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Fibrosis in genotype 3 chronic hepatitis C and nonalcoholic fatty liver disease: Role of insulin resistance and hepatic steatosis.
Hepatology 2006; 44(6):1648-55Hep

Abstract

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.

Authors+Show Affiliations

Gastroenterology Department, University of Turin, Italy. ebugianesi@yahoo.itNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17133473

Citation

Bugianesi, Elisabetta, et al. "Fibrosis in Genotype 3 Chronic Hepatitis C and Nonalcoholic Fatty Liver Disease: Role of Insulin Resistance and Hepatic Steatosis." Hepatology (Baltimore, Md.), vol. 44, no. 6, 2006, pp. 1648-55.
Bugianesi E, Marchesini G, Gentilcore E, et al. Fibrosis in genotype 3 chronic hepatitis C and nonalcoholic fatty liver disease: Role of insulin resistance and hepatic steatosis. Hepatology. 2006;44(6):1648-55.
Bugianesi, E., Marchesini, G., Gentilcore, E., Cua, I. H., Vanni, E., Rizzetto, M., & George, J. (2006). Fibrosis in genotype 3 chronic hepatitis C and nonalcoholic fatty liver disease: Role of insulin resistance and hepatic steatosis. Hepatology (Baltimore, Md.), 44(6), pp. 1648-55.
Bugianesi E, et al. Fibrosis in Genotype 3 Chronic Hepatitis C and Nonalcoholic Fatty Liver Disease: Role of Insulin Resistance and Hepatic Steatosis. Hepatology. 2006;44(6):1648-55. PubMed PMID: 17133473.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fibrosis in genotype 3 chronic hepatitis C and nonalcoholic fatty liver disease: Role of insulin resistance and hepatic steatosis. AU - Bugianesi,Elisabetta, AU - Marchesini,Gulio, AU - Gentilcore,Elena, AU - Cua,Ian Homer Y, AU - Vanni,Ester, AU - Rizzetto,Mario, AU - George,Jacob, PY - 2006/11/30/pubmed PY - 2007/1/6/medline PY - 2006/11/30/entrez SP - 1648 EP - 55 JF - Hepatology (Baltimore, Md.) JO - Hepatology VL - 44 IS - 6 N2 - 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. SN - 0270-9139 UR - https://www.unboundmedicine.com/medline/citation/17133473/Fibrosis_in_genotype_3_chronic_hepatitis_C_and_nonalcoholic_fatty_liver_disease:_Role_of_insulin_resistance_and_hepatic_steatosis_ L2 - https://doi.org/10.1002/hep.21429 DB - PRIME DP - Unbound Medicine ER -