016 Type III hyperlipidaemia, related to PI treatment, is not caused by homozygosity for apoE2

Abstract

Objective: To determine the prevalence of PI-induced Type III hyperlipidaemia and its relation with apoE2 homozygosity. Methods: Sixty-seven HIV+ patients on PI for a median of 26.5 months were tested for fasting cholesterol, triglyceride, HDL cholesterol, lipoprotein (a) and glucose. Lipoprotein electrophoresis was performed when cholesterol was > 6.5 mmol/L or triglyceride > 4.5 mmol/L. ApoE phenotype was determined using isoelectric focusing followed by Western blotting. Lipodystrophy was diagnosed clinically. Results: Fifty patients were dyslipidaemic 42 with triglyceride > 2.3 mmol/L, 32 with cholesterol > 6.5 mmol/L and 34 with HDL cholesterol < 0.9 mmol/L. 20 had a lipoprotein (a) > 300 mg/L. Sixteen patients had lipodystrophy. Eleven patients (19.3%) had a Type III hyperlipidaemia pattern, seven with associated lipodystrophy. Only one was homozygous for E2 phenotype and none had diabetes. Mean interval between the start of PI and dyslipidaemia was 240 days. Conclusion: Type III hyperlipidaemia is common in this group and unlike HIV-negative subjects is often not associated with the apo-E2/E2 isoform. HIV protease inhibitors may interfere with lipoprotein-receptor-related protein.