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Nicotinic acid is good therapeutic agent in hyperlipidemic patients

Major risk factors associated with the development of CHD include gender, age, cigrete smoking, diabetes mellitus, hypertension and hyperlipidemia.13 A HDL-C level, independently of high LDL-C level, is also major risk factor for CHD.Moreover a substantial portion of patients with CHD have low HDL-C concentrations.4, 19-20

There are various drugs which decrease total cholesterol, triglycerides, LDL-C and increase HDL-C in primary hyperlipidemic patients, but Niacin is the best HDL-C raising agent among the lipid lowering drugs.11 Niacin inhibits the activity of hormone sensitivity lipase causing decrease in lipolysis and so decreased VLDL secretion from hepatocytes.14 Factors responsible for decreased production of VLDL include inhibition of lipolysis with a decrease in free fatty acids in plasma, decreased hepatic esterification of triglycerides, and a possible direct effect on the hepatic production of apolipoprotein-B. Niacin also increases HDL-C by reducing its catabolism. It also decreases plasma fibrinogen levels and increase tissue plasminogen activator. All of these factors influence the process of atherogenesis and CHD.13-15 Some recent studies also suggest that Niacin also decreases blood pressure. Possible mechanism is that Niacin causes vasodilatation due to production of prostaglandin-3.9-12, 16

PATIENTS AND METHODS

This study was conducted at department of Pharmacology and therapeutics, Basic Medical Sciences Institute, Jinnah Postgraduate Medical Centre, Karachi, from January to July 2002.Forty patients of primary hyperlipidemia were initially enrolled in this study, selected from ward and OPD of National Institute of Cardiovascular Diseases, Karachi.Newly diagnosed and untreated primary hyperlipidemic patients of either sex, age range from 17 to 70 years were randomly selected. Patients with diabetes mellitus, peptic ulcer, renal disease, hepatic disease, hypothyroidism and alcoholism were excluded from the study by available laboratory investigation, history and clinical examination. After explaining the limitations, written consent was obtained from all study participants. The study period consisted of 90 days with fortnightly follow up visits. The required information such as name, age, sex, occupation, address, previous medication, date of follow up visit and laboratory investigations, etc of each patient was recorded on a proforma, especially designed for this study. Initially a detailed medical history and physical examination of all patients were carried out. All the base line assessments were taken on the day of inclusion (Day-0) in the study and a similar assessment was taken on Day-90 of of research design. After fulfilling the inclusion criteria patients were randomly divided into two groups, i.e.Drug-1(tab: Niacin 2gm) and Drug-2(placebo capsules, containing equal amounts of partly grinded wheat) groups. Patients of drug-1 group were advised to take Tab: Niacin (250 mg), half tablet thrice daily, after meal for 2 days, then by increasing the dose one tablet, TID, after meal for 2 days, then 2 tablets, thrice daily after meal for 2 days, then the maintaibnace dose of 3 tablets per day after meal, thrice daily, till end of the study period, i.e.up to day-90. This regimen of dose of drug (called titration of Niacin) was applied due to avoidance of it’s adverse effects produced by starting with higher doses of the Niacin.17 Patients of drug-2 group were provided placebo capsules, i.e.one capsule, TID, after meal for 90 days. Patients were called every 2 weeks for follow up to check blood pressure, weight, pulse rate and general appearance of the individual. Drug compliance to the regimen was monitored by interview and counseling at each clinical visits. Serum HDL-cholesterol was determined by direct method, at day-0 and day-90, using kit # 303210040 by Eli tech diagnostic, France.Data were expressed as the mean + SD and “t” test was applied to determine statistical significance as the difference. A probability value of <0.05 was the limit of significance.

