OBJECTIVE: Risk factors for the HIV-associated lipodystrophy syndrome (HALS) were studied in a single-centre, cross-sectional study. - PATIENTS AND METHODS: 278 consecutive HIV-infected outpatients at a German tertiary care centre were enrolled. Changes in body shape were quantified using linear analogue scales. Cumulative treatment duration for each antiretroviral drug, CD4 cells, viral load and age were investigated as potential risk factors for a clinical diagnosis of lipodystrophy syndrome by logistic regression. RESULTS: HALS was diagnosed in 88 patients. The risk of HALS increased significantly with longer protease inhibitor treatment (relative risk 1.61 (95% confidence interval, 1. 24 to 2.09, per year); older age and a history of low CD4 cell counts were cofactors in this multivariate model, but nucleoside analogues did not contribute significantly. Neither pattern nor severity of disease were predicted by these risk factors. Treatment durations and other risk factors were highly correlated with each other. CONCLUSIONS: These findings support a pathogenetic role for protease inhibitor toxicity, advanced HIV disease, and ageing. No evidence for an additional effect of nucleoside analogues was found. The high correlation of potential risk factors indicates that this and other available studies may be too small to detect multiple risk factors without major confounding.
OBJECTIVE: Risk factors for the HIV-associated lipodystrophy syndrome (HALS) were studied in a single-centre, cross-sectional study. - PATIENTS AND METHODS: 278 consecutive HIV-infected outpatients at a German tertiary care centre were enrolled. Changes in body shape were quantified using linear analogue scales. Cumulative treatment duration for each antiretroviral drug, CD4 cells, viral load and age were investigated as potential risk factors for a clinical diagnosis of lipodystrophy syndrome by logistic regression. RESULTS: HALS was diagnosed in 88 patients. The risk of HALS increased significantly with longer protease inhibitor treatment (relative risk 1.61 (95% confidence interval, 1. 24 to 2.09, per year); older age and a history of low CD4 cell counts were cofactors in this multivariate model, but nucleoside analogues did not contribute significantly. Neither pattern nor severity of disease were predicted by these risk factors. Treatment durations and other risk factors were highly correlated with each other. CONCLUSIONS: These findings support a pathogenetic role for protease inhibitor toxicity, advanced HIV disease, and ageing. No evidence for an additional effect of nucleoside analogues was found. The high correlation of potential risk factors indicates that this and other available studies may be too small to detect multiple risk factors without major confounding.
Authors: Keith W Crawford; John Spritzler; Robert C Kalayjian; Teresa Parsons; Alan Landay; Richard Pollard; Vicki Stocker; Michael M Lederman; Charles Flexner Journal: AIDS Res Hum Retroviruses Date: 2010-06 Impact factor: 2.205
Authors: Isaac O Abah; Wetkos D Dayom; Dauda A Dangiwa; Roseline Aderemi-Williams; Joseph Anejo-Okopi; Oche O Agbaji; Phyllis Kanki; John C Aguiyi Journal: Afr Health Sci Date: 2021-09 Impact factor: 0.927