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  8th International Congress on
Drug Therapy in HIV Infection
November 12-16, 2006
Glasgow, Scotland
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What's Better for High Lipids: Antilipid Drugs or NNRTI Switch?
  8th International Congress on Drug Therapy in HIV Infection November 12-16, 2006
Glasgow, Scotland
Mark Mascolini
Lipid-lowering therapy cut total cholesterol and dangerous low-density lipoprotein (LDL) cholesterol in people with HIV better than switching to a nonnucleoside (NNRTI), according to results of a cohort study [1]. But swapping a protease inhibitor (PI) for an NNRTI boosted "good" high-density lipoprotein (HDL) cholesterol better than antilipid drugs.
Mark van der Valk from Amsterdam's Academic Medical Center and D:A:D cohort coworkers analyzed the relative effects of lipid-lowering therapy and antiretroviral switching because a 130-person randomized trial suggested that a fibrate or a statin deflated total cholesterol better than switching to efavirenz or nevirapine after 12 months of follow-up [2]. The D:A:D team focused on NNRTI-naive people who had taken a PI for more than 6 months and had a total cholesterol level above 6 mmol/L (230 mg/dL) on two consecutive tests. They compared lipid trends in three subgroups--221 people who started antilipid therapy but kept taking a PI, 208 people who traded their PI for an NNRTI, and 1463 people who did neither and did not change antiretroviral therapy for the 12 months of follow-up. The analysis excluded anyone who tried to lower lipids by combining tactics or switching from one tactic to the other.
The antilipid and switch groups were significantly older than controls (45 versus 41 years, P = 0.0001) and included more men (86% versus 82% of switchers and 79% of controls, P = 0.08). More antilipid drug takers had a history of cardiovascular disease (4.5% versus 0% versus 1.2%, P = 0.0005), took drugs for heart disease (15% versus 8% versus 7%, P = 0.0004), and had diabetes (10% versus 4% versus 2%, P = 0.0001). The antilipid contingent also took ritonavir with or without lopinavir more often than other groups. Switchers had higher CD4 counts (534) than the antilipid group (484) or the control group (488) (P = 0.0003). Baseline total cholesterol, LDL cholesterol, total-to-HDL ratio, and triglycerides were all significantly higher in the antilipid group than in the other two groups, while HDL cholesterol was significantly higher in the control group. The three groups did not differ in body mass index or smoking history.
After a year of follow-up, total cholesterol had fallen about 1 mmol/L in the lipid-lowering group (P < 0.0001 versus control) and about 0.6 mmol/L in the switch group (P = 0.02 versus control). But the switch group gained more than 0.15 mmol/L of "good" HDL cholesterol (P = 0.001 versus control) while the antilipid group gained about 0.8 mmol/L, a nonsignificant improvement compared with controls (P = 0.27).
Improvement in total-to-HDL cholesterol ratio was equivalent in the antilipid and switch groups and superior to controls in both intervention groups. LDL cholesterol fell about 0.9 mmol/L in the antilipid group (P = 0.0004 versus control) and about 0.7 mmol/L in the switch group (P = 0.06 versus control), while triglycerides dropped about 0.8 mmol/L in the antilipid group (P = 0.007 versus control) and about 1.1 mmol/L in the switch group (P = 0.0001 versus control).
D:A:D statisticians determined that lipid-lowering therapy controlled total and LDL cholesterol best in people with high baseline values. But van der Valk concluded that using antilipid drugs had "minimal" effects on HDL cholesterol. Switching to an NNRTI jacked up HDL cholesterol regardless of baseline HDL readings.
This analysis has limits, van der Valk warned. Because cohort members were not randomized to a lipid-controlling strategy, selection bias could affect the results. By excluding people who tried switching to an NNRTI then started antilipid drugs, the study may have excluded a set of patients with hard-to-control hyperlipidemia. Also, the D:A:D researchers had no information on possible lifestyle changes, specific antilipid drugs used, or whether lipid samples were drawn after fasting.
1. van der Valk M, Friis-Moller N, Sabin CA, et al. Effect of interventions to improve dyslipidaemia. 8th International Congress on Drug Therapy in HIV Infection, November 12-16, 2006, Glasgow. Abstract PL9.5. 2. Calza L, Manfredi R, Colangeli V, et al. Substitution of nevirapine or efavirenz for protease inhibitor versus lipid-lowering therapy for the management of dyslipidaemia. AIDS. 2005;19:1051-1058.