CHRONIC TYPE-B GASTRITIS AS AN IMPORTANT DENOMINATOR OF PEPTIC-ULCER HEALING

Objective: To examine the influence of chronic type B gastritis in duo denal ulcer healing and the risk of duodenal ulcer relapse. Patients a nd methods: We studied 60 patients with Helicobacter pylori-associated duodenal ulcers who were randomly treated with either 40 mg omeprazol e twice a day for 10 days followed by 20 mg once a day till day 42, or a combination of omeprazole + 1 g amoxycillin twice a day for the fir st 10 days followed by 20 mg omeprazole once a day as monotherapy unti l day 42. Results: We followed 25 patients in the omeprazole group and 27 in the omeprazole + amoxycillin group. No patient was allowed to t ake any anti-ulcer medication during the follow-up. The cumulative rel apse rates within 12 months were 52% in the omeprazole group and 7% in the omeprazole + amoxycillin group, all in patients with persistent H . pylori infection. The 24-month cumulative relapse rates were 76 and 22%, respectively. Only two duodenal ulcer relapses occurred in patien ts in whom H. pylori had been eradicated and these were re-infected at the time of relapse. We studied the effects of treatment on gastritis by measuring various parameters before treatment, at the end of treat ment, 4 weeks after treatment, 1 year after treatment and 2 years afte r treatment, including the extent of gastritis (infiltration by lympho cytes and plasma cells), H. pylori colonization, gastritis activity, d egeneration of the gastric foveolar epithelium and gastric mucus deple tion, in two antral and two body biopsy specimens. All these parameter s were assessed on a score of 0-4. Duodenal ulcer relapses within 24 m onths were dependent on the gastritis score at the end of treatment (6 % 2, 61% 3, 91% 4), and on the H. pylori score 4 weeks after the end o f the treatment (9% 0, 62% 3, 92% 4). Conclusions: The data show that long-term eradication of H. pylori is possible with high-dose omeprazo le + amoxycillin treatment. In the case of persistent H. pylori infect ion, duodenal ulcer relapses depend on the extent of gastritis and the level of H. pylori colonization.