Impairment of gastric secretion modulation in duodenal ulcer and in long-term PPI treatment - Quantitative morphologic findings and pathophysiologic implications

Helicobacter pylori affects gastric secretion. This functional effect might have a morphometric counterpart. Therefore, the gastric cell secretory com partment was morphometrically assessed in different pathophysiologic condit ions related to Helicobacter pylori infection. Nineteen Helicobacter pylori -positive nonduodenal ulcer subjects, 15 omeprazole chronically treated sub jects, and 19 duodenal ulcer patients were studied against 19 controls. Som atostatin, gastrin, enterochromaffin-like, and parietal cell density was as sessed in gastric biopsies. No differences in any cell type density were fo und between Helicobacter pylori-positive nonduodenal ulcer subjects and con trols. On the contrary, differences were significant when comparing omepraz ole and duodenal ulcer patients to controls (higher density of gastrin, ent erochromaffin-like, and parietal cells, lower density of somatostatin cells ). In duodenal ulcer a reversion to control values followed Helicobacter py lori eradication and ulcer healing. A direct linear correlation between ent erochromaffin-like, gastrin, and parietal cell density was demonstrated. An almost complete map of mucosal cells involved in gastric secretion is prov ided by this study. The cell density pattern, identical to the omeprazole g roup, points to an impaired feedback control of secretion in duodenal ulcer . The reversion to control values after Helicobacter pylori eradication and ulcer healing demonstrates the pathogenetic role of Helicobacter pylori-ho st interaction in these changes.