Our analysis indicates that H. heilmannii gastritis is due to its transmission to humans by domestic animals or pets. Concomitant infections by H. heilmannii and H. pylori are very rare, and it is possible that H. heilmannii might protect from infection with H. pylori. However, the results of our retrospective analysis will have to be tested against those of a prospective study investigating the day-to-day situation of the individual patients in greater detail and also be compared with patients not infected with H. heilmannii.

Confusion in the nomenclature of gastric polyps and the resulting uncertainties regarding prognosis and treatment have made a new classification necessary, consisting of focal hyperplasia, polyp of manifold aetiology, adenoma, and benign hyperplasiogenic polyp, the latter the most common one, found only in the stomach. But 110 cases of polypoid mucosal changes could not be classified. These "polyps" grow to be at most 8 mm in diameter and are characterized histologically by non-inflammatory cysts of varying size located within the intact fundal glands. Possible causes are hamartoma or functional secretory disorders. These glandular cysts have not previously been described. They do not fit the pattern of cystic gastritis. The clinical significance lies in the differentiation from gastric polyposis.

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To elucidate conflicting evidence concerning the role of Helicobacter pylori (HP) in the evolution of gastric carcinoma, a retrospective analysis was performed on the corpus mucosa of gastric surgical specimens removed from patients with gastric carcinoma (n = 53) and pancreatic carcinoma (n = 45). Prevalence, activity and degree of chronic active gastritis (CAG) were investigated. Furthermore, proliferative activity was determined by the expression of the Ki67 antigen in epithelial cells of the neck region and the foveolae using immunohistochemistry. CAG and intestinal metaplasia were significantly more prevalent in patients with gastric than with pancreatic neoplasms. Degree and activity of CAG were higher in the group of patients with gastric carcinomas. Numbers of Ki67-positive nuclei were significantly higher in pronounced than in mild CAG. Our data are in keeping with the assumption that HP-associated CAG contributes to the development of gastric adenocarcinoma. As possible pathomechanism, it may be assumed that a conspicuously expressed inflammatory reaction triggers epithelial proliferation, with resulting higher vulnerability to mutagenic effects.