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  • 1
    ISSN: 1435-5922
    Keywords: hypergastrinemia ; omeprazole ; pirenzepine ; gastric acid secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Omeprazole effectively suppresses acid secretion, resulting in the long-term elevation of intragastric pH and serum gastrin level. Pirenzepine has been reported to inhibit gastrin secretion. This study was carried out to examine the effects of additional pirenzepine treatment on the hypergastrinemia and gastric acid suppression induced by omeprazole. Concentrations of serum gastrin and plasma somatostatin were measured in 28 peptic ulcer patients before treatment, after omeprazole treatment (20 mg/day) for 2 weeks, and after omeprazole and pirenzepine (100 mg/day) treatment for 2 weeks. The acid inhibitory effect of pirenzepine treatment in addition to omeprazole was evaluated by 24-h intragastric pH measurement in six healthy volunteers. Serum gastrin level was increased significantly, to 2.4-fold the pretreatment level, by omeprazole treatment. Additional treatment with pirenzepine suppressed serum gastrin level to 0.6-fold the omeprazole-treatment level. The serum somatostatin level was not altered significantly either by omeprazole treatment or by omeprazole and pirenzepine treatment. In healthy volunteers whose pH 3 holding time on 24-h intragastric pH monitoring was 70% by omeprazole treatment, omeprazole and pirenzepine treatment markedly increased the pH 3 holding time, to 89%. These findings suggest that pirenzepine is useful in reducing the undesirable effects of omeprazole-induced hypergastrinemia, i.e., the excessive trophic effect of omeprazole on the acid-secreting part of the stomach and the overstimulation of acid secretion. The additional pirenzepine treatment is also effective in suppressing acid secretion.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 38 (1993), S. 1422-1425 
    ISSN: 1573-2568
    Keywords: bezoar ; gastric emptying ; gastric acid secretion ; pathogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Bezoars are conglomerates of undigested material in the stomach. Previous reports have shown that a decrease in secretion of pepsin and gastric acid and a delay in gastric emptying might contribute to their formation. To clarify the pathogenesis of the formation of gastric bezoars, we studied gastric emptying in five patients who presented with a bezoar. In addition, gastric acid secretion was studied in three of the cases. Gastric emptying was not delayed in any case, and there was no trend toward a decrease in gastric acid secretion. The five patients were successfully treated by the endoscopic fragmentation and enzymatic dissolution of the benzoars. We conclude that, in Japanese, factors other than a delay in gastric emptying are the main contributors to bezoar formation.
    Type of Medium: Electronic Resource
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