No abstract

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...

Infirmary at Leeds, Leeds summARY A total of 98 patients who had either undergone gastric surgery (23) or who had peptic ulcers (56), or who had normal endoscopic findings (19), all underwent gastric biopsy, together with measurement of pH and total bile acid concentration in their fasting gastric juice. The biopsy specimens were graded "blind" for the presence of foveolar hyperplasia; oedema and smooth muscle fibres in the lamina propria; vasodilation and congestion of superficial mucosal capillaries; and a paucity of both acute and chronic inflammatory cells in the belief that these features constituted a distinctive histological picture related to reflux of alkaline duodenal content into the stomach.We found a strong association between severe grades of each of these histological variables and both hypochlorhydria (pH > 4) and increased bile acid concentrations in the stomach. Furthermore, when the individual grades were added together to give a composite "reflux score," there was a significant difference in the incidence of hypochlorhydria (p < 0'01) and raised bile acid concentrations (p < 0'005) between those patients with a reflux score above and below 10. Although we do not claim that reflux is invariably accompanied by a distinctive histological picture, we suggest that recognition of this hitherto poorly documented combination of features as reflux gastritis may assist in the selection of patients for specific treatment and minimise the overdiagnosis of premalignant dysplasia (with which the lesion may be confused) in the postoperative stomach.

To determine the relevance of gastric juice factors to gastric carcinogenesis, 56 patients with unoperated stomachs undergoing endoscopy for dyspepsia had gastric juice aspirated and analysed for pH, ascorbic acid, total bile acids, nitrite, nitrate and total nitroso compounds (NOCs). Plasma was obtained for vitamin C estimation. Antral and body biopsies were assessed for gastritis, Helicobacter pylori, atrophy and intestinal metaplasia (IM). Patients with chronic atrophic gastritis (n = 17) had lower gastric juice ascorbic acid concentrations (P less than 0.001), higher pH (P less than 0.05) and higher incidence of H. pylori infection (P less than 0.001) than normal subjects (n = 12). Patients with reflux gastritis (n = 9) had higher total bile acids (P less than 0.01). Patients with chronic gastritis and IM (n = 11) had higher gastric juice pH (P less than 0.01) and total bile acid concentrations (P less than 0.05), and lower gastric ascorbic acid concentrations (P less than 0.01) than those with chronic gastritis and no IM (n = 24). In chronic gastritis, high nitrite concentrations were associated with high pH (P less than 0.01). However, there were no significant differences in plasma vitamin C or gastric nitrite, nitrate or total NOC concentrations in relation to gastric histology. We conclude that the premalignant condition IM is associated with H. pylori infection, low gastric ascorbic acid levels and elevated total bile acids, but not to elevation in nitrite or total NOCs in fasting gastric juice.