Effect of long-term treatment with omeprazole on serum gastrin and serum group A and G pepsinogens in patients with reflux esophagitis

Jansen, J. B. M. J.; Klinkenberg‐Knol, Elly C.; Meuwissen, S. G. M.; Bruijne, J.W. de; Festen, H. P. M.; Snel, P.; Lückers, Anton E.G.; Biemond, I.; Lamers, C. B. H. W.

doi:10.1016/0016-5085(90)90946-x

Cited by 111 publications

(70 citation statements)

References 21 publications

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“…This leads to an increase in gastrin production from the antral-G cells and sustained increases in serum gastrin, usually to a mild degree (two to four times basal) (63). The question of whether these changes in serum gastrin might produce dangerous trophic effects on the gastric mucosa with long-term use of PPIs remains to be completely resolved, although both omeprazole and lanzoprazole are now approved for 1 yr of continuous usage.…”

Section: Acid Suppression Is the Mainstay Of Therapy For Gerd Protonmentioning

confidence: 99%

Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease

DeVault¹

1999

The American Journal of Gastroenterology

143

178

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PREAMBLEGuidelines for the diagnosis and treatment of gastroesophageal reflux disease (GERD) were published by the American College of Gastroenterology in 1995 (1). These and other guidelines undergo periodic review. Significant advances have been made in the area of GERD over the past several years, leading us to review and revise our previous guidelines statements. These advances have included an increase in our comfort with the chronic use of proton pump inhibitors and an increased acceptance of laparoscopic antireflux surgery, among other factors. These and the original guidelines are intended to apply to all physicians who address GERD and are intended to indicate the preferable, but not only acceptable, approach. Physicians must always choose the course best suited to the individual patient and the variables that exist at the moment of the decision. These guidelines are intended to apply to adult patients with the symptoms, tissue damage, or both that result from the reflux of gastric contents into the esophagus. For the purpose of these guidelines GERD is defined as chronic symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus.Both these and the original guidelines were developed under the auspices of the American College of Gastroenterology and its Practice Parameters Committee, and approved by the Board of Trustees. The world literature was reviewed extensively for the original guidelines and was once again reviewed using the National Library of Medicine database. All appropriate studies were reviewed and any additional studies found in the reference list of these papers were obtained and reviewed. Evidence was evaluated along a hierarchy, with randomized controlled trials given the greatest weight. Abstracts presented at national and international meetings were only used when unique data from ongoing trials were presented. When scientific data were lacking, recommendations were based on expert consensus. During preparation, the guidelines were reviewed

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Section: Acid Suppression Is the Mainstay Of Therapy For Gerd Protonmentioning

confidence: 99%

Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease

DeVault¹

1999

The American Journal of Gastroenterology

143

178

View full text Add to dashboard Cite

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“…Thirdly, treatment with proton pump inhibitor drugs or histamine type-2 receptor antagonists results in significant elevation of gastrin (owing to loss of negative feedback), up to two-fold, the reference range. 123,127,128 In patients who have been on long-term treatment with these drugs, gastrin does not return to baseline for many months after withdrawal of therapy. 129 Withdrawal of treatment for 3 d will show a significant reduction in circulating gastrin concentrations.…”

Section: Gastrin Assaymentioning

confidence: 99%

Circulating markers for endocrine tumours of the gastroenteropancreatic tract

Ardill

2008

Ann Clin Biochem

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The diffuse endocrine system (DES) includes a wide range of secretory cells that may be the source of tumours. Gastroenteropancreatic endocrine (GEP) tumours arising within the DES secrete a variety of peptides and amines that are found in the circulation and are responsible for the syndromes associated with these tumours. In this review, the most common tumours of the GEP tract are outlined and the circulating products of these tumours identified. Where differential diagnosis is difficult these points are addressed. The peptides most commonly secreted by GEP neuroendocrine tumours are identified and described and their biological activities are discussed. Current methods available for measurement of these peptides are described. Attention is drawn towards molecular specificity where appropriate, as many pancreatic and gut peptides fall within families which show considerable homology, such as the tachykinin family or the glucagon family. Other peptides such as gastrin circulate in multiple molecular forms. This homology and diversity may cause difficulty in the interpretation of peptide measurements in the clinical situation if assays are not specific.

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“…30,32,33 Up to 30% of patients on chronic PPI therapy may have gastrin blood levels greater than 500 ng/L or more than 6-fold greater than the upper limit of normal. 30,31,33 Even short-term administration of omeprazole has been shown to increase serum gastrin levels, 34 however, levels return to normal after discontinuation. Although raised as a potential issue at the time of their initial approval 25 years ago, the concern regarding PPI-induced hypergastrinemia has not disappeared completely.…”

Section: Risk Factors For Gastric Cancermentioning

confidence: 99%

Gastrin and gastric cancer

&NA;

1993

European Journal of Gastroenterology & Hepatology

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SUMMARYThe gastrointestinal peptide, gastrin, stimulates growth of gastric adenocarcinoma (gastric cancer) through the cholecystokinin-B receptors that are overexpressed in this malignancy. Serum gastrin levels may be increased secondary to chronic administration of proton pump inhibitors, atrophic gastritis, Helicobacter pylori infection, or from de novo gastrin expression from the gastric cancer epithelial cells. Strategies to interrupt the interaction of gastrin at the cholecystokinin-B receptor may provide a novel approach to the treatment of gastric cancer.Gastric cancer is the third leading cause of cancer-related mortality worldwide. Despite progress in understanding its development, challenges with treatment remain. Gastrin, a peptide hormone, is trophic for normal gastrointestinal epithelium. Gastrin also has been shown to play an important role in the stimulation of growth of several gastrointestinal cancers including gastric cancer. We sought to review the role of gastrin and its pathway in gastric cancer and its potential as a therapeutic target in the management of gastric cancer. In the normal adult stomach, gastrin is synthesized in the G cells of the antrum; however, gastrin expression also is found in many gastric adenocarcinomas of the stomach corpus. Gastrin's actions are mediated through the G-protein-coupled receptor cholecystokinin-B (CCK-B) on parietal and enterochromaffin cells of the gastric body. Gastrin blood levels are increased in subjects with type A atrophic gastritis and in those taking high doses of daily proton pump inhibitors for acid reflux disease. In experimental models, proton pump inhibitor-induced hypergastrinemia and infection with Helicobacter pylori increase the risk of gastric cancer. Understanding the gastrin:CCK-B signaling pathway has led to therapeutic strategies to treat gastric cancer by either targeting the CCK-B receptor with small-molecule antagonists or targeting the peptide with immune-based therapies. In this review, we discuss the role of gastrin in gastric adenocarcinoma, and strategies to block its effects to treat those with unresectable gastric cancer. (Cell Mol Gastroenterol Hepatol 2017;4:75-83; http://dx

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Effect of long-term treatment with omeprazole on serum gastrin and serum group A and G pepsinogens in patients with reflux esophagitis

Cited by 111 publications

References 21 publications

Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease

Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease

Circulating markers for endocrine tumours of the gastroenteropancreatic tract

Gastrin and gastric cancer

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