Evolution of hepatic steatosis in patients with advanced hepatitis C: Results from the hepatitis C antiviral long-term treatment against cirrhosis (HALT-C) trial
dc.contributor.author | Lok, Anna Suk-Fong | en_US |
dc.contributor.author | Everhart, James E. | en_US |
dc.contributor.author | Chung, Raymond T. | en_US |
dc.contributor.author | Kim, Hae-Young | en_US |
dc.contributor.author | Everson, Gregory T. | en_US |
dc.contributor.author | Hoefs, John C. | en_US |
dc.contributor.author | Greenson, Joel K. | en_US |
dc.contributor.author | Sterling, Richard K. | en_US |
dc.contributor.author | Lindsay, Karen L. | en_US |
dc.contributor.author | Lee, William M. | en_US |
dc.contributor.author | Di Bisceglie, Adrian M. | en_US |
dc.contributor.author | Bonkovsky, Herbert L. | en_US |
dc.contributor.author | Ghany, Marc G. | en_US |
dc.contributor.author | Morishima, Chihiro | en_US |
dc.date.accessioned | 2009-07-06T15:38:37Z | |
dc.date.available | 2010-08-02T17:56:56Z | en_US |
dc.date.issued | 2009-06 | en_US |
dc.identifier.citation | Lok, Anna S.; Everhart, James E.; Chung, Raymond T.; Kim, Hae-Young; Everson, Gregory T.; Hoefs, John C.; Greenson, Joel K.; Sterling, Richard K.; Lindsay, Karen L.; Lee, William M.; Di Bisceglie, Adrian M.; Bonkovsky, Herbert L.; Ghany, Marc G.; Morishima, Chihiro (2009). "Evolution of hepatic steatosis in patients with advanced hepatitis C: Results from the hepatitis C antiviral long-term treatment against cirrhosis (HALT-C) trial Potential conflict of interest: Financial relationships of the authors with Hoffmann-La Roche, Inc., are as follows: A.S. Lok is a consultant; R. T. Chung receives research support; G.T. Everson is a consultant, on the speaker's bureau, and receives research support; J.C. Hoefs is on the speaker's bureau; R.K. Sterling is a consultant, on the speaker's bureau, and receives research support; K.L. Lindsay is a consultant and receives research support. W.M. Lee receives research support; A.M. Di Bisceglie is a consultant, on the speaker's bureau, and receives research support; H.L. Bonkovsky receives research support. Authors with no financial relationships related to this project are: J.E. Everhart, H-Y Kim, J.K. Greenson, M.G. Ghany, and C. Morishima. ." Hepatology 49(6): 1828-1837. <http://hdl.handle.net/2027.42/63058> | en_US |
dc.identifier.issn | 0270-9139 | en_US |
dc.identifier.issn | 1527-3350 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/63058 | |
dc.description.abstract | Hepatic steatosis is a common histologic feature in patients with chronic hepatitis C (CHC) but there are no large longitudinal studies describing the progression of steatosis in CHC. We examined changes in steatosis on serial biopsies among CHC patients participating in the Hepatitis C Antiviral Long-term Treatment against Cirrhosis (HALT-C) Trial. All 1050 patients in the trial had advanced fibrosis at baseline biopsy and were documented not to have had a sustained virological response to peginterferon and ribavirin. Most (94%) patients had genotype 1 infection. At least one protocol follow-up biopsy was read on 892 patients, and 699 had the last biopsy performed 3.5 years after randomization. At enrollment, 39% had cirrhosis and 61% had bridging fibrosis; 18%, 41%, 31%, and 10% had steatosis scores of 0, 1, 2, and 3 or 4, respectively. The mean steatosis score decreased in the follow-up biopsies in both the interferon-treated patients and controls with no effect of treatment assignment ( P = 0.66). A decrease in steatosis score by ≥1 point was observed in 30% of patients and was associated with both progression to cirrhosis and continued presence of cirrhosis ( P = 0.02). Compared to patients without a decrease in steatosis, those with a decrease in steatosis had worse metabolic parameters at enrollment, and were more likely to have a decrease in alcohol intake, improvement in metabolic parameters, and worsening liver disease (cirrhosis, esophageal varices, and deterioration in liver function). Conclusion: Serial biopsies demonstrated that in patients with CHC, steatosis recedes during progression from advanced fibrosis to cirrhosis. Decreased alcohol intake and improved metabolic parameters are associated with a decline in steatosis and may modulate hepatitis C progression. (H EPATOLOGY 2009.) | en_US |
dc.format.extent | 416367 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | Wiley Subscription Services, Inc., A Wiley Company | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Hepatology | en_US |
dc.title | Evolution of hepatic steatosis in patients with advanced hepatitis C: Results from the hepatitis C antiviral long-term treatment against cirrhosis (HALT-C) trial | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Internal Medicine and Specialties | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Division of Gastroenterology, University of Michigan Medical Center, Ann Arbor, MI ; fax: (734) 936-7024. ; Division of Gastroenterology, University of Michigan Health System, 3912 Taubman Center, SPC 5362, Ann Arbor, MI 48109 | en_US |
dc.contributor.affiliationum | Department of Pathology, University of Michigan Medical School, Ann Arbor, MI | en_US |
dc.contributor.affiliationother | Division of Digestive Diseases and Nutrition, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD | en_US |
dc.contributor.affiliationother | Gastrointestinal Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA | en_US |
dc.contributor.affiliationother | New England Research Institutes, Watertown, MA | en_US |
dc.contributor.affiliationother | School of Medicine, University of Colorado Denver, Aurora, CO | en_US |
dc.contributor.affiliationother | Division of Gastroenterology, University of California – Irvine, Irvine, CA | en_US |
dc.contributor.affiliationother | Hepatology Section, Virginia Commonwealth University Medical Center, Richmond, VA | en_US |
dc.contributor.affiliationother | Division of Gastrointestinal and Liver Diseases, Keck School of Medicine, University of Southern California, Los Angeles, CA | en_US |
dc.contributor.affiliationother | Divisions of Digestive and Liver Diseases and Infectious Diseases,UT Southwestern Medical Center, Dallas, TX | en_US |
dc.contributor.affiliationother | Division of Gastroenterology and Hepatology, Saint Louis University School of Medicine, St. Louis, MO | en_US |
dc.contributor.affiliationother | Departments of Medicine and Molecular & Structural Biology and The Liver-Biliary-Pancreatic Center, University of Connecticut Health Center, Farmington, CT | en_US |
dc.contributor.affiliationother | Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD | en_US |
dc.contributor.affiliationother | Virology Division, Department of Laboratory Medicine, University of Washington, Seattle, WA | en_US |
dc.identifier.pmid | 19291787 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/63058/1/22865_ftp.pdf | |
dc.identifier.doi | 10.1002/hep.22865 | en_US |
dc.identifier.source | Hepatology | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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