Hepatic steatosis and steatohepatitis in human immunodeficiency virus/hepatitis C virus-coinfected patients

Hepatic steatosis (HS) is frequent in human immunodeficiency virus (HIV)- and hepatitis C virus (HCV)-coinfected patients. Antiretroviral therapy (ART) and metabolic alterations could induce HS. However, a protective effect of ART has been reported in a paired biopsy study. Thus, our aim was to examine the changes and predictors of HS progression among HIV/HCV-coinfected patients with sequential biopsies. We also evaluated the rates of steatohepatitis and factors associated thereof. HIV-infected patients with detectable serum HCV RNA, who underwent two biopsies, separated at least by 1 year, were included in this retrospective study. HS progression was defined as increase in one or more HS grades. The median (interquartile range) time between biopsies was 3.3 (2.0-5.2) years. Among 146 individuals, HS at baseline was observed in 86 (60%) patients and in 113 (77%) in the follow-up biopsy (P < 0.001). Progression of HS was observed in 60 (40%) patients. HS regressed in 11 (8%) patients. Factors associated with HS progression were changes in fasting plasma glucose (FPG) between biopsies (per 10 mg/dL increase; odds ratio [OR] [95% confidence interval; CI] = 1.4 [1.04-1.8]; P = 0.024) and cumulative use of dideoxynucleoside analogs (per year; OR [95% CI] = 1.5 [1.2-1.8]; P = 0.001). Persistent steatohepatitis or progression to steatohepatitis between biopsies was observed in 27 (18%) patients. Persistence of or progression to steatohepatitis was associated with progression ≥1 fibrosis stages between biopsies (OR [95% CI] = 2.4 [1.01-5.7]; P = 0.047). Conclusions: HS progresses frequently and regression is rarely observed in HIV/HCV-coinfected patients, including in those on ART. Cumulative exposure to dideoxynucleoside analogs and increases in FPG are related with HS progression. Stetatohepatitis is frequently observed in these patients and is linked to fibrosis progression. © 2012 American Association for the Study of Liver Diseases.This study was partly supported by a grant from Consejerı´a de Salud, Junta de Andalucı´a (exp. 0022/2007), from Fundaci on para la Investigaci on y la Prevenci on del SIDA en Espa~na (FIPSE, exp. 36789/08), and from the ISCIII-RETIC RD06/006. J.B. and J.A.G.-G. are investigators from the Intensification of Research Activity Program of the Spanish National Health Service (reference I3SNS). J.A.P. and M.A.J. are recipients of intensification grants from the Fundaci on Progreso y Salud of the Consejerı´a de Salud de la Junta de Andalucı´a (references AI-0021 and AI-0003, respectively).Peer Reviewe