Cited by 99Helicobacter pylori-related gastroenterology studiesGastrointestinal motility and disordersGastroesophageal reflux and treatments

The DOI matches its Crossref record; 64 of the 65 references it cites were found in a registry or an index.

Physiologic, pathophysiologic, and pharmacologic regulation of gastric acid secretion

Schubert, Mitchell L.·2017·Current Opinion in Gastroenterology

Abstract

PURPOSE OF REVIEW: The present review summarizes the past year's literature, both clinical and basic science, regarding physiologic and pharmacologic regulation of gastric acid secretion in health and disease. RECENT FINDINGS: Gastric acid kills microorganisms, assists digestion, and facilitates absorption of iron, calcium, and vitamin B12. The main stimulants of acid secretion are the hormone gastrin, released from antral G cells; paracrine agent histamine, released from oxyntic enterochromaffin-like cells; and neuropeptide acetylcholine, released from antral and oxyntic intramural neurons. Gastrin is also a trophic hormone that participates in carcinogenesis. Helicobacter pylori may increase or decrease acid secretion depending upon the acuity and predominant anatomic focus of infection; most patients manifest hypochlorhydria. Despite the fact that proton pump inhibitors (PPIs) are amongst the most widely prescribed drugs, they are underutilized in patients at high risk for UGI bleeding. Although generally considered well tolerated, concerns have been raised regarding associations between PPI use and dementia, kidney disease, myocardial infarction, pneumonia, osteoporosis, dysbiosis, small bowel injury, micronutrient deficiency, and fundic gland polyps. SUMMARY: Our understanding of the physiologic, pathophysiologic, and pharmacologic regulation of gastric secretion continues to advance. Such knowledge is crucial for improved and safe management of acid-peptic disorders.

Overview

Integrity signals

Registry

Crossref · 10.1097/mog.0000000000000392

Cites

64 of 64 references verified0 citation errors · 0 not checkable

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Verification

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  • Helicobacter pylori infection and related gastritis represent the prototype of gastric juice alkalinization through bacterial urease activity and IL-1β and TNF-α production, and is also a frequent cause of increased need for LT4.

    “Helicobacter pylori infection and related gastritis represent the prototype of gastric juice alkalinization through bacterial urease activity and IL-1β and TNF-α production (119), and is also a frequent cause of increased need for LT4 (47).”

Citations

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1 of the 65 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. Tiriq, 2017, Association of gastric acid suppression with recurrent Clostridium difficile infection: a systematic review and meta-analysis, J Am Med Assoc Intern Med, 177, 784

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Metadata

Authors
Schubert, M. L.
Affiliations
Virginia Commonwealth University (US)
Corresponding author
Schubert, Mitchell L.
Venue
Current Opinion in Gastroenterology
Published
2017-11
Volume
33
Issue
6
Pages
430-438
ISSN
0267-1379 (ISSN-L)
OpenAlex
W2742931075
Cited by
99
References
65
Citations by year
2026: 7 · 2025: 12 · 2024: 14 · 2023: 9 · 2022: 15 · 2021: 16 · 2020: 10 · 2019: 11 · 2018: 5
FWCI
1.51
Type
journal article
Language
en
Open access
closed
Locations
  • Current Opinion in Gastroenterology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Gastroenterology › Helicobacter pylori-related gastroenterology studies
  • Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
  • Health Sciences › Medicine › Gastroenterology › Gastroesophageal reflux and treatments
Keywords
gastric acid secretion, gastrin, histamine, acetylcholine, Helicobacter pylori, proton pump inhibitors, upper gastrointestinal bleeding, hypochlorhydria, acid peptic disease, dysbiosis, fundic gland polyps, micronutrient deficiency
MeSH terms
Acetylcholine, Gastric Acid, Gastric Mucosa, Gastrins, Histamine, Humans, Helicobacter pylori, Helicobacter Infections, Proton Pump Inhibitors

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