Literature DB >> 8680534

Effects of pirenzepine on omeprazole-induced hypergastrinemia and acid suppression in peptic ulcer patients.

A Tari1, M Hamada, T Kamiyasu, Y Fukino, M Sumii, K Haruma, K Sumii, M Inoue, G Kajiyama.   

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.

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Year:  1996        PMID: 8680534     DOI: 10.1007/bf02389513

Source DB:  PubMed          Journal:  J Gastroenterol        ISSN: 0944-1174            Impact factor:   7.527


  16 in total

1.  Intracellular Ca requirements for stimulus-secretion coupling in parietal cell.

Authors:  P A Negulescu; W W Reenstra; T E Machen
Journal:  Am J Physiol       Date:  1989-02

2.  Gastric carcinoid associated with ranitidine in a patient with renal failure.

Authors:  S S Rao; K S Nayak; G Swarnalata; D N Goyal; K P Rao; F A Mitros
Journal:  Am J Gastroenterol       Date:  1993-08       Impact factor: 10.864

Review 3.  Role of gastrin as a trophic hormone.

Authors:  J H Walsh
Journal:  Digestion       Date:  1990       Impact factor: 3.216

4.  The effect of omeprazole on ultrastructural changes in gastric parietal cells.

Authors:  H Karasawa; N Tani; T Miwa
Journal:  Gastroenterol Jpn       Date:  1988-02

5.  Antral gastrin and somatostatin concentrations in peptic ulcer patients.

Authors:  K Sumii; T Fukushima; K Hirata; Y Matsumoto; E Sanuki; S Tsumaru; M Sumioka; A Miyoshi; Y Miyachi
Journal:  Peptides       Date:  1981       Impact factor: 3.750

6.  Inhibiting gastric H(+)-K(+)-ATPase activity by omeprazole promotes degeneration and production of parietal cells.

Authors:  S M Karam; J G Forte
Journal:  Am J Physiol       Date:  1994-04

7.  Role of histamine2 receptor in increased expression of rat gastric H(+)-K(+)-ATPase alpha-subunit induced by omeprazole.

Authors:  A Tari; G Yamamoto; K Sumii; M Sumii; Y Takehara; K Haruma; G Kajiyama; V Wu; G Sachs; J H Walsh
Journal:  Am J Physiol       Date:  1993-10

8.  Toxicological studies on omeprazole.

Authors:  L Ekman; E Hansson; N Havu; E Carlsson; C Lundberg
Journal:  Scand J Gastroenterol Suppl       Date:  1985

9.  Treatment of acid-related disorders with gastric acid inhibitors: the state of the art.

Authors:  A L Blum
Journal:  Digestion       Date:  1990       Impact factor: 3.216

10.  Pirenzepine-sensitive muscarinic receptors regulate gastric somatostatin and gastrin.

Authors:  R Sue; M L Toomey; A Todisco; A H Soll; T Yamada
Journal:  Am J Physiol       Date:  1985-02
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