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Hepatic steatosis associated with increased central body fat by dual-energy X-ray absorptiometry and uncontrolled HIV in HIV/hepatitis C co-infected persons

Brown, Todd Ta; Mehta, Shruti Hb; Sutcliffe, Catherineb; Higgins, Yvonnea; Torbenson, Michael Sa; Moore, Richard Da,b; Thomas, David La; Sulkowski, Mark Sa

doi: 10.1097/QAD.0b013e3283333651
Basic Science

Objective: To evaluate the relationship between regional body composition and liver disease (fibrosis or steatosis) in HIV/HCV co-infected individuals.

Methods: Whole body dual-energy X-ray absorptiometry (DXA) was performed in 173 HIV/HCV co-infected persons within 12 months of a liver biopsy. Significant fibrosis was defined as a METAVIR stage greater than 1. Steatosis was graded as: 0, none; 1, steatosis involving less than 5% of hepatocytes; 2, 5–29%; 3, 30–60%; 4 greater than 60%, and was defined as more than 0. Poisson regression with robust variance was used to estimate prevalence ratios of the outcome measures.

Results: The population was 62% male and 84% black with a median body mass index of 25.2 kg/m2 (interquartile range 22.5, 29.3 kg/m2). No differences in regional body fat or fat distribution were observed in 42 patients with significant fibrosis compared to others with less fibrosis. However, the 77 individuals (45%) with steatosis had greater central fat than those without steatosis [prevalence ratio 1.04 per kg trunk fat; 95% confidence interval (CI) 1.04, 1.11], after adjusting for hepatic fibrosis (prevalence ratio 1.77; 95% CI 1.29, 2.42), uncontrolled HIV replication (viral load >400 copies/ml) (prevalence ratio 1.57; 95% CI 1.12, 2.22), age, sex, race and diabetes mellitus.

Conclusions: In HIV/HCV co-infected individuals, measures of regional body fat or fat distribution were not associated with hepatic fibrosis. In contrast, increased central adiposity by DXA, as well as concomitant fibrosis and uncontrolled HIV, were associated with hepatic steatosis. The extent to which weight loss and effective antiretroviral therapy can reduce the risk of steatosis deserves further investigation.

aJohns Hopkins School of Medicine, USA

bJohns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA.

Received 1 July, 2009

Revised 12 September, 2009

Accepted 18 September, 2009

Correspondence to Todd T. Brown, MD, PhD, 1830 East Monument Street, Suite 333 Baltimore, MD 21287, USA. Tel: +1 410 955 2130; fax: +1 410 955 8172; e-mail: tbrown27@jhmi.edu

© 2010 Lippincott Williams & Wilkins, Inc.