title: Is portal hypertension due to liver cirrhosis a major factor in the development of portal hypertensive gastropathy?
abstract: OBJECTIVE
  The gastric mucosa of patients with portal hypertension frequently manifests changes in its appearance that are readily identifiable by endoscopy. Many of these can be sources of bleeding, and some imply the presence of systemic disease. Although portal hypertension is critical in development of portal hypertensive gastropathy (PHG), the role that other factors might play in its pathogenesis is uncertain.
  
  
  METHODS
  Four groups of subjects were studied prospectively: 37 with portal hypertension due to cirrhosis, 26 noncirrhotic subjects with portal hypertension due to extrahepatic portal vein obstruction (PVO), nine cirrhotic patients with extrahepatic PVO, and 57 control subjects. The diagnosis in each case was based on a combination of clinical data, needle liver biopsy, ultrasonography, splenoportography, and upper GI endoscopy.
  
  
  RESULTS
  Snake skin, scarlatina rash, diffuse hyperemia, and diffuse bleeding were frequent endoscopic gastric findings in cirrhotic patients. These findings were seen less frequently in noncirrhotic patients with portal hypertension due to PVO than in cirrhotic patients (p< 0.0001). The highest incidence was seen in cirrhotic patients with PVO (P< 0.001). Positive correlations existed among the endoscopic findings, the clinical estimate of the cirrhosis severity (Child-Pugh grade), and the size and appearance of esophageal varices (Beppu score). No endoscopic findings of the gastric mucosa enabled one to distinguish between groups. Hypergastrinemia was present in cirrhotics with and without PVO but not in noncirrhotic patients with portal hypertension resulting from isolated PVO.
  
  
  CONCLUSIONS
  These findings suggest that the endoscopic findings of PHG are affected by the severity of the underlying liver disease and the presence or absence of coexisting PVO. There is no association between PHG and the presence of gastric varices. Thus, the development of the gastric lesions characteristic of PHG requires not only portal hypertension but also some other consequence of parenchymal liver disease.
authors.affiliation: Department of Gastroenterology, School of Medicine, Hacettepe University, Ankara, Turkey.
authors.forename: Y
authors.initials: Y
authors.lastname: Bayraktar
authors.forename: F
authors.initials: F
authors.lastname: Balkanci
authors.forename: B
authors.initials: B
authors.lastname: Uzunalimoglu
authors.forename: A
authors.initials: A
authors.lastname: Gokoz
authors.forename: T
authors.initials: T
authors.lastname: Koseoglu
authors.forename: F
authors.initials: F
authors.lastname: Batman
authors.forename: A
authors.initials: A
authors.lastname: Gurakar
authors.forename: D H
authors.initials: DH
authors.lastname: Van Thiel
authors.forename: B
authors.initials: B
authors.lastname: Kayhan
mesh_terms: D000328:Adult; D001706:Biopsy; D016145:Endoscopy, Digestive System; D004932:Esophageal and Gastric Varices / Q000175:diagnosis / Q000209:etiology*; D005215:Fasting / Q000097:blood; D005260:Female; D005755:Gastrins / Q000097:blood; D006801:Humans; D006975:Hypertension, Portal / Q000150:complications / Q000175:diagnosis / Q000209:etiology*; D008099:Liver / Q000000981:diagnostic imaging / Q000473:pathology; D008103:Liver Cirrhosis / Q000150:complications / Q000175:diagnosis; D008297:Male; D011172:Portography; D014463:Ultrasonography
chemical_list: D005755:Gastrins