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Metabolic health across the BMI spectrum in HIV-infected and HIV-uninfected men.
Lake, JE, Li, X, Palella, FJ, Erlandson, KM, Wiley, D, Kingsley, L, Jacobson, LP, Brown, TT
AIDS (London, England). 2018;(1):49-57
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Abstract
OBJECTIVES In the general population, metabolic health often declines as BMI increases. However, some obese individuals maintain metabolic health. HIV and antiretroviral therapy have been associated with metabolic disturbances. We hypothesized that HIV-infected (HIV) men on suppressive antiretroviral therapy experience less metabolic health than HIV-uninfected (HIV) men across all BMI categories. DESIGN/METHODS In a cross-sectional analysis of 1018 HIV and 1092 HIV men enrolled in the multicenter AIDS cohort study, Poisson regression with robust variance determined associations between HIV serostatus and metabolic health prevalence (defined as meeting ≤2 of 5 National Cholesterol Education Program Adult Treatment Panel III metabolic syndrome criteria), adjusting for age, race, BMI category, smoking, and hepatitis C virus infection status. RESULTS HIV men were younger (54 vs. 59 years) and had lower median BMI (25 vs. 27 kg/m). Nonobese HIV men had lower metabolic health prevalence than HIV men (BMI ≤25 kg/m: 80 vs. 94%, P < 0.001; BMI 25-29 kg/m: 64 vs. 71%, P = 0.05), but metabolic health prevalence among obese men did not differ by HIV serostatus (BMI 30-34 kg/m: 35 vs. 39%, P = 0.48; BMI ≥35 kg/m: 27 vs. 25%, P = 0.79). In the adjusted model, nonobese HIV men were less likely to demonstrate metabolic health than nonobese HIV men. Among HIV men, per year darunavir, zidovudine, and stavudine use were associated with lower metabolic health likelihood. CONCLUSION Metabolically healthy obesity prevalence does not differ by HIV serostatus. However, among nonobese men, HIV infection is associated with lower metabolic health prevalence, with associations between lack of metabolic health and darunavir and thymidine analog nucleoside reverse transcriptase inhibitor exposure observed.
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An 84-month observational study of the changes in CD4 T-lymphocyte cell count of 110 HIV/AIDS patients treated with traditional Chinese medicine.
Wang, J, Liang, B, Zhang, X, Xu, L, Deng, X, Li, X, Fang, L, Tan, X, Mao, Y, Zhang, G, et al
Frontiers of medicine. 2014;(3):362-7
Abstract
This study aimed to evaluate the therapeutic effect of traditional Chinese medicine (TCM) by observing the changes in CD4 T-lymphocyte cell count of 110 cases with human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS) treated continuously with TCM for 84 months. Information of 110 HIV/AIDS patients from 19 provinces and cities treated with TCM from 2004 to 2013 was collected. Changes in the indexes of CD4 counts ( ≤ 200, 201-350, 351-500 and > 500 cells/mm(3)) at five time points (0, 12, 36, 60 and 84 months) and different treatments [TCM and TCM plus antiretroviral therapy (ART)] were compared. Repeated measures test indicated no interaction between group and time (P > 0.05). Degrees of increasing and decreasing CD4 count of the two groups at four different frames were statistically significant compared with the baseline. The CD4 count between the two groups was not statistically significant. For CD4 count of ≤ 200 cells/mm(3), the mean CD4 count changes were 21 and 28 cells/mm(3) per year for the TCM group and TCM plus ART group, respectively. For CD4 count of 201-350 cells/mm(3), the mean CD4 count changes were 6 and 25 cells/mm(3) per year for the TCM group and TCM plus ART group, respectively. For CD4 count of 351-500 cells/mm(3), the mean CD4 count changes were -13 and -7 cells/mm(3) per year for the TCM group and TCM plus ART group, respectively. For CD4 count of > 500 cells/mm(3), the mean CD4 count changes were -34 and -17 cells/mm(3) per year for the TCM group and TCM plus ART group, respectively. Long-term use of TCM could maintain or slow the pace of declining CD4 counts in patients with HIV/AIDS, and may achieve lasting effectiveness.
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Lower adiponectin is associated with subclinical cardiovascular disease among HIV-infected men.
Ketlogetswe, KS, Post, WS, Li, X, Palella, FJ, Jacobson, LP, Margolick, JB, Kingsley, LA, Witt, MD, Dobs, AS, Budoff, MJ, et al
AIDS (London, England). 2014;(6):901-9
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Abstract
OBJECTIVE To examine whether altered levels of adipokines, adipose-derived peptides associated with myocardial infarction in the general population, may contribute to subclinical coronary atherosclerosis in HIV-infected persons. DESIGN Nested cohort study. METHODS We studied HIV-infected (HIV+) and HIV-uninfected (HIV-) men in the Multicenter AIDS Cohort Study with noncontrast computed tomography (CT) to measure coronary artery calcium and regional adiposity; 75% additionally underwent coronary CT angiography to measure plaque composition and stenosis. Adiponectin and leptin levels were assessed. Multiple regression models were used to assess associations between adipokine levels and HIV disease parameters, regional adiposity, and plaque adjusted for age, race, HIV serostatus, and cardiovascular disease (CVD) risk factors. RESULTS Significant findings were limited to adiponectin. HIV-positive men (n=493) had lower adiponectin levels than HIV-negative men (n=250) after adjusting for CVD risk factors (P<0.0001), which became nonsignificant after adjustment for abdominal visceral and thigh subcutaneous adipose tissue. Among HIV-positive men, lower adiponectin levels were associated with higher CD4 T-cell counts (P=0.004), longer duration of antiretroviral therapy (P=0.006), and undetectable HIV RNA levels (P=0.04) after adjusting for age, race, and CVD risk factors; only CD4 cell count remained significant after further adjustment for adipose tissue. In both groups, lower adiponectin levels were associated with increased odds of coronary stenosis more than 50% (P<0.007). Lower adiponectin levels were associated with increased extent of plaque in HIV-positive and of mixed plaque in HIV-negative men. CONCLUSION Adiponectin levels were lower in HIV-infected men and related to the severity of subclinical atherosclerosis, independent of traditional CVD risk factors.