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Am Fam Physician. 2002;66(10):1980-1983

Dyslipidemia is common in persons with diabetes mellitus and contributes to increased cardiovascular disease risk. Using 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) to decrease low-density lipoprotein (LDL) cholesterol levels reduces the risk for coronary events among these patients. Niacin is another potentially useful drug to improve diabetic dyslipidemia because it blocks fatty acid release from adipose tissue and decreases release of very–low-density lipoprotein. This latter effect reduces the number of small, dense LDL particles. In addition, niacin is considered the best drug to increase risk-reducing high-density lipoprotein (HDL) cholesterol levels. Because niacin can also increase fasting blood glucose levels, a risk-benefit evaluation is important in considering the use of niacin in these patients. Extended-release forms of niacin allow once-daily dosing and avoid much of the flushing and hepato-toxicity of the intermediate and sustained-release preparations. Grundy and associates evaluated the safety and efficacy of low-dose extended-release niacin in managing dyslipi-demia in patients with diabetes mellitus.

Patients were randomized to receive placebo, 1,000 mg of extended-release niacin, or 1,500 mg of extended-release niacin daily for about 15 weeks. Patients already taking statin preparations continued taking those medications.

Increased efficacy was noted with the two extended-release niacin dosages, with both resulting in significant increases in HDL cholesterol levels. The higher-dose treatment group also showed a significant reduction in triglyceride levels and LDL cholesterol levels. In the safety analysis, there was a marginally significant increase in glycosylated hemoglobin (HbA1C) level among patients in the higher-dose group. Fasting blood glucose levels were not affected by treatment with niacin, probably as a result of alterations in antidia-betic therapies in some patients. There was no difference in adverse events between groups except flushing, which occurred significantly more often in the treated groups but rarely caused discontinuation of medication. There was no increase in liver enzyme levels of greater than three times the upper limit of normal in any patient.

The authors conclude that extended-release niacin at dosages of 1,000 and 1,500 mg daily is effective in increasing HDL cholesterol and, with the higher dosage, decreasing triglyc-erides. No important adverse events or significant changes in glucose levels have been noted, and both dosages of niacin are well tolerated. The potential negative effects of the slight increase in HbA1C in the group receiving 1,500 mg of niacin are probably offset by a reduction in dyslipidemia-induced risk. Extended-release niacin should be considered, with or without statins, in the treatment of dyslipidemia in persons with diabetes mellitus.

editor's note: The increased risk of cardiovascular disease among patients with type 2 diabetes mellitus is partly due to a highly atherogenic lipid profile. Diabetic dyslipidemia is characterized by (1) elevated triglycerides, (2) normal LDL and total cholesterol levels, (3) reduced HDL levels, and (4) a higher percentage of small, dense LDL particles. This metabolic derangement is usually preceded by the onset of insulin resistance. Treatment of diabetic dyslipidemia should be aggressive, with goals of 100 mg per dL (2.60 mmol per L) for LDL cholesterol, 200 mg per dL (5.20 mmol per L) for triglycerides, and greater than 45 mg per dL (0.50 mmol per L) for HDL cholesterol. Intensive glycemic control, weight reduction, and pharmacologic treatment are advised. For the latter, statins are the first-line treatment, and fibrates or nicotinic acid can be added if needed.—r.s.

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