an Anti-Coagulant.
13. CNS – in case of Ischemic stroke and
Dementia
HEART – on Myocardium.
LUNGS – copd.
OTHER ORGAN PROTECTIVE EFFECTS
OF STATINS
14. STATINS AND ENDOTHELIAL
FUNCTIONS
Main role of Vascular Endothelium – vasoconstriction
/relaxation.
Hypercholesterolemia adversely affects the processes by
which the endothelium modulates arterial tone.
Statins therapy enhances endothelial production of
Vasodilator NITRIC OXIDE thus leading to improve
endothelial functions.
This mechanism is Independent of change of Plasma
Cholesterol levels.
15.
16. OTHER FAVOURABLE EFFECTS ON
ENDOTHELIUM
Restores endothelial NOS activity even in presence of
HYPOXIA and OXIDIZED LDL-C.
Increases the expression of Tissue – type Plasminogen
activator(t-PA).
Inhibits expression of endothelin-1(potent vasoconstrictor).
Upregulation of Endothelial progenitor cells.
Increases half life of mRNA.
17. STATINS AND PLAQUE STABILITY
Plaque rupture is a major cause of Acute
Coronary syndrome.
Statins reduces macrophage Cholesterol
accumulation.
And also Reduces secretion of
Metalloproteinase(a proteolytic enzyme)
20. AS AN ANTI INFLAMMATORY AGENTS
Atherosclerosis is a complex inflammatory process
characterised by presence of monocytes /macrophages and T
lymphocytes in the atheroma.
Inflammatory cytokines secreted by these macrophages and
T lymphocytes can modify Endothelial functions, SMC
proliferation, collagen degradation, and Thrombosis.
21. Role of statins are-
1. Decreases T- cell recruitment and activation.
2. Reduction in expression of inflammatory cytokines and
chemokines.
3. Attenuation of expression of CD40(TNF family) in T-cells.
4. Inhibition of SMC proliferation.
22. CLINICAL EVIDENCE OF INFLAMMATION
High-sensitive C-reactive proteins(hs-CRP) is an acute phase
reactant that is produced in the liver in response to
proinflammatory cytokines.
Elevated levels of hs-CRP indicate the risk for coronary artery
disease, coronary ischemia and myocardial infarction.
23. RESEARCH ARTICLE ON hs-CRP
TOPIC- Effect of Atorvastatin on hs-CRP in Acute Coronary
Syndrome(ACS)
PUBLISHED IN- British journal of pharmacology
RESEARCH DONE AT- CMC Hospital Ludhiana
AUTHOR – Gupta et al.
AIM – to evaluate the effect of lower dose(20mg) Atorvastatin
in patients with ACS.
24. METHOD USED..
It was prospective, open study conducted on patients
enrolled for over 15months.
Patients diagnosed with ACS as per criteria were included.
Group A(n=50) received atorvastatin 20mg/day for 4 weeks
along with std anti anginal treatment.
Group B(n=50) received std anti anginal treatment without
atorvastatin.
25. RESULT
Data was analyzed using student t test, ANOVA and chi square test.
GROUPS Hs-CRP at the
begin
Hs-CRP at the
end
% change
Group A 2.32 0.57 82
Group B 1.91 1.04 54
26. CONCLUSION
hs – CRP decreased in both but decrease in group A
(p<0.001) was significant.
The use of lower dose(20mg) of atorvastatin can offer an
attractive approach for early treatment of ACS patients.
27. PROVIDES OXIDATIVE MODIFICATION OF
LDL
Key role in mediating the uptake of Lipoprotein cholesterol
by macrophages and in other process, including cytotoxicity
within lesions.
Statins reduces susceptibility of lipoproteins to oxidation of
both in vivo and ex vivo by neutralising reactive oxygen
species and NADPH oxidase activity.
28. EFFECTS OF STATINS ON MYOCARDIUM
Pressure Overload
Activation of small GTP binding proteins,
Ras, Rho, Roc and NADPH associated
with oxidative stress
Cardiac Hypertrophy
29. Cont….
In human studies it has been proved that statins could inhibit
cardiac hypertrophy through antioxidation mechanism
involving of Rac 1and NADPH oxidase.
31. STATINS AS ANTI COAGULANT
According to JUPITER trial done by (Glynn et al 2009)
concluded that there were 43% reduction in venous
thromboembolic events in patients treated with Rosuvastatin,
20mg.
Role of statin—
1. Inhibition of platelets adhesion/aggregation.
2. Reduces fibrinogen concentration.
3. Reduces blood viscosity.
32. STATINS AND ITS EFFECT ON ISCHEMIC
STROKE
Heart Protection Study(HPS) conducted study in those aged
over 70yrs and those presented with different levels of
B.P/Lipids, even when pretreatment LDL-C was below
116mg/dl were prescribed statins.
As a result there was 28% reduction in ischemic stroke in over
20,000 people with cerebrovascular diseases.
Role of statin (seen in animal studies) is by upregulating of
eNOS in prevention of ischemic stroke.
33. STATINS AND DEMENTIA
Dementia is syndrome of chronic /progressive nature with
multiple disturbances of higher cortical functions. For Eg:
Alzheimer disease.
