IS PORTAL-HYPERTENSION DUE TO LIVER-CIRRHOSIS A MAJOR FACTOR IN THE DEVELOPMENT OF PORTAL HYPERTENSIVE GASTROPATHY

Citation
Y. Bayraktar et al., IS PORTAL-HYPERTENSION DUE TO LIVER-CIRRHOSIS A MAJOR FACTOR IN THE DEVELOPMENT OF PORTAL HYPERTENSIVE GASTROPATHY, The American journal of gastroenterology, 91(3), 1996, pp. 554-558
Citations number
16
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
00029270
Volume
91
Issue
3
Year of publication
1996
Pages
554 - 558
Database
ISI
SICI code
0002-9270(1996)91:3<554:IPDTLA>2.0.ZU;2-P
Abstract
Objectives: The gastric mucosa of patients with portal hypertension fr equently manifests changes in its appearance that are readily identifi able by endoscopy. Many of these can be sources of bleeding, and some imply the presence of systemic disease. Although portal hypertension i s critical in development of portal hypertensive gastropathy (PHG), th e 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 po rtal hypertension due to extrahepatic portal vein obstruction (PVO), n ine cirrhotic patients with extrahepatic PVO, and 57 control subjects. The diagnosis in each case was based on a combination of clinical dat a, 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 cir rhotic patients. These findings were seen less frequently in noncirrho tic patients with portal hypertension due to PVO than in cirrhotic pat ients (p < 0.0001). The highest incidence was seen in cirrhotic patien ts with PVO (p < 0.0001). Positive correlations existed among the endo scopic findings, the clinical estimate of the cirrhosis severity (Chil d-Pugh grade), and the size and appearance of esophageal varices (Bepp u 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 hyp ertension resulting from isolated PVO. Conclusion: These findings sugg est that the endoscopic findings of PHG are affected by the severity o f the underlying liver disease and the presence or absence of coexisti ng PVO. There is no association between PHG and the presence of gastri c varices. Thus, the development of the gastric lesions characteristic of PHG requires not only portal hypertension but also some other cons equence of parenchymal liver disease.