Hepatic
steatosis - fat accumulation in liver cells -- is caused by a complex interaction
of host and viral factors such as metabolic syndrome, alcoholism, and genotype
3 hepatitis C virus (HCV), according to the authors of a study published in the
February 7, 2008 advance online edition of the Journal of Hepatology. Among
HIV-HCV coinfected patients,
antiretroviral therapy may also
play a role.
The authors analyzed data from participants in APRICOT (the
AIDS Pegasys Ribavirin International Coinfection Trial) who had paired liver biopsies
interpreted and graded for steatosis along with lipid evaluations and body measurements.
APRICOT included 868 HCV-HIV coinfected patients in 19 countries who were
randomly assigned to receive conventional interferon alpha plus 800 mg/day ribavirin,
pegylated interferon alfa-2a (Pegasys) plus placebo, or pegylated interferon plus
ribavirin for 48 weeks. As
previously reported, the sustained virological response (SVR) rate was highest
in the pegylated interferon plus ribavirin arm: 40% overall, 29% for patients
with HCV genotype 1, and 62% for those with genotypes 2/3.
In the current
analysis, the investigators looked at data from 283 APRICOT participants with
available paired biopsy results. They assessed the prevalence of steatosis, baseline
factors associated with steatosis, the effect of steatosis on efficacy of interferon-based
therapy, and the impact of anti-HCV treatment on steatosis.
Results
65 of 283 patients (23%) with paired biopsies showed evidence of steatosis.
Patients with steatosis were significantly more likely to have:
The only difference in body measurements was neck circumference, which was greater
in patients with steatosis and decreased significantly during treatment.
Hip circumference at baseline was predictive of steatosis.
Conclusion
Based
on these findings, the study authors concluded, "Factors associated [with]
the metabolic syndrome are important in [HIV-HCV] coinfected patients." They
added that, "Treatment outcome affected steatosis in that viral eradication
reduced steatosis in genotype 3 patients, but altogether steatosis did not affect
efficacy of treatment in any genotype."
3/21/08
Reference M
Rodriguez-Torres, S Govindarajan, R Sola, and others. Hepatic steatosis in HCV/HIV
co-infected patients: Correlates, efficacy and outcomes of anti-HCV therapy: A
paired liver biopsy study. Journal of Hepatology. February 7, 2008 [Epub ahead
of print].