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Healing the gastroduodenal mucosa through Helicobacter pylori eradication leads to a dramatic reduction in gastroduodenal ulcer relapse. Eradication of H. pylori proves to be difficult. Although the organism is sensitive to many antibiotics in vitro, the in vivo eradicating efficacy is often disappointing. This overview summarizes the most commonly used currently-available eradication schemes and the consequences of successful eradication in peptic ulcer disease.

SUMMARY One hundred and twenty-five patients with duodenal ulcer disease were given continuous ranitidine therapy after initial acute healing. Cumulative remission rates indicated that 95 % of patients were ulcer-free after 1 year, 89% at 2 years, 81% at 3 years, 70% at 4 years and 60% at 5 and 6 years. Nine patients had a second recurrence after healing of the first. No patient developed an ulcer complication. These results support the view that long-term continuous ranitidine therapy prevents ulcer recurrence and complications.

It has long been assumed that the mucosa in areas of grossly 'healed' gastric or duodenal ulcers returns to normal, either spontaneously or after treatment. This assumption is based almost entirely upon visual, superficial examination by endoscopy. Few, if any, histological and ultrastructural studies examined the deeper mucosa in the areas of grossly healed ulcers. In several experimental studies, we analysed the development, evolution, and healing of acetic acid-induced gastric ulcers in rats and assessed the histological and ultrastructural features (structure and cellular composition) of the gastric mucosa in areas of grossly healed ulcers. The gastric mucosa of grossly 'healed' ulcers showed re-epithelialization of the mucosal surface at every study interval (2 weeks, 2, 3, and 4 months), but the subepithelial mucosa displayed prominent abnormalities. Two patterns of scarring were distinguished: (a) the mucosa in the area of healed ulcer was thinner (25-45% thinner than normal mucosa) with increased connective tissue and poor differentiation and/or degenerative changes in the glandular cells; and (b) the mucosa displayed a marked dilation of gastric glands with poor differentiation of the glandular cells and a reduction in the supportive microvascular network. It is theorized that these abnormalities could interfere with oxygenation, nutrient supply, and mucosal resistance and defence; therefore, they could be a basis for ulcer recurrence. These observations indicate that the quality of mucosal structural restoration rather than the speed of ulcer healing is the most important factor in determining risk of ulcer recurrence. The clinical relevance of these findings is supported by a preliminary study in which marked histological abnormalities were found in the subepithelial mucosa in patients with 'healed' duodenal ulcers.

Fifty-seven patients who developed asymptomatic recurrence of duodenal ulceration during maintenance treatment with ranitidine were followed up to assess the risk of developing symptoms or complications of ulcer disease. The risk of development of symptomatic ulcer recurrence was 4% in the first year of follow-up during continuous maintenance treatment, irrespective of whether or not the asymptomatic ulcer had been actively treated (by doubling the dose of ranitidine used for maintenance therapy). The asymptomatic duodenal ulceration during maintenance treatment did not predispose to complications such as haemorrhage or perforation. It seems, therefore, that patients receiving maintenance treatment for duodenal ulceration do not require endoscopic re-examination unless symptoms have recurred, because the asymptomatic recurrences of duodenal ulceration occurring during maintenance treatment are clinically benign, usually heal spontaneously if maintenance treatment is continued, and do not require active medical intervention.

One hundred and twenty patients with gastric ulcer disease, who had been receiving maintenance treatment with ranitidine (150 or 300 mg/day) for periods up to 7 years, were studied retrospectively. The proportion of patients remaining free from symptomatic recurrence of ulcer during maintenance treatment was 97% after 1 year; 90% after 3 years; and 79% after 5 years. No patient developed haemorrhage or perforation during maintenance treatment. None of the demographic features was shown to be associated with a significantly increased risk of ulcer recurrence during maintenance treatment. Comparison of the recurrence rates during maintenance treatment with those during periods without active anti-ulcer therapy, using life table and incidence density analysis, showed a significant difference in favour of maintenance treatment. We conclude that maintenance treatment with ranitidine for 5 years significantly reduces the risk of symptomatic ulcer recurrence in patients with gastric ulcer.

SUMMARY Ninety-five patients with healed gastric ulcers were treated with ranitidine 150 mg at night plus either Caved-S two tablets twice daily, or an identical placebo preparation. Treatment was continued for 2 years: the recurrence rate after 1 year was 12.5% for single therapy and 19% for combined therapy, and 30 and 40% respectively after 2 years (differences not significant). No serious side-effects were encountered, but patients found the combination therapy difficult to take, and it conferred no clinical advantage. In a 3 month follow-up after stopping maintenance therapy, 11% of the patients had a symptomatic ulcer recurrence. It is therefore recommended that elderly patients with gastric ulceration should remain on maintenance therapy for life.