Lipodystrophic syndromes and hyperlipidemia in a cohort of HIV-1-infected patients receiving triple combination antiretroviral therapy with a protease inhibitor

Citation
B. Rakotoambinina et al., Lipodystrophic syndromes and hyperlipidemia in a cohort of HIV-1-infected patients receiving triple combination antiretroviral therapy with a protease inhibitor, J ACQ IMM D, 27(5), 2001, pp. 443-449
Citations number
32
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
ISSN journal
15254135 → ACNP
Volume
27
Issue
5
Year of publication
2001
Pages
443 - 449
Database
ISI
SICI code
1525-4135(20010815)27:5<443:LSAHIA>2.0.ZU;2-5
Abstract
Objectives: To assess the frequency and features of lipodystrophic syndrome s in HIV-1-infected patients receiving highly active antiretroviral therapy (HAART) with a protease inhibitor (PI), and examine whether clinical and b iologic abnormalities are always associated in these conditions. Methods: Retrospective-prospective single-center observational study of 175 patients. Comparisons for continuous variables by t-test and paired t-test , and Kaplan-Meier analysis of time to onset of lipodystrophy were performe d. Results: In all, 51 patients (29%) had morphologic changes, after a mean HA ART duration of 20.0 +/- 6.1 months, and were categorized into pure lipoatr ophy (n = 16), mixed syndrome (truncal fat accumulation and face or limb li poatrophy) (n = 30) or pure truncal fat accumulation (In = 5). Because of t he small number, the latter group was not analyzed statistically. No differ ences were found among patients with lipoatrophy, mixed syndrome, or no lip odystrophy, in terms of gender, CD4 count, and HIV RNA plasma load at time of HAART initiation, nor in response to treatment. Patients with a mixed sy ndrome were older. Patients with lipoatrophy had longer duration of HIV dis ease, pre-HAART exposure to nucleoside analog therapy, and HAART. Baseline and pre-HAART fasting triglyceride levels were higher in patients who devel oped lipoatrophy, whereas weight and fasting cholesterol were higher in pat ients who developed a mixed syndrome. After 12 and 24 months on HAART, trig lycerides and cholesterol rose significantly in all patients, independently of lipodystrophy, whereas these parameters were not increased during nucle oside analog therapy. Conclusions: Nucleoside analog exposure appears as a risk factor for lipoat rophy. Age and nutritional status (reflected by baseline weight, triglyceri des and cholesterol) may influence the evolution to lipoatrophy or a mixed syndrome. Hyperlipidemia is observed in the absence of lipodystrophy and de pends on PI exposure.