Prevalence of gastric metaplasia in the duodenal bulb and distribution of Helicobacter pylori in the gastric mucosa. A clinical and histopathologicalstudy in 96 consecutive patients

Background, Consecutive untreated patients with duodenal ulcer (n=49) or ga stric ulcer (n=47) were compared with regard to the presence of gastric met aplasia in the duodenal bulb, gastric distribution of Helicobacter pylori a nd histopathological findings to assess differences which may contribute to either duodenal ulcer or gastric ulcer development. Methods. Serial sections of corpus, antral and duodenal mucosal biopsies we re stained by haematoxylin-eosin stain for histopathological evaluation, im munohistochemistry for the detection of Helicobacter pylori, and duodenal b iopsies alone by the PAS/Alcian blue stain to assess the presence of gastri c metaplasia in the duodenal bulb. Results. Helicobacter pylori was found in 81.6% of duodenal ulcer and in 83 .0% of gastric ulcer patients. In duodenal ulcer and gastric ulcer patients , Helicobacter pylori was found in 79.6% and 79.5% of corpus, 77.6% and 72. 3% of antral, and 16.7% and 20.0% of duodenal bulb biopsies, respectively. In duodenal ulcer patients, the density of Helicobacter pylori was signific antly lower in corpus compared to antrum biopsies (p<0.001). Furthermore, t he Helicobacter pylori density was higher in corpus of gastric ulcer than o f duodenal ulcer patients. Inflammatory scores followed the density of Heli cobacter pylori infection. In the duodenal bulb of both duodenal ulcer and gastric ulcer patients, the occurrence and extent of gastric metaplasia wer e comparable. Gastric metaplasia was present in 5 out of 8 Helicobacter pyl ori positive duodenal biopsies of duodenal ulcer patients and in 3 out of 9 Helicobacter pylori positive duodenal biopsies of gastric ulcer patients. Conclusions, No evidence was found for a role of gastric metaplasia in. the differential pathogenesis of duodenal ulcer or gastric ulcer Differences i n the gastric topography of Helicobacter pylori density and inflammatory sc ores between duodenal ulcer and gastric ulcer may contribute to differences in development and presentation of both peptic ulcer conditions.