Ann L. Silverman, Stuart C. Gordon, David J. Ternes, Heather H. Wolak, Mamtha Balasubramaniam, Neal S. Goldstein, William Beaumont Hosp, Royal Oak, MI.

A correlation with hepatic steatosis (fat accumulation in liver), body mass index (BMI) (weight) and fibrosis was described among Australian hepatitis C carriers (Hepatology 1999;29:1215). Among Italian patients (Hepatology 1999;30:1530), a correlation was found between HCV genotype 3a and steatosis, independent of BMI. It was recently proposed (PNAS 1999;96:12766) that one potential mechanism for HCV entry into cells was via the LDL receptor, leading to the hypothesis that higher HCV RNA levels might be associated with increased hepatic steatosis. We sought to determine a potential association between hepatic steatosis, fibrosis, BMI and viral load in an American cohort of HCV carriers.

Methods: We studied the records of 49 untreated nonalcoholic patients with chronic HCV; subjects with high and low viral loads were selected for review. 7/49 did not have biopsies done at our institution and 1/49 did not have a recorded weight. The remaining 41 patients were designated H (high viral levels), n=27, (>2.4 x 106 copies/ml; mean, 17.2 x 106) and L (low viral levels), n=14, (<1.5 x 106 copies/ml; mean, 6.7 x 105). Quantitative HCV RNA determinations were based on the NGl assay. Steatosis was graded on a scale of 0-3, corresponding to none to marked. Fibrosis was scored using the Metavir Fibrosis Scale.

Results: There was no difference in steatosis, hepatic fibrosis, or genotype between the H and L groups. In the total cohort, 5 patients were genotype 3a; 4/5 had little or no (grade 0-1) steatosis, and 1/5 had grade 3 steatosis. Considering the 41 patients as one cohort, we found that there was no correlation between BMI, degree of steatosis, or hepatic fibrosis.

Conclusions: In an American cohort of HCV carriers, we found that viral load does not correlate with steatosis, BMI or fibrosis. Overall, there was no association between BMI and fibrosis or steatosis.