title: Development and progression of portal hypertensive gastropathy in patients with chronic hepatitis C.
abstract: OBJECTIVE
  The objective of this study was to determine the incidence and risk factors associated with new-onset and worsening portal hypertensive gastropathy (PHG) in patients with chronic hepatitis C (CHC).
  
  
  METHODS
  A total of 831 CHC patients with bridging fibrosis or cirrhosis at the time of entry were prospectively monitored for clinical and histological liver disease progression while receiving either low-dose peginterferon α2a or no antiviral therapy in the HALT-C (Hepatitis C Antiviral Long-term Treatment against Cirrhosis) trial. Upper endoscopy with grading of PHG was performed at baseline and at year 4 of the study. The presence and severity of PHG were determined using the NIEC (New Italian Endoscopy Conference) criteria, and worsening PHG was defined as a score increase of ≥1 point.
  
  
  RESULTS
  During a median follow-up of 3.85 years, 50% of 514 subjects without PHG developed new-onset PHG, whereas 26% of 317 patients with baseline PHG had worsening PHG. Independent predictors of new-onset PHG included higher alkaline phosphatase and being diabetic, whereas predictors of worsening PHG were Caucasian race, lower albumin, as well as higher serum aspartate transaminase/alanine transaminase ratio and homeostatic model assessment levels. New-onset and worsening PHG were significantly associated with clinical and histological progression. They were also associated with new-onset and worsening gastroesophageal varices.
  
  
  CONCLUSIONS
  New-onset and worsening PHG develop at a rate of 12.9% per year and 6.7% per year, respectively, in non-responder CHC patients with advanced fibrosis. If confirmed in other studies, endoscopic surveillance for PHG may need to be tailored to individual patient risk factors.
authors.affiliation: Division of Gastroenterology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA. rfontana@med.umich.edu
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Fontana
authors.forename: Arun J
authors.initials: AJ
authors.lastname: Sanyal
authors.forename: Marc G
authors.initials: MG
authors.lastname: Ghany
authors.forename: Herbert L
authors.initials: HL
authors.lastname: Bonkovsky
authors.forename: Timothy R
authors.initials: TR
authors.lastname: Morgan
authors.forename: Heather J
authors.initials: HJ
authors.lastname: Litman
authors.forename: Andrea E
authors.initials: AE
authors.lastname: Reid
authors.forename: William M
authors.initials: WM
authors.lastname: Lee
authors.forename: Deepa
authors.initials: D
authors.lastname: Naishadham
mesh_terms: D000998:Antiviral Agents / Q000627:therapeutic use; D018450:Disease Progression; D004932:Esophageal and Gastric Varices / Q000209:etiology / Q000473:pathology; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000188:drug therapy; D006801:Humans; D006975:Hypertension, Portal / Q000150:complications*; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use; D008103:Liver Cirrhosis / Q000150:complications / Q000821:virology; D011092:Polyethylene Glycols / Q000627:therapeutic use; D011994:Recombinant Proteins; D013272:Stomach Diseases / Q000209:etiology* / Q000473:pathology*
chemical_list: D000998:Antiviral Agents; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; C100416:peginterferon alfa-2a