Background-Helicobacter pylori is an independent risk factor for gastric cancer, and this association may be due to the bacterium causing reactive oxygen species mediated damage to DNA in the gastric epithelium. High dietary ascorbic acid intake may protect against gastric cancer by scavenging reactive oxygen species. Aims-To assess reactive oxygen species activity and damage in gastric mucosa in relation to gastric pathology and mucosal ascorbic acid level, and to determine the eVect of H pylori eradication on these parameters. Patients-Gastric biopsy specimens were obtained for analysis from 161 patients undergoing endoscopy for dyspepsia. Methods-Reactive oxygen species activity and damage was assessed by luminol enhanced chemiluminescence and malondialdehyde equivalent estimation respectively. Ascorbic acid concentrations were measured using HPLC. Results-Chemiluminescence and malondialdehyde levels in gastric mucosa were higher in patients with H pylori gastritis than in those with normal histology. Successful eradication of the bacterium led to decreases in both parameters four weeks after treatment was completed. Gastric mucosal ascorbic acid and total vitamin C concentrations were not related to mucosal histology, but correlated weakly with reactive oxygen species activity (chemiluminescence and malodialdehyde levels). Conclusions-Data suggest that reactive oxygen species play a pathological role in H pylori gastritis, but mucosal ascorbic acid is not depleted in this condition. (Gut 1998;42:768-771)

The 'intestinal' form of gastric cancer, which is the commonest type, develops against a background of chronic gastritis, atrophy, and intestinal metaplasia.1 2 Helicobacter pylori is the cause of (type B) chronic gastritis and has been shown in epidemiological studies to be a major risk factor for the development of gastric cancer.3-6 Increased mucosal cell proliferation increases the likelihood of the development of a neoplastic clone of epithelial cells7 where there is chronic epithelial injury associated with H pylori positive gastritis. However, little is known about cell proliferation in H pyloni associated gastritis. The aims of the study were, firstly, to compare antral mucosal cell proliferation in normal gastric mucosa with H pylori positive and negative chronic gastritis and, secondly, to determine the effect of H pylori eradication treatment on cell proliferation. MethodsPatients undergoing routine diagnostic endoscopy were recruited after informed consent. Those taking non-steroidal anti-inflammatory drugs, H2 antagonists, proton pump inhibitors, or bismuth salts, or those who had undergone gastric surgery, were excluded from the study. Using standard biopsy forceps, tissue specimens were taken from the gastric antrum (three) and corpus (two) for histological and immunohistochemical studies. The study was approved by the hospital ethical committee. HISTOLOGYTwo antral and two corpus biopsy specimens from each site were routinely processed, and stained with haematoxylin and eosin.H PYLORI H pylori status was determined using a modified Giemsa stain on the antral and corpus sections and a biopsy urease test (CLO/DeltaWest) on the third antral biopsy specimen. To establish eradication of the micro-organism, both tests had to be negative. IMMUNOHISTOCHEMISTRYTwo antral biopsy specimens for immunostaining were put immediately into RPMI (without L-Glutamine) (Gibco) containing bromodeoxyuridine (5 mg/10 ml). They were immersed in a waterbath for 60 minutes at 37°C then placed on filter paper and fixed in 346 on 10 May 2018 by guest. Protected by copyright.

Background-There is increasing evidence that reflux of bile plays a part in the pathogenesis of Barrett's oesophagus. Bile injury to the gastric mucosa results in a "chemical" gastritis in which oedema and intestinal metaplasia are prominent. Aim-To determine if patients with Barrett's oesophagus have more bile related changes in antral mucosa than patients with uncomplicated gastro-oesophageal reflux disease (GORD) or non-ulcer dyspepsia (NUD). Patients and methods-Patients were identified by a retrospective search of pathology records and those with a clinically confirmed diagnosis of either Barrett's oesophagus or reflux oesophagitis who had oesophageal and gastric biopsies taken at the same endoscopy and had no evidence of Helicobacter pylori infection entered the study. Control biopsies were taken from H pylori negative NUD patients. Antral biopsies were examined "blind" to clinical group and graded for a series of histological features from which the "reflux gastritis score" (RGS) and "bile reflux index" (BRI) could be calculated. The reproducibility of these histological scores was tested by a second pathologist. Results-There were 100 patients with Barrett's, 61 with GORD, and 50 with NUD. The RGSs did not diVer between groups. BRI values in the Barrett's group were significantly higher than those in GORD subjects (p=0.014) which in turn were higher than those in NUD patients (p=0.037). Similarly, the frequency of high BRI values (>14) was significantly greater in the Barrett's group (29/100; 29%) than in the GORD (9/61; 14.8%) or NUD (4/50; 8%) group. However, agreement on BRI values was "poor", indicating limited applicability of this approach. Conclusion-Patientswith Barrett's oesophagus have more evidence of bile related gastritis than subjects with uncomplicated GORD or NUD. The presence of bile in the refluxate could be a factor in both the development of "specialised" intestinal metaplasia and malignancy in the oesophagus. (Gut 2001;49:359-363) Keywords: Barrett's oesophagus; reflux gastritis; bile; duodenogastro-oesophageal reflux; intestinal metaplasia Barrett's oesophagus is widely considered to be a consequence of longstanding acid induced injury commencing as an erosive oesophagitis and progressing over years to columnar and intestinal metaplasia of the squamous epithelium. The process of metaplasia represents a non-neoplastic change in cellular phenotype which is thought to be a response to a sustained adverse environment.1 The change may be a consequence of somatic mutation in the epithelial stem cells or an epigenetic event whereby divergent diVerentiation in progeny cells produces the altered phenotype.2 Whatever the precise mechanism, the resulting cell lineage has a survival advantage over "native" epithelium so that selection pressures promote the emergence and dominance of the metaplastic population. Examples in the gastrointestinal tract include gastric metaplasia in the duodenum in response to acid injury, 3 intestinal metaplasia in the stomach in longstanding Helicobacte...