1.
Interaction of magnesium oxide with gastric acid secretion inhibitors in clinical pharmacotherapy.
Yamasaki, M, Funakoshi, S, Matsuda, S, Imazu, T, Takeda, Y, Murakami, T, Maeda, Y
European journal of clinical pharmacology. 2014;(8):921-4
Abstract
PURPOSE Magnesium oxide (MgO), a short-term osmotic laxative, is converted into MgCl2 under acidic condition in the stomach and then Mg(HCO3)2 in the intestinal tract, where Mg(HCO3)2 induces the water exudation into the intestine. This indicates that the laxative effect of MgO could be attenuated under the suppressed gastric acid secretion. In this study, the possible interaction of MgO with gastric acid secretion inhibitors was evaluated by using electronic patient records of MgO dosage levels. METHODS Defecation was controlled with MgO alone in some patients after colon surgery (n = 67) and after total gastric resection (n = 4). Some other patients were treated with a combination use of MgO and H2 receptor antagonist (H2RA) (n = 14) or proton pump inhibitor (PPI) (n = 27). The possible drug interaction of MgO with H2RA or PPI was evaluated by comparing dosage levels of MgO used in controlling defecation. RESULTS In controlling defecation, the daily dosage levels of MgO in patients taking H2RA or PPI and patients with total gastric resection were significantly higher than those patients taking MgO alone after colon surgery. The ratios of good constipation control (controlled well at the dosing level of 1,000 mg MgO) in patients taking H2RA or PPI were significantly lower than that in patients treated with MgO alone. In an in vitro study, the solubility of MgO at pH 4.5 was quite low, as compared with that at pH 1.2. CONCLUSIONS When patients received H2RA or PPI, the laxative effect of MgO is decreased possibly due to the low solubility of MgO at the higher gastric pH and less generation of MgCl2 and Mg(HCO3)2. Higher dosing level of MgO or another laxative should be used in patients taking H2RA or PPI, as well as the case of patients with total gastric resection.
2.
Gastric acid and salivary bicarbonate. Is there a relationship in duodenal ulcer patients?
Namiot, Z, Stasiewicz, J, Markowski, AR, Namiot, DB, Jaroszewicz, W, Kemona, A, Górski, J
Roczniki Akademii Medycznej w Bialymstoku (1995). 2004;:75-9
Abstract
PURPOSE Since saliva protects the oesophageal and oral mucosa against hydrogen ions, the aim of the study was to establish the relationship between the secretion of gastric acid and salivary bicarbonate. MATERIAL AND METHODS The study involved 43 Helicobacter pylori positive duodenal ulcer patients receiving: 1. omeprazole alone (O), 2. omeprazole and amoxicillin (OA) or 3. omeprazole, amoxicillin and tinidazole (OAT). In each study group the examination was performed twice, before and at the end of a two-week treatment, both under basal conditions and during a gastric secretory test with pentagastrin. Concentrations of gastric hydrogen ions and salivary bicarbonate were evaluated by the titration method. RESULTS In all therapeutic groups analysed separately, the secretion of gastric acid as well as salivary bicarbonate decreased at the end of the treatment, however only in OA and OAT groups the differences in bicarbonate reached statistical significance. As the changes in the concentration and output of both salivary bicarbonate and gastric acid had the same direction, the three therapeutic groups (O, OA, OAT) were subjected to combined analysis. It showed that under basal conditions and during stimulation with a gastric catheter or catheter and pentagastrin, bicarbonate concentration and output were higher before than at the end of the treatment. However, no direct correlation between gastric acid secretion and salivary bicarbonate was found in groups subjected to either separate or combined analysis. CONCLUSIONS The results of our study provide evidence for the partial involvement of hydrogen ions of gastric origin in the regulation of salivary bicarbonate secretion in duodenal ulcer patients.
3.
Regulation of gastric function by endogenous gastrin releasing peptide in humans: studies with a specific gastrin releasing peptide receptor antagonist.
Hildebrand, P, Lehmann, FS, Ketterer, S, Christ, AD, Stingelin, T, Beltinger, J, Gibbons, AH, Coy, DH, Calam, J, Larsen, F, et al
Gut. 2001;(1):23-8
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Abstract
BACKGROUND AND AIMS The main goal of our study was to characterise the activity of BIM26226 as a peripheral gastrin releasing peptide (GRP) receptor antagonist in healthy human subjects and to determine if endogenous GRP is a physiological regulator of gastric acid secretion and gastrin release. METHODS Our study consisted of three parts. In part I, subjects received saline or BIM26226 followed by graded doses of intravenous human GRP in a four period crossover design. In part II, subjects received BIM26226 or saline during oral meal ingestion or modified sham feeding. In part III, subjects received an acidified meal in the presence and absence of BIM26226 in a two period crossover design. In addition, gastrin and somatostatin mRNA were measured in biopsy specimens during saline and BIM26226 infusion. RESULTS BIM26226 dose dependently inhibited GRP induced acid output. Acid secretion after oral liquid meal intake and sham feeding was significantly inhibited by BIM26226 (p<0.01) whereas plasma gastrin release remained unchanged. Gastrin and somatostatin mRNAs were not significantly different after saline or BIM26226. CONCLUSIONS BIM26226 is a potent GRP antagonist in humans. Endogenous GRP may be a physiological regulator of gastric acid secretion. Gastrin release does not seem to be under the control of GRP.