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Steatosis in chronic hepatitis C: Relative contributions of obesity, diabetes mellitus, and alcohol
Hepatology Sept 2002, Vol 36, Number 3
  Steatosis is accumulation of fat in the liver. This study discussed below finds body mass index contribute to developing steatosis & thus to faster progression of liver diseasse, and suggests diabetes contributes to steatosis & faster liver disease progression. HIV+ individuals may develop this more than HIV- negative individuals due to elevated cholesterol and triglycerides for patients on HAART or perhaps moreso on protease inhibitors. Poor diet, lack of exercise, smoking cigarettes, and a sedentary lifestyle can contribute to elevated lipids. HIV+ persons are at greater risk for developing insulin resistance and diabetes at an compared to HIV- individuals, also apparently due to protease inhibitor use. Protease inhibitor sparing regimens may help control lipids, insulin resistance, and sugar.
Steatosis has emerged as a histologic finding of importance to the progression of hepatitis C virus (HCV)-associated liver disease. However, most studies of HCV-associated steatosis have excluded alcohol drinkers and individuals with diabetes and thus have not addressed the relative contribution of known causes of steatosis to liver injury in HCV-associated disease. To address this issue, we studied 297 consecutive patients with HCV who met inclusion criteria. Alcohol consumption, demographics, and serologic tests were correlated with degrees of steatosis and fibrosis on liver biopsy. Liver biopsy specimens were also examined for evidence of significant alcohol or nonalcoholic steatohepatitis (NASH) injury. In univariate analysis, steatosis correlated with type 2 diabetes mellitus (P = .005) and body mass index (BMI) (P = .0001) but not with the intensity of alcohol intake (in grams per day). In multivariate analysis, BMI (P = .0002) and genotype 3a infection (P = .02) were independent predictors of steatosis. When patients with risk factors for NASH were excluded, genotype 3a infection was the only independent predictor of steatosis. Steatosis (P = .04) and inflammation (P < .0001) scores on liver biopsy were the only independent predictors of fibrosis. Significant alcohol or NASH injury was found in only 6% of biopsy specimens. In conclusion, steatosis in HCV infection is associated with risk factors for NASH, particularly obesity, rather than alcohol consumption. (HEPATOLOGY 2002;36:729-736.)
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