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Mechanism of action of Roter (bismuth subnitrate) in patients with duodenal ulcer disease and healthy volunteers
Author(s) -
PUGH S.,
LEWIN M. R.
Publication year - 1990
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.1990.tb01413.x
Subject(s) - medicine , antacid , gastroenterology
The effects of Roter (compound bismuth subnitrate) on antacid activity and mucosal prostaglandin E 2 (PGE 2 ) 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 0.01). Endogenous PGE 2 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 PGE 2 synthesis in untreated patients compared with controls (P 0.005). However, following 4 weeks' treatment with Roter, there was a 90% rate of healing accompanied by a significant increase in PGE 2 synthesis (P 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.