Mechanism of action of Roter (bismuth subnitrate) in patients with duodenal ulcer disease and healthy volunteers.

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Pugh S, Lewin MR

Mechanism of action of Roter (bismuth subnitrate) in patients with duodenal ulcer disease and healthy volunteers.

J Gastroenterol Hepatol. 1990 Jul-Aug;5(4):382-6.

PubMed ID
2129809 [ View in PubMed
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Abstract

The effects of Roter (compound bismuth subnitrate) on antacid activity and mucosal prostaglandin E2 (PGE2) synthesis were variously investigated in patients with duodenal ulcer disease and healthy volunteers. Roter had a significant but small antacid activity with a buffering capacity of 10.9 mmol per tablet. In healthy volunteers, this was assessed by 24 h gastric pH monitoring on matched days with and without Roter treatment. The percentage of time that gastric pH was above 3 and the time after a standard meal that the pH was above 3, were both significantly increased by treatment with Roter (II tds post-cibal) (P less than 0.01). Endogenous PGE2 synthesis was measured in endoscopic duodenal biopsies taken both before and after Roter treatment in patients with acute untreated duodenal ulceration. There was a significant deficiency of mucosal PGE2 synthesis in untreated patients compared with controls (P less than 0.005). However, following 4 weeks' treatment with Roter, there was a 90% rate of healing accompanied by a significant increase in PGE2 synthesis (P less than 0.05) up to control levels. These findings suggest that Roter heals by the combined effects of a modest antacid neutralizing capacity and the ability to restore mucosal prostaglandins to normal levels, thereby mediating prostaglandin-dependent defence mechanisms.

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