OBJECTIVES: Liver steatosis is a common histopathological finding in patients infected with hepatitis C virus. Patients with chronic hepatitis C having both steatosis and factors causing oxidative stress may be at a higher risk of fibrogenesis. In a subset of patients with a definite date of contamination, our study aimed to assess the potential synergistic interaction between steatosis and factors likely to induce oxidative stress-namely, alcohol intake, iron overload, and drugs. METHODS: Out of 700 anti-HCV-positive screened patients, 142 untreated patients with liver biopsy and with one known risk factor were selected. Liver fibrosis, inflammation, and necrosis were graded according to the Knodell score, and steatosis as moderate to severe if more than 30% of hepatocytes were affected. Drinkers were defined as having daily mean alcohol intakes of more than 30 g in men and 20 g in women. RESULTS: In multivariate analysis, two factors were independently associated with extensive fibrosis: the degree of severity of piecemeal necrosis (OR = 3.27, CI = 1 .17-9.16) and a combination of moderate to severe steatosis and alcohol intake (OR = 7.02, CI = 1.12-44). The median progression rate of fibrosis was about twice as high among drinkers with steatosis than among drinkers without steatosis or nondrinkers with or without steatosis (0.25 vs 0. I vs 0.13 vs 0.08, respectively; p = 0.02). Independent parameters significantly associated with moderate to severe steatosis were body mass index (OR = 1.13, CI = 1.02-1.26) and infection with genotype 3 (OR = 5.5, CI = 1.88-16), but not alcohol consumption. CONCLUSIONS: As well as the key role of the severity of piecemeal necrosis, the study underlines the synergistic interaction between steatosis and even low alcohol consumption as a contributory factor in extensive liver fibrosis.
OBJECTIVES:Liver steatosis is a common histopathological finding in patients infected with hepatitis C virus. Patients with chronic hepatitis C having both steatosis and factors causing oxidative stress may be at a higher risk of fibrogenesis. In a subset of patients with a definite date of contamination, our study aimed to assess the potential synergistic interaction between steatosis and factors likely to induce oxidative stress-namely, alcohol intake, iron overload, and drugs. METHODS: Out of 700 anti-HCV-positive screened patients, 142 untreated patients with liver biopsy and with one known risk factor were selected. Liver fibrosis, inflammation, and necrosis were graded according to the Knodell score, and steatosis as moderate to severe if more than 30% of hepatocytes were affected. Drinkers were defined as having daily mean alcohol intakes of more than 30 g in men and 20 g in women. RESULTS: In multivariate analysis, two factors were independently associated with extensive fibrosis: the degree of severity of piecemeal necrosis (OR = 3.27, CI = 1 .17-9.16) and a combination of moderate to severe steatosis and alcohol intake (OR = 7.02, CI = 1.12-44). The median progression rate of fibrosis was about twice as high among drinkers with steatosis than among drinkers without steatosis or nondrinkers with or without steatosis (0.25 vs 0. I vs 0.13 vs 0.08, respectively; p = 0.02). Independent parameters significantly associated with moderate to severe steatosis were body mass index (OR = 1.13, CI = 1.02-1.26) and infection with genotype 3 (OR = 5.5, CI = 1.88-16), but not alcohol consumption. CONCLUSIONS: As well as the key role of the severity of piecemeal necrosis, the study underlines the synergistic interaction between steatosis and even low alcohol consumption as a contributory factor in extensive liver fibrosis.
Authors: T Asselah; N Boyer; M-C Guimont; D Cazals-Hatem; F Tubach; K Nahon; H Daïkha; D Vidaud; M Martinot; M Vidaud; C Degott; D Valla; P Marcellin Journal: Gut Date: 2003-11 Impact factor: 23.059