Optimal dose of oral omeprazole for maximal 24 hour decrease of intragastric acidity.

Sharma, Bhawna; Walt, R P; Pounder, R. E.; Gomes, M D; Wood, Elizabeth; Logan, Laurie

doi:10.1136/gut.25.9.957

Cited by 238 publications

(77 citation statements)

References 18 publications

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“…3 Discontinuing treatment may prove dif®cult in some patients even if the dose of proton pump inhibitor is slowly tapered, due to the dose±response curves for these drugs. 49,50 In these cases the use of high doses of H 2 -receptor antagonists or antacids should be considered.…”

Section: Clinical Consequencesmentioning

confidence: 99%

Review article: the pharmacological inhibition of gastric acid secretion—tolerance and rebound

Sandvik

Brenna

Waldum

1997

Aliment Pharmacol Ther

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During the last decade our understanding of the regulation of gastric acid secretion has changed considerably. The recognition that gastrin acts mainly by releasing histamine from the enterochromaffin‐like (ECL) cell is of major importance. It is now necessary to review and seek new explanations for the development of tolerance and for the post‐treatment acid hypersecretion that may be observed when treatment with acid‐secretory inhibitors is discontinued. Tolerance and rebound related to H2‐receptor antagonists has previously been explained as upregulation of gastrin and/or histamine H2‐receptors, and/or an increased parietal cell mass. Experimental evidence for these theories is scarce. On the other hand, tolerance can now be explained by a gastrin‐induced increase in ECL cell‐derived histamine at the parietal cell H2‐receptor competing with the antagonist. The lack of tolerance to proton pump inhibitors may be explained by their mode of action, being non‐competitive and acting at the H+, K+‐ATPase rather than at stimulatory receptors. Post‐treatment rebound acid hypersecretion can be understood as gastrin upregulating and/or stimulating growth of the ECL cell, leading to increased amounts of releasable histamine post‐treatment. Novel experimental data strongly support this view of the development of tolerance and post‐treatment rebound acid hypersecretion.

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Section: Clinical Consequencesmentioning

confidence: 99%

Review article: the pharmacological inhibition of gastric acid secretion—tolerance and rebound

Sandvik

Brenna

Waldum

1997

Aliment Pharmacol Ther

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“…Loxtidine was the so-called unsurmountable H-2 blocker (63), and this compound was not developed into a drug due to the NETs seen in rodents. The PPIs are very efficient drugs in inhibiting gastric acid secretion (67), but at the same time risky due to hypergastrinemia. Rather early, it was shown that PPI treatment induced ECL cell hyperplasia (68), which caused rebound acid hypersecretion (69).…”

Section: Gastrin and Gastric Netsmentioning

confidence: 99%

Gastrin and gastric cancer

Waldum¹,

Petersen²,

Brenna³

1993

European Journal of Gastroenterology & Hepatology

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Gastric cancer although occurring in reduced frequency is still an important disease, partly because of the bad prognosis when occurring in western countries. This decline in occurrence may mainly be due to the reduced prevalence of Helicobacter pylori (Hp) infection, which is the most important cause of gastric cancer. There exist many different pathological classifications of gastric carcinomas, but the most useful seems to be the one by Lauren into intestinal and diffuse types since these types seldom transform into the other and also have different epidemiology. During the nearly 30 years that have passed since the groundbreaking description of Hp as the cause of gastritis and gastric cancer, a continuous search for the mechanism by which Hp infection causes gastric cancer has been done. Interestingly, it is mainly atrophic gastritis of the oxyntic mucosa that predisposes to gastric cancer possibly by inducing hypoacidity and hypergastrinemia. There are many arguments in favor of an important role of gastrin and its target cell, the enterochromaffin-like cell, in gastric carcinogenesis. The role of gastrin in gastric carcinogenesis implies caution in the long-term treatment with inhibitors of gastric acid secretion inducing secondary hypergastrinemia, in a common disease like gastroesophageal reflux disease.Keywords: carcinogenesis, classification of cancer, gastric cancer, gastrin, hormones, neuroendocrine neoplasia Gastric cancer has been one of the most prevalent cancers and combined with a high mortality, gastric cancer has been among the leading causes of cancer death. However, there has been a continuous decline in the prevalence of gastric cancers during the last decades. Unfortunately, in spite of widespread use of upper gastrointestinal endoscopy, the prognosis in patients affected in the western world has not been much improved. This is in contrast to Japan where gastric cancer often is diagnosed at an early phase allowing removal and a better prognosis (1, 2). This is partly due to special screening programs in Japan having a high prevalence of gastric cancer (1, 2), resulting in diagnoses at a curable stage. In most western countries, the prevalence is much lower (3), and therefore, no such program has been implemented. The cause of the geographical differences in the prevalence of gastric cancer most probably is increased prevalence of Helicobacter pylori (Hp) in East Asia as well as a higher frequency of atrophic oxyntic gastritis (4). The prognosis of gastric cancer is better in patients from East Asia even when living in the west possibly due to less aggressive biology (5). In this review, we will focus on the role of gastrin in the etiology of gastric cancer and at the same time give an explanation of the decline in frequency. We will only cover cancers originating from epithelial cells (carcinomas) and will not discuss the importance of Epstein-Barr virus that plays a role neither in gastric carcinogenesis (6) nor in human papilloma virus, which has a less established impact (7).

