Does High Body Mass Index Affect Hepatic Fibrosis, Steatosis and Inflammation in Patients with Chronic Hepatitis C?
Mohamed A. Metwally, Claudia O. Zein, Nizar N. Zein, Rochester, MN
It has been reported that high body mass index (BMI) may have a negative impact on the rate of fibrosis progression in HCV patients. Steatosis is a common histopathological finding in liver biopsy of chronic HCV patients, but hepatic fibrosis is the responsible factor for the complication of chronic hepatitis C. Body mass index is a well known to be associated with hepatic steatosis in obese and diabetic patients and the lowering of BMI may potentially decrease hepatic steatosis in these patients. The impact of high BMI on hepatic fibrosis, steatosis and inflammatory activity in patients with chronic HCV is still under investigation.
The aim of this study is to assess the potential association between body mass index and stage of hepatic fibrosis in HCV patients.
209 consecutive previously untreated chronic HCV patients were enrolled. Chronic HCV was confirmed by serological, virological and histological investigations. Other confounding liver diseases were excluded. Liver biopsies were reviewed for stage of fibrosis, degree of inflammation and degree of steatosis. Laboratory and demographic data at time of liver biopsy including alcohol intake and diabetes mellitus were collected. Univariate analysis was used to compare mean BMI against levels of hepatic fibrosis, inflammatory activity, and steatosis. Demographic data were compared also against levels of hepatic fibrosis, inflammatory activity, and steatosis. T test for continuous data chi-square test or Fishers exact test for categorical data was used for the analysis. Multivariate analysis against level of hepatic fibrosis was done to control for confounding variables including diabetes mellitus and alcohol intake.
Higher BMI values were associated with more advanced hepatic fibrosis (Stage III/IV) in unvariate analysis (P=0.02) and was still significant after controlling for alcohol intake and diabetes in multivariate analysis (P=0.04). High BMI was also associated with hepatic steatosis (P=0.03), although there was no statistically significant association between steatosis and fibrosis stages suggesting that the association between BMI and fibrosis is independent of that of BMI and steatosis. BMI was not associated with hepatic inflammatory activity (P=0.6). There was no significant association between hepatic steatosis and alcohol intake (p=0.5) nor diabetes mellitus (p=0.6). There was no significant association between stage of hepatic fibrosis and degree of steatosis.
In summary, higher BMI values were associated with more severe hepatic fibrosis in patients with chronic HCV infection. Whether high BMI in HCV patients contribute directly to progression of hepatic fibrosis and whether dietary lowering of BMI will slow the progression of HCV associated liver disease remains to be determined.
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