CONGESTIVE GASTROPATHY - FACTORS INFLUENCING DEVELOPMENT, ENDOSCOPIC FEATURES, HELICOBACTER-PYLORI INFECTION, AND MICROVESSEL CHANGES

Objectives: To study 1) the factors influencing the development of con gestive gastropathy (CG) in patients with portal hypertension (PHT), 2 ) the changes in gastric microvessels in patients with PHT with and wi thout CG, and 3) to determine whether Helicobacter pylori plays any ro le in the pathogenesis of CG. Methods: One hundred eighteen patients w ith PHT (102 cirrhosis, 16 noncirrhotic portal fibrosis) were evaluate d by videogastroscopic examination. Antral biopsy tissue was examined for microvessel changes, histological gastritis, and H. pylori infecti on in 85 of 118 patients and 45 controls. Portal venous pressure (PVP) was determined by hepatic venous pressure gradient in 17 patients wit h CG. Results: CG was present in 71 (60%) patients with PHT, of whom 4 1 (58%) had mild and 30 (42%) had severe CG. CG was observed with equa l frequency in cirrhosis (63%) and noncirrhotic portal fibrosis (44%). The incidence of CG was higher in patients with severe liver disease, a past history of hemetemesis, in those with esophageal varices, and in those with gastric varices. Severe CG was commonly observed in pati ents with large size esophageal varices and in those with gastric vari ces, There was significant dilation of gastric mucosal vessels in pati ents with PHT, but in this regard there was no significant difference between patients with and without CG. The presence of H. pylori, histo logical gastritis, degree of PVP, or degree of capillary dilation did not influence the severity of CG. Conclusions: CG occurs commonly in p atients with PHT, especially those with severe liver disease, past his tory of hemetemesis, and esophagogastric varices. Patients with PHT ha ve significant gastric microvessel changes. The severity of CG appears to be independent of PVP, capillary dilation, H. pylori infection, or histological gastritis.