RESULTS

Out of 40 patients, 37 completed the over all study period. Three patients withdrew from the drug-1 group (Niacin group) due to side effects of the drug like flushing, sensation of heat, urinary and headache. Tables showing base line and post treatment values are self explainatory.When results were summed up and test parameters were compared, it was seen that, after 90 days of treatment with Niacin, HDL-Cholesterol increased from 36.41+1.96 mg/dl to 43.70+1.81 mg/dl, which is highly significant (P<0.001).Overall percentage change from day-0 to day-90 was 20.02, as shown in table no: 1. In placebo group at day-0,HDL-Cholesterol level was 35.50+1.13 mg/dl,which increased to 35.75+1.07 mg/dl,which is non-significant(P>0.05).The overall percentage increase in the parameter was 0.70.The difference between mean values among placebo group and Niacin group is 19.32 as shown in the table no:3.Mean systolic Blood pressure of patients on Niacin, reduced from 125.88+3.48 mm of Hg to 119.70+3.13 mm of Hg in 3 months, which is highly significant(P<0.001).In percentage this reduction is 4.90%,as shown in table no:1 and 3.In placebo group this reduction is 1.62%(P<0.01) and difference in mean values of these 2 groups is 3.28. Niacin has shown reduction in diastolic Blood Pressure of hyperlipidemic patients. It reduced diastolic B.P at day-0, from 89.11+1.92 mm of Hg to 84.70+1.74 mm of Hg, at day-90, which is highly significant (P<0.001).In percentage this reduction is 4.94%.Placebo group has shown little effect on diastolic B.P, i.e. only 2.67%, but this difference is significant (P<0.01).Difference in mean values of diastolic B.P among 2groups is 2.27, as depicted in table no: 2 and 3.

DISCUSSION

Among the lipid lowering drugs, Niacin appears to be the best HDL raising agent. In our study,HDL-Cholesterol levels raised by 20% in men and women with low HDL-C levels treated with a medium dose of Niacin(2 gm/day).The drug has another advantage of being inexpensive. Levels of HDL-C, not only raised by 20% but go maintained throughout 3 months of study period with the therapy. This finding coincides with the study of Martin-jadraque et al.4 Treatment with placebo capsules for 90 days, HDL-Cholesterol was increased 0.7% as compared to 3.7% increase in a study by lipid Research Clinics.18  7% increase in HDL-Cholesterol has also been quoted in another study by Rivellese et al.It was demonstrated by Miller et al5  that long distance runners have much high HDL-Cholesterol concentration than do more sedentary subjects. The rise in HDL-C concentration by physical training may be a consequence of enhanced catabolism of triglycerides rich lipoproteins (VLDL). It was observed by McKinney et al7, that high dose of crystalline Niacin increased 30% in concentration of HDL-C.This observation is in contrast with our observation, probably due to small sample size low dose of the drug.They used 6gm of Niacin in 80 patients for the period of four months.Drop out rate in our study was 15% and most of the patients discontinued treatment due to development of side effects like flushing, urticaria and sensation of heat in the body. Other patients were convinced for continuing therapy, by dose concentration regimen (titration) of Niacin or taking aspirin 250 mg OD, before taking 1st dose of drug at morning. Wilkin et al, have described the mechanism by which aspirin blocks Niacin induced flushing.8 Stern et al has mentioned that tolerance is developed for flushing, urticaria and hotness in body, by dose titration of Niacin. Niacin produces Prostaglandin D-3, which causes vasodilatat, and decreases blood pressure.

CONCLUSION

From the results of present study and data from previously published literature it is concluded that niacin decreased the risk of CHD by increasing HDL-C and decreasing blood pressure, so it could be recommend that this drug may be used as monotherapy in patients of hyperlipidemia in whom HDL-C levels are low and who are prone to develop atherogenesis.

REFERENCES

1. Krira KA, Shah SMS, Salahuddin et al (2000). Incidence of lipid disorders in offspring of patients with premature myocardial infarction. Medical Channel; 6:9-12

2. Samad A, Sahibzada WA, sheikh SA (1996). Guidelines for detection and management of lipid levels. PJC; 7:26-46.

3. Timmis AD (1991). Early diagnosis of MI.BMJ; 7:309-310.

4.Martin-Idraque R, Tato F, Mostaza JM, Vega GL, Grundy SM (1996). Effectiveness of low-dose crystalline nicotinic acid in men with low HDL-Cholesterol levels.Arch.Intern.Med; 156:1081-1088.

