Taylor Barbara S, So-Armah Kaku, Tate Janet P, Marconi Vincent C, Koethe John R, Bedimo Roger J, Butt Adeel A, Gibert Cynthia L, Goetz Matthew B, Rodriguez-Barradas Maria C, Womack Julie A, Gerschenson Mariana, Lo Re Vincent, Rimland David, Yin Michael T, Leaf David, Tracy Russell P, Justice Amy C, Freiberg Matthew S
*Medical Service/Infectious Diseases, South Texas Veterans Health Care System, San Antonio, TX; Department of Medicine, UT Health San Antonio, San Antonio, TX;†Department of Medicine, Boston University School of Medicine, Boston, MA;‡Section of General Internal Medicine, VA Connecticut Healthcare System, West Haven, CT; Department of Internal Medicine, Yale University School of Medicine, New Haven, CT;§Medical Service, VA Medical Center, Atlanta, GA; Medical Service, Emory University School of Medicine, Atlanta, GA;‖Departments of Medicine and Biostatistics, Vanderbilt University School of Medicine, Nashville, TN;¶Department of Medicine, Infectious Diseases Section, VA North Texas Health Care System; UT Southwestern Medical Center, Dallas, TX;#Center for Health Equity Research and Promotion, VA Pittsburg Healthcare System, Pittsburgh, PA; Hamad Healthcare Quality Institute, Hamad Medical Corporation, Doha, Qatar; Department of Medicine, Weill Cornell Medical College, Doha, Qatar and New York, NY;**Medical Service/Infectious Diseases, VA Medical Center, Washington, DC; Department of Medicine, George Washington University Medical Center, Washington, DC;††Department of Medicine, VA Greater Los Angeles Healthcare System, Los Angeles, CA; David Geffen School of Medicine at UCLA, Los Angeles, CA;‡‡Infectious Diseases Section, Michael E. DeBakey VA Medical Center, Houston, TX; Infectious Diseases Section, Baylor College of Medicine, Houston, TX;§§VA Connecticut Healthcare System, West Haven, CT;‖‖Cell and Molecular Biology Department, John A. Burns School of Medicine, University of Hawaii- Manoa, Honolulu, HI;¶¶Philadelphia VA Medical Center, Philadelphia, PA; Perelman School of Medicine, University of Pennsylvania, Philadelphia, VA;##Division of Infectious Diseases, Columbia University Medical Center, New York, NY;***Infectious Diseases Section, VA Greater Los Angeles Healthcare System, Los Angeles, CA; Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA;†††Departments of Pathology and Laboratory Medicine and Biochemistry, College of Medicine, University of Vermont, Burlington, VT; and‡‡‡Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN; Geriatric Research, Education, and Clinical Center, VA Tennessee Valley Healthcare System, Nashville, TN.
J Acquir Immune Defic Syndr. 2017 Aug 15;75(5):500-508. doi: 10.1097/QAI.0000000000001444.
Obesity prevalence among people living with HIV (HIV+) is rising. HIV and obesity are proinflammatory states, but their combined effect on inflammation (measured by interleukin 6, IL-6), altered coagulation (D-dimer), and monocyte activation (soluble CD14, sCD14) is unknown. We hypothesized inflammation increases when obesity and HIV infection co-occur.
The Veterans Aging Cohort Study survey cohort is a prospective, observational study of predominantly male HIV+ veterans and veterans uninfected with HIV; a subset provided blood samples. Inclusion criteria for this analysis were body mass index ≥ 18.5 kg/m and biomarker measurement. Dependent variables were IL-6, sCD14, and D-dimer quartiles. Obesity/HIV status was the primary predictor. Unadjusted and adjusted logistic regression models were constructed.
Data were analyzed for 1477 HIV+ and 823 uninfected participants. Unadjusted median IL-6 levels were significantly higher and sCD14 levels significantly lower in obese/HIV+ compared with nonobese/uninfected (P <0.01 for both). In adjusted analyses, the odds ratio for increased IL-6 in obese/HIV+ patients was 1.76 (95% confidence interval: 1.18 to 2.47) compared with nonobese/uninfected, and obesity/HIV+ remained associated with lower odds of elevated sCD14. We did not detect a synergistic association of co-occurring HIV and obesity on IL-6 or sCD14 elevation. D-dimer levels did not differ significantly between body mass index/HIV status groups.
HIV-obesity comorbidity is associated with elevated IL-6, decreases in sCD14, and no significant difference in D-dimer. These findings are clinically significant, as previous studies associated these biomarkers with mortality. Future studies should assess whether other biomarkers show similar trends and potential mechanisms for unanticipated sCD14 and D-dimer findings.
感染人类免疫缺陷病毒（HIV）的人群中肥胖患病率正在上升。HIV感染和肥胖均处于促炎状态，但它们对炎症（通过白细胞介素6即IL-6来衡量）、凝血改变（D-二聚体）及单核细胞活化（可溶性CD14即sCD14）的联合影响尚不清楚。我们推测肥胖与HIV感染同时存在时炎症会增加。
退伍军人老龄化队列研究调查队列是一项针对主要为男性的HIV阳性退伍军人和未感染HIV的退伍军人的前瞻性观察性研究；其中一部分人提供了血样。该分析的纳入标准为体重指数≥18.5kg/m且进行了生物标志物检测。因变量为IL-6、sCD14和D-二聚体四分位数。肥胖/HIV状态是主要预测因素。构建了未调整和调整后的逻辑回归模型。
对1477名HIV阳性参与者和823名未感染参与者的数据进行了分析。与非肥胖/未感染组相比，肥胖/HIV阳性组未调整的IL-6中位数水平显著更高，sCD14水平显著更低（两者P均<0.01）。在调整分析中，与非肥胖/未感染组相比，肥胖/HIV阳性患者IL-6升高的优势比为1.76（95%置信区间：1.18至2.47），且肥胖/HIV阳性与sCD14升高的较低优势比仍相关。我们未检测到HIV与肥胖同时存在对IL-6或sCD14升高有协同关联。体重指数/HIV状态组之间D-二聚体水平无显著差异。
HIV-肥胖合并症与IL-6升高、sCD14降低及D-二聚体无显著差异相关。这些发现具有临床意义，因为先前的研究将这些生物标志物与死亡率相关联。未来的研究应评估其他生物标志物是否显示出类似趋势以及sCD14和D-二聚体意外发现的潜在机制。
