Abstract
Steatosis occurs in some patients with chronic hepatitis C and has been associated with fibrosis. Steatosis may result from viral mediated factors such as genotype 3 or coexistant metabolic syndrome. The aim of this study was to evaluate the association of demographic and clinical factors with the presence of steatosis and to evaluate the association between steatosis and histologic features on biopsy and disease progression. Methods: 598 patients underwent biopsy for HCV staging over a 10 year period and were well characterized clinically and histologically. Demographic and clinical data were collected retrospectively. Liver biopsies were read by two clinicians masked to clinical data. Biopsies were systematically evaluated by histology activity index (HAI) [Knodell 1981] and steatosis was graded 0-3. Disease progression was characterized by the fibrosis index (fibrosis stage 0-4/years since first risk factor). Results: The mean age was 49 ± 9 years and the mean BMI was 30 ± 7 kg/m2. The mean duration of infection was 26 ± 9 years. The population was 61% male and was 41% African American, 39% Non-Hispanic White and 20% Hispanic. Diabetes mellitus (DM) was present in 22%, hypertension in 36%, hyperlipidemia in 10% and past alcohol use in 26%. Steatosis (fat >5%) was present in 48% of patients. Those with steatosis had higher mean ALT level (91 ± 81 vs 70 ± 57, p<0.001) and higher mean BMI (30.9 ± 6.9 vs 28.7 ± 6.8, p=0.001). Patients with genotype 3 infection were more likely to have steatosis compared to other genotypes (72% vs 47%, p=0.009). Sixty five percent of Hispanics had steatosis compared to 44% of Non-Hispanic Whites and 43% of African Americans (p<0.001). Steatosis was more common in patients with DM (64% vs 43%, p<0.001). There was no association between steatosis and AST level, duration of infection, gender, hypertension, hyperlipidemia or past alcohol abuse. In multivariate analysis, Hispanic race, BMI and DM remained associated with steatosis. Patients with steatosis on liver biopsy had higher mean levels of portal inflammation (2.3 ± 0.9 vs 2.0 ± 0.8, p<0.001), interface hepatitis (2.9 ± 1.9 vs 2.2 ± 1.8, p<0.001), lobular inflammation (1.3 ± 0.7 vs 0.9 ± 0.9, p<0.001), fibrosis (2.7 ± 1.1 vs 2.4 ± 1.2, p=0.002) and total HAI (9.1 ± 3.8 vs 7.5 ± 3.9, p<0.001). Fibrosis index was higher in those with steatosis (0.12 ± 0.07 vs 0.10 ± 0.07, p=0.021). Conclusion: The presence of steatosis on biopsywas associatedwithmore histologic activity and faster rates of disease progression by fibrosis index. BMI, DM and Hispanic race can help clinicians identify patients at risk for steatosis.
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