and genotype-3 chronic hepatitis C (CHC) are characterized by hepatic steatosis. However, the mechanisms for fat accumulation in both disorders might be different. We sought to (1) dissect the contribution of viral and metabolic factors to hepatic steatosis in NAFLD and genotype-3 CHC and (2) assess the impact on liver damage of steatosis from different aetiologies. Methods: We compared the prevalence of the metabolic syndrome (ATPIII criteria), insulin resistance (HOMA-R) and histologic parameters (steatosis, inflammation, fibrosis) in 132 consecutive patients with genotype-3 CHC and steatosis to 132 NAFLD patients matched by BMI, age and extent of hepatic steatosis. Steatosis was scored 0-3, inflammation and fibrosis 0-4 in all biopsies. Results: Despite matching for BMI and extent of steatosis, the prevalence of the metabolic syndrome was higher in NAFLD than in CHC (21% vs 9%, P= 0.026), with a higher prevalence of hypertension, hypertriglyceridemia and low HDL-cholesterol in NAFLD. HOMA-R was significantly increased in NAFLD compared to CHC (2.32 vs 4.22, P = 0.0003). Biochemical (AST, ALT) and histological (score of inflammation and fibrosis) parameters of liver damage were significantly higher in CI-IC than in NAFLD, while test of liver function (albumin, INR) and of peripheral iron burden were comparable. By logistic regression analysis (corrected for gender, age, BMI, ALT), NAFLD was associated with high HOMA-R (>75th percentile) (OR 2.72; 95%CI: 1.59-4.66; P = 0.0003). A linear correlation between steatosis and fibrosis was observedin NAFLD (rs= 0.300; P = 0.006), but not in CHC (rs = 0.147; P = 0.092). Independent predictors of severe fibrosis (grade 34) in CHC included portal inflammatory grade (4.17, 1.89-9.21, P=0.004)and HOMA-R (OR, 1.22; 1.03-1.46; P=0.023). Severe fibrosis was associated with grade-3 steatosis (2.30, 1.05-5.05, P = 0.038) in the whole population, and separately in NAFLD (3.79, 1.29-11.15, P = 0.015), but not in CHC. Conclusions: Age- and BMI-matched NAFLD patients have a higher prevalence of the metabolic syndrome compared with CHC. Hepatic necroinflammation and fibrosis are more pronounced in genotype-3 CHC than in NAFLD with a comparable amount of liver steatosis. Hepatic fibrosis is associated with the extent of steatosis in NAFLD and to the degree of inflarmnation in genotype-3 CHC.

Different contribution of metabolic and viral steatosis to liver damage

BUGIANESI, Elisabetta;VANNI, Ester;RIZZETTO, Mario;
2005

Abstract

and genotype-3 chronic hepatitis C (CHC) are characterized by hepatic steatosis. However, the mechanisms for fat accumulation in both disorders might be different. We sought to (1) dissect the contribution of viral and metabolic factors to hepatic steatosis in NAFLD and genotype-3 CHC and (2) assess the impact on liver damage of steatosis from different aetiologies. Methods: We compared the prevalence of the metabolic syndrome (ATPIII criteria), insulin resistance (HOMA-R) and histologic parameters (steatosis, inflammation, fibrosis) in 132 consecutive patients with genotype-3 CHC and steatosis to 132 NAFLD patients matched by BMI, age and extent of hepatic steatosis. Steatosis was scored 0-3, inflammation and fibrosis 0-4 in all biopsies. Results: Despite matching for BMI and extent of steatosis, the prevalence of the metabolic syndrome was higher in NAFLD than in CHC (21% vs 9%, P= 0.026), with a higher prevalence of hypertension, hypertriglyceridemia and low HDL-cholesterol in NAFLD. HOMA-R was significantly increased in NAFLD compared to CHC (2.32 vs 4.22, P = 0.0003). Biochemical (AST, ALT) and histological (score of inflammation and fibrosis) parameters of liver damage were significantly higher in CI-IC than in NAFLD, while test of liver function (albumin, INR) and of peripheral iron burden were comparable. By logistic regression analysis (corrected for gender, age, BMI, ALT), NAFLD was associated with high HOMA-R (>75th percentile) (OR 2.72; 95%CI: 1.59-4.66; P = 0.0003). A linear correlation between steatosis and fibrosis was observedin NAFLD (rs= 0.300; P = 0.006), but not in CHC (rs = 0.147; P = 0.092). Independent predictors of severe fibrosis (grade 34) in CHC included portal inflammatory grade (4.17, 1.89-9.21, P=0.004)and HOMA-R (OR, 1.22; 1.03-1.46; P=0.023). Severe fibrosis was associated with grade-3 steatosis (2.30, 1.05-5.05, P = 0.038) in the whole population, and separately in NAFLD (3.79, 1.29-11.15, P = 0.015), but not in CHC. Conclusions: Age- and BMI-matched NAFLD patients have a higher prevalence of the metabolic syndrome compared with CHC. Hepatic necroinflammation and fibrosis are more pronounced in genotype-3 CHC than in NAFLD with a comparable amount of liver steatosis. Hepatic fibrosis is associated with the extent of steatosis in NAFLD and to the degree of inflarmnation in genotype-3 CHC.
The 40th Annual Meeting of the European Association for the Study of the Liver (EASL 2005)
Parigi
13-17 Aprile 2005
42
25
26
E. Bugianesi; G. Marchesini; E. Gentilcore; I.H.Y Cua; E. Vanni; M. Rizzetto; J. George
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/131717
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