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Unlabelled: Aim of the present study has been to investigate the possible modifications of peptic secretion after a period with H2 blockers and omeprazole, evaluating in the same patient pepsinogen group A levels in gastric mucosa and pepsin in gastric juice. 54 active duodenal ulcer were studied: during an upper gastrointestinal endoscopy a sample of gastric juice and one fundus biopsy were taken before and after four weeks 300 mg/daily ranitidine (23 patients), 40 mg/daily famotidine (7 patients), 300 mg/daily nizatidine (12 patients) therapy and 40 mg/daily omeprazole (12 patients) therapy., Results: H2-blockers and omeprazole treatment determines a non statistically significant decrease of pepsin in gastric juice and in pepsinogen group A in gastric mucosa.

The clinical course of gastric and duodenal ulcer and the efficacy of H2 blockers in ulcer healing and the prevention of relapse in cirrhotic liver patients were studied. Seventy-four cirrhotic patients with endoscopically proven acute gastric ulcer (30), duodenal ulcer (34) or a combination of both gastric and duodenal ulcers (10) were treated for six weeks with either Cimetidine 800 mg/daily (27) or Ranitidine 300 mg/daily (47). Of the 77 patients 49 (66.2%) were healed after therapy, 11 cases (14.8%) remained unhealed even after two additional cycles of the same treatment and four were lost to follow-up. After an endoscopically proven healing of the active ulcer, 51 patients took part in the long-term study over a mean period of 24 months: 21.5% of the 27 patients were treated with a maintenance dosage of H2 blockers and 29.1% of the 24 patients left without therapy relapsed during the first year. We conclude that the ulcer healing rate with H2 blockers is lower and the relapse rate higher in cirrhotic patients than in the general ulcer population.

The effects of Nizatidine, an H2-receptor antagonist, and Misoprostol, a PGE1 analogue, on gastric pH, pepsin, pepsinogen group I and N-acetylneuraminic acid concentration were evaluated in a group of 20 patients with duodenal ulcer. Nizatidine decreased pepsin concentration while it increased gastric pH, although not to a significant degree and left pepsinogen group I and N-acetylneuraminic acid concentration unchanged. Misoprostol did not modify gastric pH, pepsin and N-acetylneuraminic acid values but it increased pepsinogen group I levels. These data support the view that H2-receptor antagonists, especially Nizatidine, and Misoprostol do not directly affect pepsin and/or N-acetylneuraminic acid concentration.