Association of elevated plasma inflammatory biomarker levels with age-related macular degeneration but not cataract in persons with AIDS

医学 黄斑变性 生物标志物 炎症 全身炎症 内科学 C反应蛋白 胃肠病学 急性期蛋白 前瞻性队列研究 免疫学 眼科 化学 生物化学
作者
Douglas A. Jabs,Mark L. Van Natta,Michael F. Schneider,Jeong W. Pak,Garrett Trang,Norman G. Jones,Jeffrey M. Milush,Peter W. Hunt
出处
期刊:AIDS [Ovid Technologies (Wolters Kluwer)]
卷期号:36 (2): 177-184 被引量:6
标识
DOI:10.1097/qad.0000000000003104
摘要

Objective: To evaluate the relationship between plasma biomarkers of systemic inflammation and incident age-related macular degeneration (AMD) in persons with the AIDS. Design: Case–control study. Methods: Participants with incident intermediate-stage AMD ( N = 26) in the Longitudinal Study of the Ocular Complications of AIDS (LSOCA) and controls ( N = 60) without AMD. Cryopreserved baseline plasma specimens were assayed for biomarkers of inflammation, including high-sensitivity C-reactive protein (CRP), interleukin (IL)-6, interferon-γ inducible protein (IP)-10, soluble CD14 (sCD14), soluble CD163 (sCD163), and intestinal fatty acid-binding protein (I-FABP). Results: After adjustment for age, sex, and race/ethnicity, baseline mean ± standard deviation (SD) log 10 (mg/ml) plasma levels of CRP (0.52 ± 0.60 vs. 0.20 ± 0.43; P = 0.01) and mean ± SD log 10 (pg/ml) plasma levels of sCD14 (6.31 ± 0.11 vs. 6.23 ± 0.14; P = 0.008) were significantly higher among cases (incident AMD) than among controls (no AMD). There was a suggestion that mean ± SD baseline log 10 (pg/ml) plasma IL-6 levels (0.24 ± 0.33 vs. 0.11 ± 0.29; P = 0.10) might be higher among cases than controls. In a separate analysis of 548 participants in LSOCA, elevated baseline levels of plasma inflammatory biomarkers were associated with a greater risk of mortality but not with an increased risk of incident cataract. Conclusion: These data suggest that systemic inflammatory biomarkers are associated with incident AMD but not incident cataract in persons with AIDS, and that systemic inflammation may play a role in the pathogenesis of AMD.
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