Niacin also known as vitamin B3 or nicotinic acid. Niacin is a water-soluble B-complex vitamin that functions as a vitamin only after its conversion to NAD or NADP.
Niacin with statin therapy benefits are increasing HDL-C by 3040% lowers triglycerides by 3545% reduces LDL-C levels by 2030%.
Action of niacin
In adipose tissue, niacin inhibits the lipolysis of triglycerides by hormone-sensitive lipase, which reduces transport of free fatty acids to the liver and decreases hepatic triglyceride synthesis. In liver, niacin reduces triglyceride synthesis by inhibiting both the synthesis and esterification of fatty acids. .
Reduced triglyceride synthesis decreases hepatic VLDL production, which reduces LDL levels Niacin raises HDL-C levels by decreasing fractional clearance of apoA-I in HDL rather than by enhancing HDL synthesis.
Adverse effects
Cutaneous effects include flushing and pruritus of the face and upper trunk, and rashes. Dyspepsia, nausea, vomiting . Hepatotoxicity, manifested as elevated serum transaminases and hyperglycemia.
CONTRA INDICATION
Peptic ulcer- reactivate ulcer disease Diabetes mellitus- niacin induce insulin resistance and cause severe hyperglycemia. Gout it elevates uric acid level.
THERAPEUTIC DOSE
It is especially useful in patients with both hypertriglyceridemia and low HDL-C levels. Crystalline niacin (immediate-release or regular) refers to niacin tablets that dissolve quickly after ingestion. Sustained-release niacin refers to preparations that continuously release niacin for 68 hours after ingestion
Regular or crystalline niacin in doses of 26 g/day reduces triglycerides by 3550%, and the maximal effect occurs within 47 days. Reductions of 25% in LDL-C levels are possible with doses of 4.56 g/day, but 36 weeks are required for maximal effect. Average increases in HDL-C of 1530%occur in patients with low HDL-C levels with a dose of 24g/day and the maximum effect occurs within 4-6 weeks.
DYSLIPIDEMIA
Dyslipidemia or dyslipidaemia is an abnormal amount of lipids (e.g. cholesterol and/or fat) in the blood. In developed countries, most dyslipidemias are hyperlipidemias; that is, an elevation of lipids in the blood, often due to diet and lifestyle.
Human plasma lipoproteins are separated into five major class based on the density: Chylomicrons Very-low-density lipoproteins(VLDLs) Intermediate density lipoproteins(IDLs) Low density lipoproteins(LDLs) High density lipoproteins(HDLs) Lipoprotein(a)-[Lp(a)],resembles LDL in lipid composition and has a density that overlaps LDL and HDL.
Metabolic product of B-100 VLDL Metabolic product of B-100 IDL Liver, intestine liver A-1,AB-100,Apo(a)
LDL
TG;10%; chol,50%
HDL Lp(a)
ATP III Classification of LDL, Total, and HDL Cholesterol (mg/dL) LDL Cholesterol <100 Optimal 100-129 Near optimal/above optimal 130-159 Borderline high 160-189 High 190 Very high Total Cholesterol <200 200-239 240 HDL Cholesterol <40 60
Low High
Original article
In patients with established cardiovascular disease, residual cardiovascular risk persists despite the achievement of target low-density lipoprotein (LDL) cholesterol levels with statin therapy. It is unclear whether extended-release niacin added to simvastatin to raise low levels of highdensity lipoprotein (HDL) cholesterol is superior to simvastatin alone in reducing such residual risk.
Results
A total of 3414 patients were randomly assigned to receive niacin (1718) or placebo(1696). The trial was stopped after a mean follow-up period of 3 years owing to a lack of efficacy. At 2 years, niacin therapy had significantly increased the median HDL cholesterol level from 35 mg per deciliter to 42 mg per deciliter , lowered the triglyceride level from 164 mg per deciliter to 122 mg per deciliter and lowered the LDL cholesterol level from 74 mg per deciliter to 62 mg per deciliter . The primary end point occurred in 282 patients in the niacin group (16.4%) and in 274 patients in the placebo group (16.2%).
conclusion
Among patients with atherosclerotic cardiovascular disease and LDL cholesterol levels of less than 70 mg per deciliter , there was no incremental clinical benefit from the addition of niacin to statin therapy during a 36-month follow-up period, despite significant improvements in HDL cholesterol and triglyceride levels.