[O14] A prospective cohort study on the risk for lipodystrophy in HIV-1-infected patients treated with protease inhibitor-containing regimens

2nd International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV

13-15 September 2000, Toronto, Canada

A PROSPECTIVE COHORT STUDY ON THE RISK FOR LIPODYSTROPHY IN HIV-1- INFECTED PATIENTS TREATED WITH PROTEASE INHIBITOR-CONTAINING REGIMENS

Antiviral Therapy 2000; 5(Suppl. 5):10 (abstract no. O14)

E Martínez¹, A Mocroft², MA Garcia-Viejo¹, JB Pérez-Cuevas¹, JL Blanco¹, J Mallolas¹, L Bianchi¹, I Conget¹ and JM Gatell¹
¹Hospital Clinic Universitari, Barcelona,Spain; and ²Royal Free and University College Medical School, London, UK

BACKGROUND: Risk factors for lipodystrophy (LD) in HIV-1-infected patients treated with highly active antiretroviral therapy (HAART) containing HIV-1 protease inhibitors (PI) are poorly understood.

DESIGN: 494 consecutive antiretroviral-naïve HIV-1- infected adults who initiated HAART with two nucleoside reverse transcriptase inhibitors plus at least one PI from 10/96 to 9/99 were eligible. Moderate or severe body fat changes were clinically assessed and categorized as subcutaneous lipoatrophy (SL), central obesity (CO), or both. A person-years analysis was used to calculate the incidence of types of LD and Cox proportional hazards models were used to describe the univariate and multivariate factors associated with progression to any LD.

RESULTS: Incidences of any LD, LD with SL, and LD with CO were 11.2 (95% CI: 9.2-14.2), 9.2 (95% CI: 7.0-11.4) and 7.7 (95% CI: 5.7-9.7) per 100 patient-years, respectively. An increased risk for any LD was found among females (RH 1.7; 95% CI: 1.1-2.7), heterosexuals (RH 3.5; 95% CI: 1.9-6.3) and homosexuals (RH 2.2; 95% CI: 1.2-4.1), with increasing age (RH 1.5 per 10 years older; 95% CI: 1.2-1.8) and with the duration of exposure to antiretroviral therapy (RH 1.5 per 6 months extra; 95% CI: 1.2-1.7) but not with any individual antiretroviral agent. Risk factors for LD with SL or LD with CO were similar to those associated with any LD. Duration of indinavir use but not duration of HAART was an additional risk factor for LD with CO (RH 1.3 per 6 months extra; 95% CI: 1.0-1.6, P=0.06). Duration of stavudine use was an additional risk factor for LD with SL (RH 1.2 per 6 months extra; 95% CI: 1.0-2.0).

CONCLUSIONS: Risk factors for any LD, LD with SL, and LD with CO in HIV-1-infected patients receiving PI-containing HAART are multifactorial and overlapping, and cannot be exclusively ascribed to the duration of exposure to any particular antiretroviral agent.

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