Mechanism of action of Roter (bismuth subnitrate) in patients with duodenal ulcer disease and healthy volunteers
Autor: | S. Pugh, M. R. Lewin |
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Rok vydání: | 1990 |
Předmět: |
Adult
Male medicine.medical_specialty medicine.medical_treatment Duodenal ulcer disease Gastroenterology Dinoprostone Gastric Acid Duodenal ulceration Antacid Internal medicine Healthy volunteers medicine Humans In patient Intestinal Mucosa Prostaglandin E2 Hepatology business.industry Hydrogen-Ion Concentration Middle Aged Gastric ph Mechanism of action Duodenal Ulcer Drug Evaluation Female Antacids medicine.symptom business Bismuth medicine.drug |
Zdroj: | Journal of Gastroenterology and Hepatology. 5:382-386 |
ISSN: | 1440-1746 0815-9319 |
DOI: | 10.1111/j.1440-1746.1990.tb01413.x |
Popis: | 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. |
Databáze: | OpenAIRE |
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