par Dooko, Claude Béténé A;De Wit, Stéphane ;Neuhaus, Jacqueline;Palfreeman, Adrian;Pepe, Rosalie;Pankow, James J.S.;Neaton, James
Référence Journal of acquired immune deficiency syndromes, 67, 5, page (538-546)
Publication Publié, 2014
Article révisé par les pairs
Résumé : Background: HIV infection is associated with increased levels of inflammatory markers. Inflammation is hypothesized to play a role in the development of type 2 diabetes. Data addressing this issue among HIV-positive participants are limited. Methods: A cohort of 3695 participants without diabetes, taking antiretroviral therapy and with an average CD4+ count of 523 cells/mm3, were followed for an average of 4.6 years. Diabetes risk associated with baseline levels of high sensitivity C-reactive protein (hsCRP) and interleukin-6 (IL-6) was assessed using Cox proportional hazards regression models. Analyses considered baseline levels of factors associated with diabetes risk and HIV-related measures. Results: One hundred thirty-seven patients developed diabetes requiring drug treatment during follow-up (8.18 per 1000 person-years). Median levels of IL-6 and hsCRP were significantly higher among those who developed diabetes compared with those who did not: 3.45 versus 2.50 pg/mL for IL-6 and 4.91 versus 3.29 μg/mL for hsCRP (P < 0.001). Adjusted hazard ratios associated with a doubling of IL-6 and hsCRP were 1.29 (95% confidence interval: 1.08 to 1.55; P = 0.005) and 1.22 (95% confidence interval: 1.10 to 1.36; P < 0.001), respectively. Body mass index (P < 0.001), age (P = 0.013), coinfection with hepatitis B or C (P = 0.03), nonsmoking status (P = 0.034), and use of lipid-lowering treatment (P = 0.008) were also associated with an increased risk of diabetes. Conclusions: These findings indicate that low-grade systemic inflammation is an underlying factor in the pathogenesis of diabetes.

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