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The production of tumour necrosis factor a (TNF a) and interleukin-6 by human antral mucosa during short term culture in vitro has been measured by enzyme linked immunosorbent assay. TNF a and interleukin-6 concentrations in culture supernatants were significantly greater (p<0001) in patients infected with Helicobacter pylon, all of whom had chronic gastritis, than in patients who were H pylori negative with histologically normal gastric mucosa. Among H pylon colonised patients, TNF a concentrations were significantly higher in those with active gastritis and neutrophil infiltration into the epithelium than in those with inactive gastritis. In contrast, interleukin-6 concentrations were raised in both active and inactive gastritis. This study shows that H pylon gastritis is associated with increased gastric mucosal production of TNF a and interleukin-6 and that the nature of the mucosal cytokine response varies with the immunohistology of the disease. Inflammatory cytokines generated locally within the gastric mucosa could be relevant to the gastric physiology of H pylon infection.

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Duodenal biopsy specimens from 471 adults and 47 children were examined to determine the prevalence and distribution of gastric epithelium in the duodenal bulb in relation to age, gender, gastroduodenal inflammation, smoking, alcohol and consumption of nonsteroidal anti-inflammatory drugs (NSAID). Gastric metaplasia was present in the anterior wall duodenal biopsy specimen in 31%, was significantly less common in patients under 17 than in adults, and was more common in males than females. In sixty two adults who underwent multiple radial duodenal biopsy gastric metaplasia was randomly distributed around the duodenal circumference; sixty three per cent of the patients with gastric metaplasia found on multiple biopsy were detected by just the anterior biopsy. Gastric elium'245 and is therefore able to infect the duodenum only when gastric metaplasia is present. We have proposed that the combination of H pylori and gastric metaplasia induced by acid are the prerequisites for the development of active duodenitis, and that this inflammation impairs mucosal defences, leading ultimately to duodenal ulceration.6Duodenal ulcer is a multifactorial condition.7 The aetiology is closely related to enhanced acid secretion, but has been found to be influenced by many other factors including gender, genetic predisposition, alcohol consumption, drug intake, smoking, and most recently H pylori infection. Some of these factors may also affect the occurrence of metaplastic gastric epithelium in the duodenum and consequently influence susceptibility to duodenitis and ulceration.The aim of this study was to investigate the prevalence and distribution of gastric epithelium in the duodenum in relation to age, gender, alcohol consumption, smoking, fasting gastric juice pH, ingestion of nonsteroidal anti-inflammatory drugs (NSAID) and gastroduodenal inflammation. Methods Four hundred and seventy one patients with dyspepsia who had upper gastrointestinal endoscopy with biopsy performed at defined sites as part of three dyspepsia studies were investigated. The studies had been approved by the hospital ethical committees and the patients had given informed consent. (These patients include 252 of the patients in a previous study.4) All of the patients (aged 18-84, 209 of them male) had a biopsy specimen taken from the anterior wall of the first part of the duodenal mucosa as well as specimens from constant sites in the antral and body gastric mucosa.To determine the distribution of gastric epithelium in the duodenum and to estimate

The prevalence of Helicobacter pylori was determined using an ELISA technique for IgG antibodies to H. pylori in 76 patients with end-stage renal failure who were receiving regular haemodialysis and 202 patients with functioning renal transplants. Twenty-seven (34%) of the haemodialysis group and 58 (29%) of the transplant group were positive for H. pylori IgG antibodies, and the prevalence did not differ significantly from that in 247 age-matched healthy controls. In the haemodialysis group, patients positive for H. pylori were older, median age 60 years (range 22–73), compared to those patients without H. pylori antibodies, median age 52 years (range 22–75), p < 0.05, more suffered from dyspeptic symptoms, 35 vs. 10% (p < 0.01), yet fewer had been prescribed aluminium-containing antacids, 38 vs. 78% (p < 0.01). In the transplanted group, those positive for H. pylori were more symptomatic for dyspepsia, 30 vs. 11% (p < 0.01), and had lower serum creatinine values, 136 ± 10 μmol/l (mean ± SEM) vs. 172 ± 12 μmol/l (p < 0.05), compared to those without H. pylori antibodies. Almost all the transplant patients with H. pylori antibodies were taking steroids (98%) compared to 84% of those without antibodies (p < 0.05). The prevalence of antibodies to H. pylori in this study was increased in symptomatic dyspeptic subjects and reduced in those patients prescribed aluminium-containing phosphate binders.