Background: HIV infection and ART have been associated with dyslipidemia. The utility of current treatments is limited. Though niacin lowers triglycerides levels, decreases LDL cholesterol and increases HDL cholesterol, concerns of increased insulin resistance have limited its use in people living with HIV.

Methods: We conducted a prospective open-label pilot trial to evaluate the safety and efficacy of Niaspan in HIV-infected individuals on ART with LDL ³ 130 mg/dl or triglycerides ³ 200 mg/dl. During a 4-wk lead-in period, lipid-lowering agents were discontinued and subjects received counseling for an NCEP Step I Diet. Niaspan therapy was then initiated at 500mg. The dose was increased to 1,000 mg after 2 wks and subsequently titrated upwards by 500 mg every 4 wks to a maximum of 2,000 mg per day to achieve NCEP goals. Subjects received Niaspan therapy for 14 wks. Fasting lipid profiles were evaluated every 2 wks during the first month and then monthly. A 5-hr, 11 time point oral glucose tolerance test (oGTT) was used to evaluate glucose metabolism before and after Niaspan treatment.

Results: Fourteen (14) men were enrolled; 93% Caucasian, none of them had diabetes at baseline by ADA guidelines, and 50% were glucose intolerant. Median CD4 was 420 (IQR 258–585); 79% had viral loads below 400 copies/ml. The effect of Niaspan on fasting lipids and oGTT, glucose, and insulin levels is shown in the table below.

	Before Niaspan Median (IQR)		After Niaspan Median (IQR)		% change Median (IQR)		p value
CHOL (mg/dl)	245	(205-339)	220	(183-265)	-14	(-25 to –9)	0.005
TG (mg/dl)	489	(341-715)	406	(263-471)	-34	(-42 to -17)	0.02
HDL (mg/dl)	39	(31-44)	39	(31-46)	3	(0 to 13)	0.09
LDL direct (mg/dl)	114	(75-141)	123	(64-153)	-4	(-11 to 21)	0.86
Glucose AUC	33411	(32299-39017)	34649	(33667-38991)	2	(-1 to 8)	0.37
Insulin AUC	10173	(6401-12936)	10763	(5980-19562)	36	(-7 to 50)	0.25
HOMA	1.5	(1.2-2.7)	3.4	(1.2 -5.6)	73	(-10 to 206)	0.05

Forty-three percent (43%) of the patients had flushing; 2 discontinued Niaspan. There were no grade 3 elevations of LFT, uric acid, or changes in CD4, or viral load. An additional subject became glucose intolerant after treatment.

Conclusions: Niaspan significantly decreased triglycerides and total cholesterol levels, but did not normalize them. HOMA and other indexes of insulin sensitivity worsened. The clinical utility of Niaspan for the management of dyslipidemia associated with HIV infection or its treatment should be evaluated in larger randomized trials, but its utility might be limited because of worsening insulin resistance.