Hepatic steatosis widespread among HIV/HCV coinfected patients in France

A study of 148 HIV/HCV coinfected individuals in the south of France has found a 67% prevalence rate of hepatic steatosis (fatty liver). Steatosis was of moderate or more severe degree in 30% and was associated with HCV genotype 3 and greater body mass index (BMI). The findings were published in the June 1 issue of the Journal of Acquired Immune Deficiency Syndromes.

Progression of hepatitis C is marked by progressive scarring of the liver (fibrosis) leading to cirrhosis and carcinoma (liver cancer); progression is typically much faster in people who are coinfected with HIV and hepatitis C virus (HCV). In some cases, people with HIV and/or HCV also develop hepatic steatosis, an abnormal build-up of fat within the liver cells. Studies have found varying rates of hepatic steatosis in HIV/HCV coinfected people; these variances have not yet been completely explained.

This study investigated hepatic steatosis among members of the Aquitaine Cohort – a prospective cohort of HIV-positive patients at the Bordeaux University Hospital and four other hospitals in southwestern France. Analysis included 148 coinfected patients who had liver biopsies performed during 1999 through 2003, who had not received ribavirin/interferon combination therapy. (Thirteen percent had received interferon monotherapy, which did not succeed in resolving the HCV infection.)

Characteristics of the study group were as follows: median age 38.8 years, 64% male, 65.5% infected through injection drug use, median CD4 cell count 500 cells/mm. HCV genotype was type 1 in 43% and type 3 in 31%. Ninety percent were receiving HAART at the time of biopsy. All participants were uninfected with hepatitis B (as determined by negative HBV surface antigen test).

Liver biopsy samples were evaluated for fibrosis and steatosis. Fibrosis was scored according to the METAVIR system; steatosis was graded according to how many liver cells were found to be affected: none, mild (1% to 10% of liver cells steatotic), moderate (11% to 30%), severe (31% to 60%) or massive (more than 60%). Some degree of steatosis was found in 99 of the 148 study participants (67%, 95% confidence interval [CI]: 59% to 74%). Steatosis was absent in 33.1%, mild in 36.5%, moderate in 18.9%, severe in 9.5% and massive in 2%. “Significant” steatosis – defined as moderate, severe or massive – was present in 30% (95% CI: 23% to 38%).

The only risk factor for steatosis identified by multivariate analysis was severe necroinflammatory activity (active cell death), as has been found in several studies of HCV-monoinfected patients. When this factor was removed, the HCV genotype and body mass index (BMI) were found to be significantly associated with steatosis, with HCV type 3 and greater BMI (i.e., greater obesity) being larger risks.

The researchers note that, although some previous studies report similar rates of hepatic steatosis in HIV-HCV coinfected patients (Bani-Sadr 2006, Gaslightwala 2006, McGovern 2006), many report lower rates (Sulkowski 2005, Monto 2005, Marks 2005). Differences in grading systems make direct comparisons difficult; however, only one, American, study (Sulkowski) reported dramatically lower prevalence (18%). The difference may be explained by the greater prevalence of HCV genotype 3 in the Aquitaine cohort and racial differences: American studies contain significant numbers of black participants, who may have a lower incidence of steatosis, while most Aquitaine participants were white.

The researchers conclude that, while hepatic steatosis was frequently observed overall and several risk factors were identified, “[f]further investigations are required to achieve better understanding of steatosis in HCV-HIV—coinfected patients, a complication that impairs clinical management.”