Incidence and risk factors for steatosis progression in adults coinfected with HIV and hepatitis C virus

Abstract

Background & aims: Hepatic steatosis is a common histologic finding in patients coinfected with human immunodeficiency virus (HIV) and hepatitis C virus (HCV), although little is known about its natural history. We prospectively examined the natural history of steatosis in patients coinfected with HIV and HCV who attended an urban HIV clinic.

Methods: The study cohort consisted of 222 coinfected patients (87% black, 94% with HCV genotype 1 infection) who had at least 2 liver biopsies performed between 1993 and 2008. Biopsy specimens were scored by a single pathologist; samples were classified as having trivial (<5% of hepatocytes affected) or significant (>5%) levels of fat (steatosis). We characterized progression to significant levels of fat among patients whose first biopsy samples had no or trivial levels of fat, and regression among those with significant fat, using logistic regression.

Results: Initial biopsy specimens from most patients (88%) had no or trivial amounts of fat. Among second biopsy samples, 74% had no or trivial fat and 13% had significant amounts of fat. The strongest risk factors for progression of steatosis were alcohol abuse and overweight/obesity; cumulative exposure to antiretroviral therapy between biopsies and high counts of CD4(+) T cells were associated with reduced progression of steatosis. Among the 28 patients whose initial biopsy specimen had significant fat levels, most (75%) regressed.

Conclusions: Antiretroviral therapy and high counts of CD4(+) T cells are associated with reduced progression of steatosis in patients coinfected with HIV and HCV. Efforts to diagnose and prevent steatosis should focus on persons with a high body mass index and excessive alcohol intake.

Conflict of interest statement

Conflicts of interest: None

Copyright © 2011 AGA Institute. Published by Elsevier Inc. All rights reserved.

Figures

Figure 1

Patterns of fat across multiple liver biopsies (N=222).

Figure 2

Steatosis progression at subsequent biopsy by fat score at the initial biopsy of the biopsy pair.

Figure 3

Relationship of the change of and steatosis grade and fibrosis stage (n=222).