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“…In man and animals omeprazole is a strong and long-acting inhibitor of acid secretion (Larsson et al 1983;Sharma et al 1984). A nearly 100% inhibition of gastric acid secretion can be obtained, a property not reported for other inhibitors of acid secretion such as H2-receptor blockers (Sharma et al 1984).…”

mentioning

confidence: 99%

“…This study demonstrates that omeprazole has a more longacting inhibitory effect on gastric acid secretion compared to cimetidine and accelerates healing of chronic gastric ulcers dose-dependently in rats omeprazole ; cimetidine ; chronic gastric ulcers ; gastric acid secretion ; rats Omeprazole is a substituted benzimidazole that acts directly on the parietal cell by blocking the H+, K+-adenosine triphosphatase, the proton pump of the parietal cell (Fellenius et al 1981). In man and animals omeprazole is a strong and long-acting inhibitor of acid secretion (Larsson et al 1983;Sharma et al 1984). A nearly 100% inhibition of gastric acid secretion can be obtained, a property not reported for other inhibitors of acid secretion such as H2-receptor blockers (Sharma et al 1984).…”

mentioning

confidence: 99%

Effect of omeprazole and cimetidine on healing of chronic gastric ulcers and gastric acid secretion in rats.

Olsen

Therkelsen

Poulsen

1988

Tohoku J. Exp. Med.

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The effect of omeprazole and cimetidine on healing of chronic gastric ulcers and gastric acid secretion was investigated in rats. The effect of three doses of omeprazole given orally once daily for 25 days was investigated. In controls median ulcer healing was 19.6% after 25 days. Omeprazole increased median ulcer healing from 36% at 145 ,umole/kg/day to 80% at 580,umole/kg/day. Basal and pentagastrin stimulated gastric acid secretion decresed dose-dependently by nearly 90% at a dose of 580 jimole/kg/day 22-24 hr after the last dose of omeprazole. Cimetidine given twice daily, in a dose that initially inhibits gastric acid secretion by 95%, reduced acid secretion by only 50% 11 hr after the last dose. Median ulcer healing after treatment with cimetidine for 25 days was 41%. This study demonstrates that omeprazole has a more longacting inhibitory effect on gastric acid secretion compared to cimetidine and accelerates healing of chronic gastric ulcers dose-dependently in rats omeprazole ; cimetidine ; chronic gastric ulcers ; gastric acid secretion ; rats Omeprazole is a substituted benzimidazole that acts directly on the parietal cell by blocking the H+, K+-adenosine triphosphatase, the proton pump of the parietal cell (Fellenius et al. 1981). In man and animals omeprazole is a strong and long-acting inhibitor of acid secretion (Larsson et al. 1983;Sharma et al. 1984). A nearly 100% inhibition of gastric acid secretion can be obtained, a property not reported for other inhibitors of acid secretion such as H2-receptor blockers (Sharma et al. 1984). Due to the strong antisecretory effect of omeprazole this drug might be applicable for treatment of gastric and duodenal ulcers.Healing rates of approximately 95-100% of duodenal ulcers after 4 weeks of treatment have been reported in man (Cooperative study 1984; Bardhan et al.

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Optimal dose of oral omeprazole for maximal 24 hour decrease of intragastric acidity.

Cited by 238 publications

References 18 publications

Review article: the pharmacological inhibition of gastric acid secretion—tolerance and rebound

Review article: the pharmacological inhibition of gastric acid secretion—tolerance and rebound

Gastrin and gastric cancer

Effect of omeprazole and cimetidine on healing of chronic gastric ulcers and gastric acid secretion in rats.

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