Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reduction of gastric acidity by the inhibition of secretion or neutralization is the therapeutic principle most widely used in peptic ulcer disease. From a pathophysiological standpoint, this does not appear logical, because in a majority of patients gastric acid secretion is not increased. In addition, there is some concern about the consequences of a reduction in gastric acidity, especially in the long term. And finally, all available inhibitors of gastric acid secretion have a systemic action and may thus cause systemic side effects. Carbenoxolone, sucralfate, and tri-potassium dicitrato bismuthate have been shown to accelerate healing of ulcers without appreciable acid inhibition. Despite an apparently different mode of action, the healing rates are similar to those of commonly used acid inhibitors. Several possible mechanisms of action have been claimed for each of these agents, but none has been convincingly demonstrated to be essential in ulcer healing. This may reflect ignorance of the relevant events rather than an action by a combined principle.
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PMID:Protective drugs in the treatment of gastroduodenal ulcer disease. 354 12

Carbenoxolone (Biogastrone, Berk) has been shown to reduce the peptic activity and total acidity of gastric juice obtained from anaesthetized pylorus-ligated rats without affecting significantly the volume of gastric juice secreted or the K(+) concentration. Glycyrrhetinic acid was less potent in reducing peptic activity and caused no reduction in total acidity. Antipeptic activity of carbenoxolone has also been demonstrated in vitro using the pepsin plate technique and the haemoglobin pepsin assay.It is suggested that these actions of carbenoxolone may contribute to the increased rate of healing of peptic ulcer in patients treated with the drug.
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PMID:Inhibition of peptic activity by carbenoxolone and glycyrrhetinic acid. 491

The influence of oral carbenoxolone sodium (50 mg X 3 daily) on prostaglandin E2 release into gastric juice has been examined in nine peptic ulcer patients (duodenal ulcer, n = 6; prepyloric ulcer, n = 1; gastric ulcer, n = 2) during modified sham feeding and following bolus stimulation of acid secretion by pentagastrin (6 micrograms/kg). Carbenoxolone increased the overall mean of prostaglandin E2 concentrations in gastric juice following modified sham feeding by 32 +/- 9% (mean +/- SEM; P less than 0.02) and decreased the acidity slightly but significantly (P less than 0.05). A marked rise in prostaglandin E2 levels (46 +/- 11%; n = 5; P less than 0.02) was observed in for duodenal ulcer patients and the patient with a prepyloric ulcer responding to therapy (i.e., pain relief and ulcer healing within 4 weeks of treatment). A significant peak (P less than 0.05) related to modified sham feeding was observed only during medication, while a late gradual increase in prostaglandin E2 levels--not associated with vagal stimulation--occurred both in control and carbenoxolone experiments. No significant differences were observed following pentagastrin stimulation. The initial peak in prostaglandin E2 levels observed during medication favours the notion that the mechanism of drug action relies on inhibition of enzymatic degradation while the late increase in prostaglandin E2 levels may be explained by artificial prostaglandin formation during the aspiration procedure.
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PMID:Effect of carbenoxolone on gastric prostaglandin E2 levels in patients with peptic ulcer disease following vagal and pentagastrin stimulation. 641 22