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Background: Adenocarcinoma of the gastro-oesophageal junction is rapidly increasing in incidence and there is much interest in precursor lesions. The aetiology of inflammation of the gastric cardia (carditis) and the concept of the cardia as a native zone of mucinous gastric glands are disputed., Aims: To investigate the relationship between the type of cardiac mucosa and carditis with various histological and clinical parameters., Methods: Ninety-eight sets of gastric biopsies (cardia, corpus, incisura and antrum) were obtained prospectively in young patients (median age 40 years) who presented to the outpatient clinic with symptoms of gastro-oesophageal reflux (n = 25) or other upper gastrointestinal symptoms. Patients with neoplasia or Barrett's oesophagus were excluded. The presence (n = 19) or absence of oesophagitis at endoscopy was recorded. The degree of inflammation, Helicobacter pylori density, intestinal metaplasia and atrophy were scored according to the Sydney classification and the type of cardiac mucosa (oxyntic or mucinous) was noted., Results: We found that carditis and mucinous-type cardiac mucosa were strongly associated with H. pylori-related gastritis (P = 0.00019 and P = 0.006, respectively) but not with clinical or endoscopic gastro-oesophageal reflux. Mucinous mucosa in the cardia was only seen in 17% of biopsies., Conclusion: H. pylori-related gastritis is associated with mucinous-type cardiac mucosa as well as with carditis. The former strongly points to expansion of mucinous cardiac mucosa in H. pylori gastritis. This probably represents metaplasia of oxyntic to mucinous mucosa and raises the possibility of a role in carcinogenesis of the gastro-oesophageal junction.

Background: The incidence of adenocarcinoma of the proximal stomach (cardia) is increasing. The pathophysiological processes underlying this trend are unclear. Normal cell turnover depends on cell proliferation being in balance with programmed cell death or apoptosis. It has been well documented that excessive proliferation potentiates the effects of any carcinogen that targets DNA. It is therefore accepted that excessive proliferation is a risk factor for subsequent neoplasia development., Aims: To compare apoptosis and proliferation in normal cardia tissue, carditis, and cardia intestinal metaplasia, and to determine the effect of Helicobacter pylori infection and gastro-oesophageal reflux disease., Methods: Biopsies from the cardia were obtained from consecutive dyspeptic patients and asymptomatic controls at the time of gastroscopy. Samples were assessed histologically and classified as normal, carditis, or cardia tissue with intestinal metaplasia. All samples were then examined, employing immunohistochemical techniques, for the presence of proliferating and apoptotic cells., Results: A total of 76 histological specimens were examined. There was a statistical significant difference in the proliferation index between controls and both carditis and cardia intestinal metaplasia, and also between carditis and cardia intestinal metaplasia. In contrast, there was a significant increase in the apoptotic index for carditis compared with controls, while that of intestinal metaplasia did not differ from controls. As a result, comparison of the apoptotic/proliferation ratios for each group revealed that, for both carditis and cardia intestinal metaplasia, the apoptotic index/proliferation index ratio is reduced significantly compared with controls, but as a result of different mechanisms., Conclusion: This study demonstrates that individuals with carditis and cardia intestinal metaplasia have alterations in epithelial cell kinetics. In particular, it shows that there is a persistent imbalance between proliferation and apoptosis, which may represent malignant potential.