Fibrosis in genotype 3 chronic hepatitis C and nonalcoholic fatty liver disease: Role of insulin resistance and hepatic steatosis.

Fibrosis in genotype 3 chronic hepatitis C and nonalcoholic fatty liver disease: Role of insulin resistance and hepatic steatosis. Research Abstract Details 

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Fibrosis in genotype 3 chronic hepatitis C and nonalcoholic fatty liver disease: Role of insulin resistance and hepatic steatosis. Abstract Text:

Elisabetta Bugianesi,Gulio Marchesini,Elena Gentilcore,Ian Homer Y Cua,Ester Vanni,Mario Rizzetto,Jacob George,

Hepatic steatosis has been associated with fibrosis, but it is unknown whether the latter is independent of the etiology of fat infiltration. We analyzed the relationship between clinical characteristics, insulin resistance (HOMA-R) and histological parameters in 132 patients with "viral" steatosis caused by genotype 3 chronic hepatitis C (CHC-3) and 132 patients with "metabolic" steatosis caused by nonalcoholic fatty liver disease (NAFLD), matched by age, BMI, and degree of liver fat accumulation. Tests of liver function were comparable in the two study populations. The prevalence of features of insulin resistance was higher in NAFLD, as was HOMA-R (P = .008). Logistic regression analysis confirmed that steatosis was associated with a high viral load and low serum cholesterol in CHC-3, and with high aminotransferase, glucose, ferritin and hypertriglyceridemia in NAFLD. At univariate analysis, advanced fibrosis was associated with steatosis in NAFLD, but not in CHC-3. Other parameters related to fibrosis severity were HOMA-R and a low platelet count in CHC-3, and high aminotransferases, HOMA-R, ferritin and low HDL-cholesterol in NAFLD. On multivariate analysis, only low platelet count (OR = 0.78; 95% CI, 0.67-0.92) and HOMA-R (OR = 2.98; 1.13-7.89) were independent predictors of advanced fibrosis in CHC-3. In NAFLD, severe fibrosis was predicted by fat grading (OR = 3.03; 1.41-6.53), ferritin (OR = 1.13; 1.03-1.25) and HOMA-R (OR = 1.16; 1.02-1.31). In conclusion, insulin resistance is an independent predictor of advanced fibrosis in both NAFLD and CHC-3, but the extent of steatosis contributes to advanced disease only in NAFLD. Virus-induced hepatic steatosis as seen in CHC-3 does not contribute significantly to liver fibrosis.

Fibrosis in genotype 3 chronic hepatitis C and nonalcoholic fatty liver disease: Role of insulin resistance and hepatic steatosis. Publishing Authors By Initials

E Bugianesi,G Marchesini,E Gentilcore,IH Cua,E Vanni,M Rizzetto,J George,

For similar investigative techniques: epidemiologic methods: statistics as topic: probability: risk: risk factors research abstracts see: investigative techniques: epidemiologic methods: statistics as topic: probability: risk: risk factors research

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Fibrosis in genotype 3 chronic hepatitis C and nonalcoholic fatty liver disease: Role of insulin resistance and hepatic steatosis. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Hepatology (Baltimore, Md.)

VOLUME: 44

Page Numbers: 1648-55

Journal Abbreviation: Hepatology

ISSN: 0270-9139

DAY: 3

MONTH: Dec

YEAR: 2006

Fibrosis in genotype 3 chronic hepatitis C and nonalcoholic fatty liver disease: Role of insulin resistance and hepatic steatosis. Information

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LANGUAGE: eng

NlmUniqueID: 8302946

Fibrosis in genotype 3 chronic hepatitis C and nonalcoholic fatty liver disease: Role of insulin resistance and hepatic steatosis. Keywords Mesh Terms:

KEYWORDS: Risk Factors

MESH TERMS: etiology

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Grant and Affiliation Information for Fibrosis in genotype 3 chronic hepatitis C and nonalcoholic fatty liver disease: Role of insulin resistance and hepatic steatosis.

AFFILIATION: Gastroenterology Department, University of Turin, Italy. ebugianesi@yahoo.it

Country: United States

AGENCY: United States NIDDK

GRANT: DK56402

ACRONYM: DK

MEDLINETA: Hepatology

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