1st International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV 26–28 June 1999 - San Diego, CA, USA

RITONAVIR USE AND HYPERLIPIDAEMIA IN HIV-INFECTED PATIENTS

Antiviral Therapy 1999; 4(Suppl. 2):57 (abstract no.43)

F Terheggen, EJG Sijbrands, K Brinkman, HM Weigel and PHJ Frissen
Department of Internal Medicine, Onze Lieve Vrouwe Gasthuis, Amsterdam, The Netherlands

BACKGROUND: HIV protease inhibitors (ritonavir, indinavir, saquinavir) have been shown to exhibit a variety of metabolic effects, including glucose intolerance, abnormal fat distribution and hyperlipidaemia. The latter phenomenon is particularly associated with ritonavir. The purpose of this study was to quantify the hyperlipidaemic effect of ritonavir and to identify risk factors predictive for developing hyperlipidaemia in patients on ritonavir.

DESIGN: A consecutive series of unrelated patients (n=102) treated with ritonavir from April 1996 until June 1998 were included. The patient's file and a questionnaire were used to collect the following data: demographic data, a full medical history, family history (e.g. hyperlipidaemia, coronary heart disease and diabetes mellitus), diet, alcohol and smoking habits, diuretics or beta-blocker usage, body mass index, ALAT, glucose, C-peptide, CD4 lymphocyte count and plasma HIV-1 RNA. Random serum concentrations of cholesterol and triglyceride were measured before and after 4, 8 and 12 weeks of treatment.

RESULTS: Hypertriglyceridaemia (triglyceride >3.4 mmol/l) occurred in 54% and hypercholesterolaemia (cholesterol >6.5 mmol/l) occurred in 36% of HIV-1-infected patients on ritonavir. Isolated hypertriglyceridaemia and hypercholesterolaemia occurred in respectively 25% and 8% of the treated patients. A combined increase occurred in 29%. The mean serum concentration of triglyceride increased significantly during treatment from 1.9 to 5.9 mmol/l (range 0.73-47.3 mmol/l; P<0.0001). The mean serum concentration of cholesterol increased significantly from 4.4 to 6.4 mmol/l (range 3.5-16.6 mmol/l; P<0.0001). The maximum increase occurred during the first 4 weeks. The patients with hypertriglyceridaemia during treatment showed a significantly higher C-peptide measured prior to treatment (P=0.007). Prior use of a PI (P=0.02) and HIV-1 risk factor (infection not by intravenous drug use; P=0.02) predicted also hypertriglyceridaemia. Baseline serum levels of triglycerides higher than 3.4 mmol/l showed a trend in predicting hypertriglyceridaemia during treatment (P=0.08). No other risk factors could be identified.

CONCLUSIONS: Hyperlipidaemia occurred in a significant proportion of ritonavir treated HIV patients. C-peptide prior to treatment, HIV-1 risk factor (infection not by intravenous drug use) and prior use of PIs were predictive for the development of hyperlipidaemia. Despite the marked hypertriglyceridaemia (>20 mmol/l in three patients) no clinical sequelae i.e. pancreatitis were observed. Follow-up was too short to assess long-term effects, i.e. atherosclerosis.

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