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  • Title: Effect of Helicobacter pylori eradication on gastric histology, serum gastrin and pepsinogen I levels, and gastric emptying in patients with gastric ulcer.
    Author: Maconi G, Lazzaroni M, Sangaletti O, Bargiggia S, Vago L, Bianchi Porro G.
    Journal: Am J Gastroenterol; 1997 Oct; 92(10):1844-8. PubMed ID: 9382049.
    Abstract:
    OBJECTIVE: The evolution of gastritis and the behavior of basal and meal-stimulated gastrin release, pepsinogen levels, and gastric emptying of solids were studied in a series of consecutive patients with Helicobacter pylori-positive, uncomplicated, non-NSAID-related type I gastric ulcer over a follow-up period of 3 months after eradication therapy was begun. METHODS: Before starting treatment (consisting of omeprazole 40 mg a day for 1 month and amoxycillin 1 g three times daily for 14 days), and for 3 months after ulcer healing, 16 patients had a series of functional examinations, including basal and meal-stimulated serum gastrin concentration, serum pepsinogen I levels, evaluation of gastric emptying of solids by means of serial ultrasonographic measurement of the gastric antrum area, and histological assessment of antral and corpus gastritis. RESULTS: Double therapy resulted in the successful eradication of H. pylori in eight of 16 evaluable patients. In the group of H. pylori-eradicated patients, the mean scores of gastritis activity and inflammation in the antrum and corpus had fallen, 3 months after eradication. No significant changes in mean gastritis scores were observed in the case and control group with regard to intestinal metaplasia and atrophy in the antrum and corpus. In H. pylori-eradicated patients, the integrated gastrin response to meal, but not fasting gastrin concentration, fell significantly during follow-up, and serum pepsinogen I levels significantly decreased, compared with baseline. In contrast, the fasting and maximal antral area and the gastric emptying of solids remained unchanged over time. In the control group (but not the H. pylori-eradicated group), no significant modifications of any of the above-mentioned parameters were observed during follow-up. CONCLUSION: Our findings suggest that in non-NSAID-related type I gastric ulcers, the eradication of H. pylori significantly reduces gastritis activity and inflammatory scores, but not atrophy and intestinal metaplasia, and modifies gastrin and pepsinogen I release in a short follow-up period. In contrast, H.pylori eradication does not significantly affect gastric emptying of solids, at least within a period of 3 months from therapy.
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