Correlation between serum gastrin and cellular proliferation in Barrett’s esophagus

Abstract

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.