Journal
DIABETES CARE
Volume 33, Issue 10, Pages 2244-2249Publisher
AMER DIABETES ASSOC
DOI: 10.2337/dc10-0633
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Funding
- AIDS Clinical Trials Group of the National Institute for Allergy and Infectious Disease [U01-A1-068636, AI-068634, AI-069501]
- Johns Hopkins Bayview General Clinical Research Center Advanced Chemistry Laboratory (National Institutes of Health [NIH] Institute for Clinical and Translational Research) [5UL1-RR-025005]
- National Center for Complementary and Alternative Medicine, NIH [5K23-AT-2862]
- Merck
- GlaxoSmithKline
- BMS
- Gilead
- Pfizer
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OBJECTIVE - To determine whether systemic inflammation after initiation of HIV-antiretroviral therapy (ART) is associated with the development of diabetes. RESEARCH DESIGN AND METHODS - We conducted a nested case-control study, comparing 55 previously ART-naive individuals who developed diabetes 48 weeks after ART initiation (case subjects) with 55 individuals who did not develop diabetes during a comparable follow-up (control subjects), matched on baseline BMI and race/ethnicity. Stored plasma samples at treatment initiation (week 0) and 1 year later (week 48) were assayed for levels of high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and the soluble receptors of tumor necrosis factor-et (sTNFR1 and sTNFR2). RESULTS - Case subjects were older than control subjects (median age 41 vs. 37 years, P = 0.001), but the groups were otherwise comparable. Median levels for all markers, except hs-CRP, decreased from week 0 to week 48. Subjects with higher levels of hs-CRP, sTNFR1, and sTNFR2 at 48 weeks had an increased odds of subsequent diabetes, after adjustment for baseline marker level, age, BMI at week 48, CD4 count at week 48 (< vs. >200 cells/mm(3)), and indinavir use (all P-trend <= 0.05). After further adjustment for week 48 glucose, effects were attenuated and only sTNFRI. remained significant (odds ratio, highest quartile vs. lowest 23.2 [95% CI 1.28-423], P = 0.03). CONCLUSIONS Inflammatory markers 48 weeks after ART initiation were associated with increased risk of diabetes. These findings suggest that systemic inflammation may contribute to diabetes pathogenesis among HIV-infected patients.
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