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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
    ISSN: 1573-2568
    Keywords: hypergastrinemia ; somatostatin ; pirenzepine ; omeprazole ; gene expression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Pirenzepine has inhibitory effects on gastrin secretion bothin vivo andin vitro. The aim of this study was to determine the mechanism responsible for the suppression of omeprazole-induced hypergastrinemia that occurs with pirenzepine treatment. The effects were measured in rats treated with oral omeprazole plus intraperitoneal pirenzepine or saline once daily for seven days in the antrum. The serum gastrin level increased significantly by more than sixfold with omeprazole treatment; additional treatment with pirenzepine suppressed this increase by 48%. Pirenzepine treatment did not change the level of gastrin mRNA but significantly increased the level of somatostatin mRNA. Combination treatment with omeprazole plus pirenzepine significantly decreased the gastrin mRNA level to half and significantly increased the somatostatin mRNA level up to 1.4-fold of the levels achieved with omeprazole treatment alone. These results suggest that the stimulatory effect of omeprazole on gastrin synthesis is partially blocked by pirenzepine via mediation of somatostatin synthesis in the antrum.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-2568
    Keywords: ENPROSTIL ; OMEPRAZOLE ; HYPERGASTRINEMIA ; INTRAGASTRIC PH MEASUREMENT ; HELICOBACTER PYLORI
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study was performed to examine the effectsof additional enprostil administration onhypergastrinemia and gastric acid suppression induced byomeprazole. Serum gastrin concentrations were measured in 10 peptic ulcer patients (six Helicobacterpylori-positive and four Helicobacter pylori-negativepatients) before treatment, after two weeks ofomeprazole (20 mg/day), and after two weeks ofomeprazole and enprostil (50 μg/day). The additionalacid inhibitory effect of enprostil was evaluated by24-hr intragastric pH measurements in five healthyHelicobacter pylori-negative volunteers. Afteromeprazole treatment, the serum gastrin level ofHelicobacter pylori-positive patients (3.5-fold ofcontrol) was markedly higher than that of Helicobacterpylori-negative patients (1.7-fold of control).Additional treatment with enprostil suppressed serumgastrin levels to 0.4-fold and 0.7-fold of omeprazoletreatment levels in Helicobacter pylori-positive andHelicobacter pylori-negative patients, respectively. In healthy volunteers, median pH recordedduring the nonmeal daytime interval increasedsignificantly with additional enprostil. Thus, enprostilreduces undesirable omeprazole-induced hypergastrinemia, especially in Helicobacter pylori-positivepatients, and effectively suppresses acidsecretion.
    Type of Medium: Electronic Resource
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