Portal Hypertensive Gastropathy in Chronic Hepatitis C Patients with Bridging Fibrosis and Compensated Cirrhosis: Results from the HALT-C Trial
Authors: Fontana, Robert J.1; Sanyal, Arun J.2; Mehta, Savant3; Doherty, Michael C.4; Neuschwander-Tetri, Brent A.5; Everson, Gregory T.6; Kahn, Jeffrey A.7; Malet, Peter F.8; Sheikh, Muhammad Y.9; Chung, Raymond T.10; Ghany, Marc G.11; Gretch, David R.12
Source: The American Journal of Gastroenterology, Volume 101, Number 5, May 2006 , pp. 983-992(10)
Publisher: Blackwell Publishing
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Abstract:
OBJECTIVES: The clinical significance of portal hypertensive gastropathy (PHG) in patients with compensated liver disease is not well established. The aim of this study was to determine the prevalence and correlates of PHG in a large cohort of patients with chronic hepatitis C virus (HCV) infection and bridging fibrosis/compensated cirrhosis entering the randomized phase of the Hepatitis C Antiviral Long-term Treatment against Cirrhosis trial (HALT-C).METHODS: The presence and severity of PHG in 1,016 HCV patients with no prior history of gastrointestinal bleeding was determined at surveillance endoscopy using the New Italian Endoscopy Club criteria.RESULTS: Overall, 37% of HALT-C patients had PHG with 34% having mild and 3% with severe changes. The mucosal mosaic pattern was identified in 33%, red marks in 15%, and gastric antral vascular ectasia (GAVE) features in only 3%. Independent correlates of PHG included biochemical markers of liver disease severity (lower serum albumin, higher bilirubin), portal hypertension (lower platelet count), insulin resistance (higher glucose), and non-African American race. Independent correlates of GAVE included a history of smoking, nonsteroidal anti-inflammatory drugs (NSAIDs) use within the past year, and higher serum bilirubin and glucose levels. There was a strong positive association between the presence of PHG and esophageal varices ( p < 0.0001). CONCLUSIONS: PHG is associated with the histological and biochemical severity of liver disease in patients with HCV and advanced fibrosis but is mild in most patients. The clinical relevance of these findings will be further explored during the randomized phase of the HALT-C study.(Am J Gastroenterol 2006;101:983–992)Document Type: Research article
DOI: 10.1111/j.1572-0241.2006.00461.x
Affiliations: 1: Division of Gastroenterology, University of Michigan Medical Center, Ann Arbor, Michigan 2: Division of Gastroenterology, Virginia Commonwealth University Health System, Richmond, Virginia 3: Gastroenterology Division, University of Massachusetts Medical Center, Worcester, Massachusetts 4: New England Research Institutes, Watertown, Massachusetts 5: Division of Gastroenterology and Hepatology, Saint Louis University School of Medicine, St. Louis, Missouri 6: Section of Hepatology, Division of Gastroenterology and Hepatology, University of Colorado School of Medicine, Denver, Colorado 7: Division of Gastrointestinal and Liver Diseases, Keck School of Medicine, University of Southern California, Los Angeles, California 8: Division of Digestive and Liver Diseases, University of Texas Southwestern Medical Center, Dallas, Texas 9: Division of Gastroenterology, University of California—Irvine, Irvine, California 10: Gastrointestinal Unit (Medical Services), Massachusetts General Hospital and the Department of Medicine, Harvard Medical School, Boston, Massachusetts 11: Liver Diseases Branch, 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, Maryland 12: Departments of Laboratory Medicine and Medicine, University of Washington, Seattle, Washington
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