TY - JOUR
T1 - Hepatic Steatosis in Hepatitis C
T2 - Comparison of Diabetic and Nondiabetic Patients in the Hepatitis C Antiviral Long-Term Treatment Against Cirrhosis Trial
AU - Lok, Anna S F
AU - Everhart, James E.
AU - Chung, Raymond T.
AU - Padmanabhan, Latha
AU - Greenson, Joel K.
AU - Shiffman, Mitchell L.
AU - Everson, Gregory T.
AU - Lindsay, Karen L.
AU - Bonkovsky, Herbert L.
AU - Di Bisceglie, Adrian M.
AU - Lee, William M.
AU - Morgan, Timothy R.
AU - Ghany, Marc G.
AU - Morishima, Chihiro
N1 - Funding Information:
Financial relationships of the authors with Hoffmann-La Roche, Inc., are as follows: A.S.F.L. is a consultant and receives research support; R.T.C. receives research support; M.L.S. is a consultant, on the speaker’s bureau, and receives research support; G.T.E. is a consultant, on the speaker’s bureau, and receives research support; K.L.L. is a consultant and receives research support; H.L.B. is a consultant and on the speakers bureau; A.M.D. is a consultant, on the speaker’s bureau, and receives research support; W.M.L. is on the speaker’s bureau and receives research support; and T.R.M. is on the speaker’s bureau and receives research support. In addition, A.S.F.L. receives research support from Eisai, J.K.G. receives research support and other compensation from Metabolic Solutions; G.T.E. receives support from Metabolic Solutions, W.M.L. receives research support from Bayer Diagnostics, T.R.M. receives research grants and is on the speaker’s bureau of Scherling Plough and receives research grants and is a consultant for Valcant; and C.M. receives research support from Bayer Diagnostics. This study also was supported by the National Institute of Diabetes & Digestive & Kidney Diseases. Additional support was provided by the National Institute of Allergy and Infectious Diseases, the National Cancer Institute, the National Center for Minority Health and Health Disparities, and by General Clinical Research Center grants from the National Center for Research Resources, National Institutes of Health. Additional funding to conduct this study was supplied by Hoffmann-La Roche, Inc., through a Cooperative Research and Development Agreement with the National Institutes of Health. The insulin assays were performed in the Michigan Diabetes Research and Training Center, which is supported by an National Institute of Diabetes & Digestive & Kidney Diseases grant (P60 DK020572-28).
PY - 2007/2
Y1 - 2007/2
N2 - Background & Aims: Hepatic steatosis often is observed in patients with chronic hepatitis C and has been reported to be associated with hepatic fibrosis and impaired treatment response in some studies. Our aim was to determine the prevalence of and risk factors for hepatic steatosis among Hepatitis C Antiviral Long-term Treatment against Cirrhosis patients, and to determine the relationship between steatosis, fibrosis, and sustained virologic response (SVR) to re-treatment with pegylated interferon and ribavirin. Methods: Baseline data from 1143 Hepatitis C Antiviral Long-term Treatment against Cirrhosis patients, with a mean body mass index of 30, 5% with genotype 3, 38% with cirrhosis, and 24% with diabetes were analyzed. Results: Steatosis scores of 0, 1, 2, 3, and 4 were observed in 19%, 42%, 30%, 8%, and 1% of patients, respectively. High body mass index, triglyceride and alanine aminotransferase levels, and genotype 3 were associated with higher grades of steatosis. Among nondiabetic patients, steatosis scores of 0-2 but not scores of 3-4 were associated significantly with cirrhosis. For diabetic patients, there was no association between steatosis and cirrhosis. Similarly, steatosis scores of 2-4 were associated with a lack of SVR among nondiabetic but not among diabetic patients. Conclusions: In this cohort with predominantly hepatitis C virus genotype 1 infection, steatosis was associated strongly with metabolic factors that contribute to nonalcoholic fatty liver disease. Steatosis correlated with increasing stages of fibrosis up to but not including cirrhosis. Steatosis had a negative impact on SVR among nondiabetic but not diabetic patients. The discordant findings between nondiabetic and diabetic patients indicate that these 2 groups should be considered separately when analyzing metabolic factors and liver disease outcomes.
AB - Background & Aims: Hepatic steatosis often is observed in patients with chronic hepatitis C and has been reported to be associated with hepatic fibrosis and impaired treatment response in some studies. Our aim was to determine the prevalence of and risk factors for hepatic steatosis among Hepatitis C Antiviral Long-term Treatment against Cirrhosis patients, and to determine the relationship between steatosis, fibrosis, and sustained virologic response (SVR) to re-treatment with pegylated interferon and ribavirin. Methods: Baseline data from 1143 Hepatitis C Antiviral Long-term Treatment against Cirrhosis patients, with a mean body mass index of 30, 5% with genotype 3, 38% with cirrhosis, and 24% with diabetes were analyzed. Results: Steatosis scores of 0, 1, 2, 3, and 4 were observed in 19%, 42%, 30%, 8%, and 1% of patients, respectively. High body mass index, triglyceride and alanine aminotransferase levels, and genotype 3 were associated with higher grades of steatosis. Among nondiabetic patients, steatosis scores of 0-2 but not scores of 3-4 were associated significantly with cirrhosis. For diabetic patients, there was no association between steatosis and cirrhosis. Similarly, steatosis scores of 2-4 were associated with a lack of SVR among nondiabetic but not among diabetic patients. Conclusions: In this cohort with predominantly hepatitis C virus genotype 1 infection, steatosis was associated strongly with metabolic factors that contribute to nonalcoholic fatty liver disease. Steatosis correlated with increasing stages of fibrosis up to but not including cirrhosis. Steatosis had a negative impact on SVR among nondiabetic but not diabetic patients. The discordant findings between nondiabetic and diabetic patients indicate that these 2 groups should be considered separately when analyzing metabolic factors and liver disease outcomes.
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U2 - 10.1016/j.cgh.2006.11.002
DO - 10.1016/j.cgh.2006.11.002
M3 - Article
C2 - 17296533
AN - SCOPUS:33846881160
SN - 1542-3565
VL - 5
SP - 245
EP - 254
JO - Clinical Gastroenterology and Hepatology
JF - Clinical Gastroenterology and Hepatology
IS - 2
ER -