S779 Lack of Gastrin Hormone Physiological Reaction in Patients With Gastric Bypass Surgery

Introduction: Hypergastrinemia is a physiological reaction found in 16% of the users of gastric acid suppression treatment (protein pump inhibitors [PPI] and H2 Blockers). Hypergastrinemia incidence also increased in the presence of gastric acid modifiers such as bile reflux. Other certain gastric hormones such as ghrelin and glucagon-like peptide-1 (GLP-1) action changes were found in patients with bariatric surgery. This study was designed to evaluate the gastrin hormone physiologic reaction in patients with gastric bypass surgery. Methods: One hundred forty-three patients with dyspepsia from gastroesophageal reflux disease or peptic ulcer disesase were involved. All patients had serum gastrin hormone measured on the morning of endoscopy. Forty-seven of the tested patients had gastric bypass surgery, and 23 were taking PPI or H2 Blockers. Ninety-six patients did not have bariatric surgery, and 56 were users of PPI or H2 Blockers. The incidence of hypergastrinemia was reported and compared among all 4 groups. Patients with bile reflux and chronic atrophic gastritis were excluded. Results: There was no incidence of hypergastrinemia detected in patients with gastric bypass surgery, including the users and non-users of acid suppression treatment. Eighteen percent (10/56) had hypergastrinemia in acid suppression treatment users of the patients without bariatric, (P < 0.05). No hypergastrinemia incidence was found in patients without surgery and without acid suppression treatment. Conclusion: There was no physiological reaction of gastrin hormone to the use of acid suppression treatment in patients who had gastric bypass surgery. However, this hormonal response could be different in patients with sleeve gastrectomy because of the possibility of bile reflux which will be studied separately. This is the first observation of gastrin hormone in gastric bypass patients, where further and larger studies should be done in the future. The absence of the gastrin reaction in gastric bypass patients has different etiology comparing to patients with previous Billroth I and II surgery because of the resected gastric antrum in the ulcer surgery patients. Direct contact of the gastric contents with the G cell tissues of the antrum could be essential for the stimulation of Gastrin hormone. The clinical improvement of gastroesophageal reflux disease following gastric bypass surgery could be attributed to this gastrin hormonal changes, however more studies are needed.

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Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001130576.79579.fc
Primary Topic
Bariatric Surgery and Outcomes
Type
article
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article

S779 Lack of Gastrin Hormone Physiological Reaction in Patients With Gastric Bypass Surgery

A. Distante, Mumtaz Tabbaa
The American Journal of Gastroenterology
Bariatric Surgery and Outcomes
article

S779 Lack of Gastrin Hormone Physiological Reaction in Patients With Gastric Bypass Surgery

A. Distante, Mumtaz Tabbaa
article en

Abstract

Introduction: Hypergastrinemia is a physiological reaction found in 16% of the users of gastric acid suppression treatment (protein pump inhibitors [PPI] and H2 Blockers). Hypergastrinemia incidence also increased in the presence of gastric acid modifiers such as bile reflux. Other certain gastric hormones such as ghrelin and glucagon-like peptide-1 (GLP-1) action changes were found in patients with bariatric surgery. This study was designed to evaluate the gastrin hormone physiologic reaction in patients with gastric bypass surgery. Methods: One hundred forty-three patients with dyspepsia from gastroesophageal reflux disease or peptic ulcer disesase were involved. All patients had serum gastrin hormone measured on the morning of endoscopy. Forty-seven of the tested patients had gastric bypass surgery, and 23 were taking PPI or H2 Blockers. Ninety-six patients did not have bariatric surgery, and 56 were users of PPI or H2 Blockers. The incidence of hypergastrinemia was reported and compared among all 4 groups. Patients with bile reflux and chronic atrophic gastritis were excluded. Results: There was no incidence of hypergastrinemia detected in patients with gastric bypass surgery, including the users and non-users of acid suppression treatment. Eighteen percent (10/56) had hypergastrinemia in acid suppression treatment users of the patients without bariatric, (P < 0.05). No hypergastrinemia incidence was found in patients without surgery and without acid suppression treatment. Conclusion: There was no physiological reaction of gastrin hormone to the use of acid suppression treatment in patients who had gastric bypass surgery. However, this hormonal response could be different in patients with sleeve gastrectomy because of the possibility of bile reflux which will be studied separately. This is the first observation of gastrin hormone in gastric bypass patients, where further and larger studies should be done in the future. The absence of the gastrin reaction in gastric bypass patients has different etiology comparing to patients with previous Billroth I and II surgery because of the resected gastric antrum in the ulcer surgery patients. Direct contact of the gastric contents with the G cell tissues of the antrum could be essential for the stimulation of Gastrin hormone. The clinical improvement of gastroesophageal reflux disease following gastric bypass surgery could be attributed to this gastrin hormonal changes, however more studies are needed.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 48%
Bariatric Surgery and Outcomes
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