@article{6e4d3d6838b441b98f76b5728d5b9dce,
title = "The Association of Inflammatory Markers With Nonalcoholic Fatty Liver Disease Differs by Human Immunodeficiency Virus Serostatus",
abstract = "Background. We aimed to determine the relationship of circulating adipokines and inflammatory biomarkers with fatty liver among men in the Multicenter AIDS Cohort Study. Methods. Noncontrast computed tomography was used to assess fatty liver and measure abdominal visceral adipose tissue (VAT) area in 526 participants without history of cardiovascular disease, heavy alcohol use, or viral hepatitis infection. Multivariable logistic regression was used to assess associations of circulating biomarker levels with fatty liver. Results. Three hundred twenty-nine human immunodeficiency virus (HIV)-infected men had higher levels of several inflammatory biomarkers compared with 197 HIV-uninfected men. Among HIV-uninfected men, increased adiponectin was associated with lower odds of fatty liver (odds ratio [OR] = 0.51 per doubling, P = .02), whereas higher odds of fatty liver was observed with increased levels of the proinflammatory markers intercellular adhesion molecule (ICAM)-1 (OR = 5.30, P = .004), C-reactive protein (OR = 1.66, P = .002), interleukin (IL)-6 (OR = 1.67, P = .03), and tumor necrosis factor α receptor 2 (OR = 6.55, P = .003). Among HIV-infected men, ICAM-1 was the only proinflammatory marker associated with greater odds of fatty liver (OR = 2.67, P = .02), whereas higher adiponectin (OR = 0.57, P = .003), and osteoprotegerin levels (OR = 0.48, P = .03) were associated with lower odds. These associations were all independent of VAT. Conclusions. Fatty liver is associated with a heightened inflammatory state independent of visceral adiposity in HIV-uninfected men but not in HIV-infected men. However, a heightened anti-inflammatory state may protect against fatty liver regardless of HIV serostatus.",
keywords = "HIV, NAFLD, adiponectin, biomarkers, fatty liver",
author = "Price, {Jennifer C.} and Ruibin Wang and Seaberg, {Eric C.} and Budoff, {Matthew J.} and Kingsley, {Lawrence A.} and Palella, {Frank J.} and Witt, {Mallory D.} and Post, {Wendy S.} and Thio, {Chloe L.}",
note = "Funding Information: In contrast to our inflammatory marker findings, adiponectin was protective of fatty liver regardless of HIV serostatus, underscoring the importance of the anti-inflammatory properties of adiponectin in fatty liver disease. This finding is supported by increasing evidence linking adiponectin dysregulation to HIV-associated metabolic complications. Circulating adiponectin levels are reduced in patients with HIV-associated lipodystrophy and inversely correlated with insulin resistance [44, 45]. Moreover, certain antiretroviral medications, including elvite-gravir, efavirenz, stavudine, ritonavir, and ritonavir-boosted lopinavir, impair adipocyte adiponectin gene expression [46– 49]. In contrast, raltegravir does not reduce adiponectin gene expression, and, in fact, switching from stavudine to raltegravir increased gene expression in a group of patients with lipodystrophy [47]. We found an inverse correlation between cumulative dideoxynucleoside use and adiponectin levels, which perhaps explains in part our observed association between this medication class and fatty liver in our cohort. There was not enough raltegravir use in our cohort to determine whether this was protective against fatty liver. Further research is warranted in this area. Funding Information: Financial support. The MACS Cardiovascular Disease study is funded by National Heart, Lung, and Blood Institute (NHLBI): RO1 HL095129 (Post). MACS (Principal Investigators): Johns Hopkins University Bloomberg School of Public Health (Joseph Margolick), U01-AI35042; Northwestern University (Steven Wolinsky), U01-AI35039; University of California, Los Angeles (Roger Detels), U01-AI35040, Los Angeles Biomedical Research Institute, UL1TR001881; University of Pittsburgh (Charles Rinaldo), U01-AI35041; the Center for Analysis and Management of MACS, Johns Hopkins University Bloomberg School of Public Health (Lisa Jacobson), UM1-AI35043. The MACS is funded primarily by the National Institute of Allergy and Infectious Diseases, with additional cofunding from the National Cancer Institute, the National Institute on Drug Abuse, and the National Institute of Mental Health. Targeted supplemental funding for specific projects was also provided by the NHLBI Funding Information: and the National Institute on Deafness and Communication Disorders. MACS data collection is also supported by UL1-TR001079 (Johns Hopkins University ICTR) from the NCATS, a component of the NIH, and NIH Roadmap for Medical Research and the Los Angeles Biomedical Research Institute at Harbor-UCLA Clinical and Translational Sciences Institute, UL1TR000124. This work was also supported by an American College of Gastroenterology Junior Faculty Development Award (to J. C. P.), the UCSF Open Access Publishing Fund, and the University of California San Francisco Liver Center (P30 DK026743). Publisher Copyright: {\textcopyright} 2022 The Author.",
year = "2017",
month = jun,
day = "1",
doi = "10.1093/OFID/OFX153",
language = "English (US)",
volume = "4",
journal = "Open Forum Infectious Diseases",
issn = "2328-8957",
publisher = "Oxford University Press",
number = "3",
}