INFLAMMATORY RESPONSES AND INTENSITY OF HELICOBACTER-PYLORI INFECTION IN PATIENTS WITH DUODENAL AND GASTRIC-ULCER - HISTOPATHOLOGIC ANALYSIS WITH A NEW STAIN

Background: The basic histopathologic patterns of Helicobacter pylori gastritis have been described, but the details of the interaction between bacteria, epithelial cells and inflammatory cells are poorly understood. One of the limiting factors is the lack of a staining technique allowing the simultaneous visualization of bacteria and the morphologic details of the infected mucosa. Purpose: To use a new stain to analyze intensity and distribution of H. pylori and gastritis in patients with H. pylori gastritis without ulcer, with duodenal ulcer, and with gastric ulcer, in an attempt to elucidate the role of H. pylori in the pathogenesis of peptic ulcer disease. Methods: patients underwent esophagogastro-duodenoscopy and gastric biopsies were obtained from 3 sites on the antral lesser curvature, 2 on the antral greater curvature, and 6 on the corpus. Formalin-fixed biopsy specimens were processed, oriented, embedded in paraffin, cut in 4-mu m sections and stained with a combined stain developed in our laboratory (a combination of hematoxylin and eosin with a silver stain and Alcian Blue at pH2.5). This stain allows the simultaneous visualization of H. pylori, the gastric mucosal morphology, and the inflammatory infiltrate. Density of H. pylori, neutrophils and mononuclear cells were scored on each specimen using a scale from 0 to 5. Results: Density and distribution of H. pylori were essentially similar in the non-ulcer infected patients and in patients with gastric ulcer. Patients with duodenal ulcer had a higher density of bacteria in the antrum than in the corpus. All patients had significantly greater inflammatory responses in the antrum than in the corpus, but this gradient was much more pronounced in patients with duodenal ulcer than in those with gastric ulcer and those with no ulcer. Surprisingly, the strongest intensity of gastritis (both in the antrum and corpus) was found in this latter group. Conclusions: The gastritis gradient is more important than the intensity of inflammatory responses per se in determining the outcome of H. pylori infection with respect to the development of peptic ulcer. Larger studies, using new methodologies that allow a better assessment of the numbers of bacteria in the gastric mucus, should be performed to better elucidate the relationship between magnitude of infection, intensity of the mucosal inflammatory responses, and outcome of H. pylori gastritis.