5.Miller NE, Rao S, Lewis B, et al (1979). HDL and physical activity. Lancet; 1:111

6.Kris-Etherton PM, Pearson TA, Wan Y et al (1999). High-monounsaturated fatty acid diets lower both plasma cholesterol and triglycerides concentration.Am.J.Clin.Nutr; 70:1009-1015.

7.Mckenny JM, Proctor JD, Harris S, Chinchili VM (1994). A comparison of the efficacy and toxic effects of sustained vs immediate-release Niacin in hypercholesterolemic patients. JAMA; 271:672-677.

8.Wilkin JK, Wilkin O, Kapp R, Donachie R, Chernosky ME, Buckner J(1982).Aspirin blocks nicotinic acid-induced flushing.Clin.Pharmacol.Ther;31:478-482.

9. Stern RH, Spence JD, Freeman DJ, Parbtani A, (1991). Tolerence to Nicotinic acid flushing.Clin.PharmacolTherap; 50:66-70.

10.Tato F, Vega GL, Grundy SM, (1998). Effects of crystalline nicotinic acid-induced hepatic dysfunction on serum LDL-Cholesterol and lecithin cholesteryl Acyl transferase.Am.J.Cardiol; 81:805-807.

11. Garg A, Grundy SM (1990). Nicotinic acid as therapy for dyslipidemia in non-insulin dependent DM.JAMA; 264:723-726.

12. Levy RI, Fredrickson DS, Shulman R,(1972).Dietary and drug treatment of primary hyperlipedemia.Ann.Int.Med; 77:267-294.

13. Qizilbash N, Jones L, Warlow C, Mann J, (1991). Fibrinogen and lipid concentrations as risk factors for transient Ischemic attacks and minor ischemic strokes. BMJ; 303:605-609.

14. Rivelles AA, Auletta P, Marotta G, et al (1994). Long term metabolic effects of two dietary methods of treating hyperlipidemia. BMJ; 5:10-14.

15. Roche HM, Gibney MJ (2000). Effect of long chain n-3 polyunsaturated fatty acids on fasting and postprandial triglycerolmetabolism.AM.J.Clin.Nutr; 71:232S-237S.

16. Chisholm A, Mann J, Sutherland W, Duncan A, Skeoff M, Frampton C (1996). Effect on lipoprotein profile of replacing butter with margarine in a low fat diet. BMJ; 312:931-939.

17. Crouse JR, (1996). New developments in the use of Niacin for treatment of hyperlipedemia. Coron Artery Dis; 7:321-326.

18. Delong DM, Delong ER, Wood PD, Lippel K, Rifkind BM (1986). A comparison of methods for the estimation of plasma lowand very low-density lipoprotein cholesterol. JAMA; 256:2372-2377.

19. Kanne W B, Castell W P, Gordon T, (2002). Cholesterol in prediction of atherosclerosis. New perspective based on Framinghan study.Ann.Intern.Med; 90:85-91.

20. Grundy SM, Denke MA (1999). Dietary influence on serum lipids and lipoproteins Lipids Res 1999(3): 1; 1149-1172.

21.Valverda MA, V.tolo MR, Patin RV,(1999).Changes in lipid profile in obese children and adolescents.Arch Lantinoam Nutr;49:338-343.

About the Author

Ashraf Memon,Shah Murad,Ghulam Rasool Bhurgari,Nighat Kafil,Muhsin Turab,Shehzad Rasheed

What is the scope for Bio Medical Engineering in Canada.?

My wife is a Bio-Medical Engineer(Masters from Mumbai University,India) with 1 year experience installation/setup of 5 parameter,7 parameter patient monitors,ambulatory blood pressure monitors,holter monitors etc.

My biggest advice for your wife would be to take any additional education in Canada. As I understand it employers in Canada in professional fields do not have a great record at recognizing extremely talented people who happen to have a degree from a non-western university.

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