THE EFFECTS OF HELICOBACTER-PYLORI COLONIZATION ON GASTRIC FUNCTION AND THE INCIDENCE OF PORTAL HYPERTENSIVE GASTROPATHY IN PATIENTS WITH CIRRHOSIS OF THE LIVER

Objectives: To investigate the prevalence of Helicobacter pylori infec tion in 50 cirrhotic patients with biopsy-proven cirrhosis with and wi thout portal hypertensive gastropathy and to study whether or not the effects of H. pylori colonization of the stomach on gastric acid and p epsin secretion, serum gastrin and pepsinogen I levels, gastric mucus, and gastric emptying contributed to the development of portal hyperte nsive gastropathy in cirrhotics. Methods: All patients underwent an up per GT endoscopy followed by determination of basal and pentagastrin a nd insulin-stimulated gastric acid and pepsin secretion and serum gast rin and pepsinogen I levels. The gastric biopsies were stained to dete ct H. pylori infection, portal hypertensive gastropathy, and gastritis . The amount of gastric mucus was estimated by a microanalytical techn ique. The rate of gastric emptying was assessed by the radionuclide me thod using a semi-solid meal. Results: Thirty-three (66%) patients had endoscopic evidence of portal hypertensive gastropathy, 10 with the s evere (20%) and 23 with mild form (46%). Twenty (40%) patients had his tological evidence of H. pylori infection. Eleven out of 33 (33%) pati ents with endoscopic portal hypertensive gastropathy had microscopic e vidence of H. pylori infection. Eighteen out of 20 (90%) patients with chronic active gastritis had concomitant H. pylori colonization. In c ontrast, the gastric mucosa was histologically normal in 21 of the 30 patients (70%) not infected with H. pylori. Marked hypochlorhydria and reduced pepsin secretion associated with a tendency to hypergastrinem ia were observed in cirrhotic patients colonized with H. pylori compar ed with those without. However, there was no significant difference in serum pepsinogen I concentrations, the ratio of polymeric to degraded gastric mucus, or the rate of gastric emptying between cirrhotics wit h and without H. pylori colonization of the stomach. Furthermore, thes e parameters were not significantly different in patients with portal hypertensive gastropathy with and without H. pylori infection. Conclus ion: These observations suggest that H. pylori infection is unlikely t o be involved in the pathogenesis of portal hypertensive gastropathy.