Related Experiment Video
Updated: May 31, 2026

An Immunofluorescent Method for Characterization of Barrett’s Esophagus Cells
Published on: July 20, 2014
Correlation between serum gastrin and cellular proliferation in Barrett's esophagus
Daniel A Green1, Carrie M Mlynarczyk, Benjamin J Vaccaro
1Department of Medicine, Columbia University College of Physicians & Surgeons, New York, NY, USA.
Background:
Patients with Barrett's esophagus (BE) are commonly treated with proton-pump inhibitors (PPIs) to minimize the exposure of esophageal mucosa to stomach acid. However, the use of these medications can lead to significant hypergastrinemia in a subset of patients, which is concerning due to the known tumorigenic and proliferative effects of gastrin. The present pilot study aims to investigate a potential correlation between serum gastrin and cellular proliferation in BE.
Methods:
We performed a cross-sectional analysis of patients with nondysplastic BE on PPI therapy. Fasting serum gastrin was measured on the same day as esophageal biopsies were obtained. These biopsies were then stained with Ki-67 nuclear antibody. Pearson's correlation coefficient was calculated to assess the relationship between Ki-67 index and ln(gastrin).
Results:
A total of 10 patients were included in the study. The mean age was 62.6 (±8.4) years and 5 patients were male. The median serum gastrin level was 45.2 pM (interquartile range [IQR] 33-113) and the median Ki-67 index was 49.6% (IQR 23-64). We found a statistically significant positive correlation between Ki-67 index and ln(gastrin) (r = 0.64; p = 0.05).
Conclusions:
In nondysplastic BE patients on PPI therapy, serum gastrin levels were significantly correlated with cellular proliferation. These pilot data lend support to a potential causal effect of gastrin on neoplastic progression in BE. Longitudinal studies of patients with BE are needed to determine whether hypergastrinemia is a risk factor for the development of dysplasia and adenocarcinoma or could be used as a biomarker for disease progression.
Related Concept Videos
Barrett Esophagus-I: Introduction
This constant acid exposure transforms the esophagus's pink mucosal lining (stratified squamous epithelium) into a type of lining more similar...
Barrett Esophagus-II: Clinical Manifestations and Management
To diagnose Barrett's esophagus, healthcare providers often recommend an endoscopy for those showing symptoms of acid reflux. The procedure entails...
Gastritis II: Pathophysiology
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Mucosal Barrier of the Stomach
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.

