Ultrastructural examination of biopsies showing Helicobacter pylon associated chronic gastritis reveals close attachment between gastric surface epithelial celis and the organism. The finding of 'adhesion pedestals', which represents a cellular response to the presence of the organism, is analogous to the response ofintestinal cells to enteropathogenic E coli. Thus the development of bacterial attachment sites in H pylori associated gastritis might be an indication of pathogenicity. We have therefore explored the relationship between the proportion of organisms forming attachment sites and histological indices of disease 'activity'. Antral biopsies from 40 patients with Hpyloni positive gastritis were examined histologically and ultrastructurally, and the percentage of attached organisms compared with subjective assessments of epithelial degeneration, mucin depletion, polymorphonuclear and chronic inflammatory cell infiltration. We found a significant increase in the proportion of attached bacteria in cases showing histological epithelial degeneration, and a significant decrease in cases showing intraepithelial polymorph infiltration. The direct relationship between bacterial attachment and cellular degeneration lends further support to a pathogenic effect. Reduced attachment in the face of polymorph infiltration might indirectly reflect aspects of the immune responsenamely, blocking of adhesion by IgA, with complement activation and generation of leucotactic factors.

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Aim: To determine associations between enterogastric bile reflux and gastric mucosal pathology. Method: A retrospective study using fasting gastric juice bile acid measurements and antral or prestomal biopsy specimens from 350 patients, 66 of whom had previously undergone surgery that either bypassed or disrupted the pyloric sphincter.Results: Bile reflux was positively associated with reactive gastritis and negatively with Helicobacter pylon density. After stratification for previous surgery, age, and H pylon status, the histological feature most strongly associated with bile reflux was intestinal metaplasia, including all its subtypes. The aim of this study was therefore to determine the role of bile reflux in the causation of gastric mucosal pathology, specifically controlling for the presence of H pylon, in patients both with and without previous gastric surgery. A large study population was required to disentangle the effects of bile reflux from those of H pyloni infection. We achieved this by performing a meta analysis on gastric biopsy results and gastric juice bile acid measurements obtained during the course of our studies over the past 10 years. In particular, we sought to examine more closely the association we have previously reported between bile reflux and reflux or reactive gastritis, to report on the relative importance of the individual components of the histological reflux score we have previously proposed,' and to confirm and further explore the association between bile reflux and intestinal metaplasia. We also attempted to derive a histological index predicting the presence of abnormal bile reflux. MethodsBiopsy and gastric juice bile acid results were available from 350 patients who had participated in five published studies.'45-7 The 168 patients in the first three studies had been selected for their known pathology or previous gastric surgery; 60 of these had also undergone surgery that had destroyed or bypassed the pylorus. The fourth study comprised 135 consecutive patients attending an open access endoscopy clinic, excluding those with neoplastic disease. The 47 patients in the last study were attending diagnostic endoscopy lists and were selected on criteria of convenience of the timing of sample collection and of absence of previous gastric surgery. All patients had at least two biopsy specimens taken from the antrum, or in the 35 with Billroth gastrectomies, from the remnant of stomach within 5 cm of the stoma.All patients gave informed consent. The studies were individually approved by the local research ethics committee.Gastric juice was aspirated through a nasogastric tube in the first two studies, and at the time of endoscopy in the latter three. Bile acid concentration was then determined by the steroid dehydrogenase method8 in the same laboratory throughout.The biopsy specimens were fixed in 10% formalin. After routine processing sections were taken at three levels and stained with haematoxylin and eosin. Additional sections were stained with alcian blue (pH 2 5) and pe...

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Ascorbic acid, the reduced form of vitamin C, may protect against gastric cancer and is secreted by the normal stomach. Secretion is impaired in Helicobacter pylori (H pylon) associated chronic gastritis. This study examined if eradication of H pylon improves gastric juice ascorbate values. Fasting gastric juice and plasma samples were collected at endoscopy from patients participating in trials of H pylori eradication for duodenal ulcer disease and intestinal metaplasia before and up to 15 months after attempted eradication. Ascorbic acid and total vitamin C concentrations were determined by high performance liquid chromatography. In 12 patients in whom H pylon was successfully eradicated gastric juice ascorbate and total vitamin C concentrations and the ratio of juice to plasma vitamin C rose after treatment. Analysis after treatment suggested that the rise was greatest in patients with high final plasma vitamin C concentrations, even though these did not change with treatment. By contrast, in 22 patients in whom H pylon eradication was unsuccessful there were no significant changes in juice or plasma concentrations after treatment. It is concluded that successful eradication of H pylori improves secretion of vitamin C into gastric juice. It is speculated that this increases protection against gastric cancer.