In a nested case control study, based on the UK-based
General Practice Research Database showed that among
people of aged over 50yrs with statin therapy, risk for
developing dementia was significantly reduced, independent
of their lipid status.
34. STATINS IN PULMONARY DISEASE
COPD- statins have Immunomodulatory effects including –
1. Reducing Neutrophil migration
2. Cytokine production
3. Adverse matrix remodelling
4. Reducing small airway inflammation.
35. ASTHMA –
1. In laboratory animals , statins have shown
immunomodulatory role in allergic lung
inflammation.
2. In human trials statins have shown negative , or
perhaps only modest benefit.
36. ORIGINAL RESEARCH ARTICLE
TOPIC – Statin therapy and Vitamin D
RESEARCH DONE AT- Chettinad Hospital and Research
Institute Chennai TN.
PUBLISHED IN – International Journal of Basic and Clinical
Pharmacology.
37. AIM AND METHOD USED..
AIM- To Evaluate association between statins and vitamin D.
METHOD- the study was a prospective cross-sectional study. 125
participants who fulfilled the selection criteria were enrolled in the
study. 65 subjects belonged to control group and 60, statin group.
The blood sample were collected for vitamin D estimation. The
result were correlated with demographic profile, nature of statin
and muscular side effects and compared with control group.
38. SELECTION CRITERIA-
1. Statin group- all subjects who were on any one of statins for
more than 1 year.
2. Control group- apparently healthy individuals.
3. Subjects who were on vitamin D supplementation were
excluded from both groups.
39. METHOD CONT….
From the eligible subjects, 5ml of blood was collected by
direct venous puncture
Vitamin D(total) was estimated with High sensitivity
chemiluminescence immunoassay method.
Vitamin D level in blood was classified as –
1. Sufficient – 30-100ng/ml
2. Insufficient – 20-29ng/ml
3. Deficient - <20ng/ml.
40. RESULT
Statistical comparison was made for vitamin D level using
Independent samples t- test as well as vitamin D status using chi
square test.
The mean vitamin D level in statin group was 15.82ng/ml and
20.57ng in control group.
This difference was found to be statistically significant(p=0.006 and
0.033)
Myalgia was reported by 30 among 60 subjects(50%) in statin
group and 5 among 65 subjects (7.69%) in control group.
41. CONT….
13.85% in control group and 10% in statin group had
sufficient vitamin D level.
18.33% in control group and 36.92% in statin group
insufficient vitamin D level.
49.23% in control group and 71.67% in statin group had
deficiency of vitamin D level.
42. DATA OF VITAMIN D LEVEL IN STATIN
GROUP.
Age(years) N Mean vitamin
D(ng/ml)
SD
<40 0
40-60 14 15.03 12.22
>60 46 15.26 12.35
Gender
Male 28 16.65 10.02
Female 32 13.94 13.90
43. DATA OF VITAMIN D LEVEL IN
CONTROL GROUP.
Age(years) N Mean Vitamin
D(ng/ml)
SD
<40 12 15.13 6.46
40-60 29 20.64 7.11
>60 24 23.04 6.53
Gender
Male 35 22.48 6.68
Female 30 18.20 7.29
44. VITAMIN D LEVEL IN STATIN AND
CONTROL GROUP(ng/ml)
0
5
10
15
20
25
Statin Group Control Group
Series 1
45. VITAMIN D STATUS
Vitamin D status Statin group(%) Control group(%)
Sufficient 6(10.00) 9(13.85)
Insufficient 11(18.33) 24(36.92)
Deficiency 43(71.67) 32(49.23)
47. SUMMARY..
STATIN PLEIOTROPY BENEFITS
Increased synthesis of Nitric oxide Improved endothelial dysfunction
Inhibition of free radical release
Decreased synthesis of endothelin-1
Inhibition of LDL-C oxidation
Upregulation of endothelial progenitor
cell
Reduced number and activities of
inflammatory cells
Reduced inflammatory response
Reduced levels of c-reactive proteins
Reduced macrophages cholesterol
accumulation
Stabilization of atherosclerotic plaques
Inhibition of platelets aggregation Reduced thrombogenic response
Reduced fibrinogen concentration
Reduced blood viscosity
48. BIBLIOGRAPHY
1. Goodman and Gilman. The Pharmacological basis of
therapeutics.12th ed.china.McGraw-Hill,2011.
2. Bertram G. Katzung. Basic & clinical Pharmacology. 14th ed.
Chennai. McGraw-Hill, 2018.
3. Liao JK, Laufs U. Pleiotropic effect of statins. Annu Rev
Pharmacol Toxicol, 2005; 45: 89-118.
4. Roth L et al. cholesterol- independent effects of Atorvastatin.
Vascular Pharmacology, 2016; 80:50-58.
49. CONT…
5.Krishna RK et al. Pleiotropic effects of the HMG CoA inhibitors
in pulmonary diseases. Pul pharma & therapeutics., 2015 ;30:
134-140.
6.Davignon J. Pleiotropic effects of pitavastatins. Br J Clin
Pharmacol, 2011; 73:4, 518-535.
7.Gupta et al. Effect of Atorvastatin on hs-CRP in ACS. Br J clin
Pharmacol, 2008 ; 66:3, 411-413.
8.Radhakrishanan A et al. statin therapy and vitamin D. IJBCP,
2005; 4:6 1113-1117.