Effect of Helicobacter pylori eradication on histologic lesions of gastric mucosa.: An 18-month follow-up study

Objective. To evaluate the effect of Helicobacter pylori eradication on pathologic lesions over the gastric mucosa during an 18-month follow-up period. Patients and methods. A total of 122 duodenal ulcer patients infected with H. pylori were prospectively studied. Patients were randomized to receive: ranitidine alone, ranitidine plus antibiotics, or bismuth plus antibiotics. An endoscopy was performed at 3, 6, 12 and 18 months. Haematoxylin-eosin, Giemsa, and Warthin-Starry staining methods were used. Histologic lesions were classified according to the following score: normal (0); superficial chronic gastritis (CG): mild (0.5), moderate (1) and severe (1.5); atrophic CG: mild (2), moderate (3) and severe (4); intestinal metaplasia: absence (0), mild (1), moderate (2) and severe (3). The acute inflammatory activity (active CG) was scored from 0 to 3 (absence, mild, moderate, severe) regarding: inflammatory density in the lamina propria, density of polymorphonuclear leukocytes in the lamina propria, density of intra-epithelial polymorphonuclear leukocytes and superficial erosions. Results. H. pylori eradication was achieved in 31% of patients (0% in the group of ranitidine alone and 48% in patients who received antibiotics). The score corresponding to CG declined progressively after H. pylori eradication, with average values of 2.1+/-1.3, 1.98 +/- 1.4, 1.73 +/- 1.6, 1.43 +/- 1.9 and 1.38 +/- 1.9 (p < 0.0001) at 0, 3, 6, 12 and 18 months, respectively. The corresponding score for active CG also improved progressively after eradication: 7.82 +/- 1, 2.51 +/- 0.7, 1.24 +/- 0.6, 0.45 +/- 1.6 and 0.12 +/- 0.5 (p < 0.0001). Nevertheless, no changes were observed regarding atrophia or intestinal metaplasia conditions. Conclusions. H. pylori eradication is associated with a histologic improvement of gastric mucosa. It begins early and continues for the 18 months after therapy. The improvement in the overall inflammatory component is slow and progressive. In contrast, improvement of the acute component in gastritis is more marked early, and is observed immediately after eradication. Nevertheless, H. pylori eradication is not followed by an improvement in atrophy or intestinal metaplasia.