SUMMARY The presence of Campylobacterpylori, histologically diagnosed gastritis, and antibodies to C pylori were determined in a series of 113 patients undergoing endoscopy. Paired biopsy specimens from the fundus, body, and antrum were collected from 59 patients and from the antrum of 54 patients. The presence of Cpylori was confirmed by either culture or silver stain in 30 of 59, 31 of 59, and 54 of 103 biopsy specimens from the fundus, body, and antrum, respectively. Ofthe specimens which contained C pylori 20 of 30 (66%) from the fundus, 25 of 31 (80%) from the body, and 54 (100%) from the antrum showed gastritis. Cpylori and gastritis were shown in seven of nine (78 1 %) of patients with gastric ulcers and in nine of 11 (82%) of patients with duodenal ulcers. Using an enzyme linked immunosorbent assay (ELISA) technique to detect IgG antibody to C pylori, all patients with histologically diagnosed gastritis and organisms present had titres of > 640; eight of 39 (21 %) ofpatients without gastritis and without organisms gave similar titres. Hence the presence of C pylori was associated with gastritis and with raised titres of IgG antibody. Spiral organisms have been described in the stomach of man and other animals by several authors since the 1920s.`5 Following the reports of Warren6 and Marshall7 there has been an increase in interest in the organism which these authors named C pyloridis and which has since been redesignated C pylori.8 These Campylobacter-like organisms and others9 have been isolated from gastric biopsy specimens using techniques which were developed for the isolation of intestinal campylobacters.Despite the profusion of short reports there have been few detailed substantiative prospective studies, especially in Great Britain. We therefore present the results of our study in which 113 patients were investigated endoscopically, histologically, bacteriologically and serologically. Part of this study was designed to determine the distribution of Campylobacter-like organisms in infected or colonised stomachs, an aspect which has not clearly been established. The survey was also undertaken so that we could substantiate the association of these organisms with histologically diagnosed gastritis, gastric, and duodenal peptic ulceration. Furthermore, we inves-

Endoscopically sited gastric mucosal biopsies were taken from 98 patients with hepatic cirrhosis, and from 48 control patients. Nineteen patients with cirrhosis were found to have gastric ulcers, including eight with multiple erosions. In four of these eight, erosions were shown to arise in histologically normal mucosa. Among the remaining 79 patients with cirrhosis, the prevalence of chronic gastritis was not increased compared with controls of the same age-group. There was no increase in chronic gastritis in patients with alcoholic cirrhosis compared with either controls or patients with chronic active hepatitis and cirrhosis. The increased proneness of patients with cirrhosis to acute and chronic gastric mucosal lesions cannot be explained on the basis of an underlying chronic gastritis.