NEW YORK (Reuters Health) – The results of the largest and longest study of gastrin biology in Barrett’s esophagus to date provide further evidence that long-term therapy with proton pump inhibitors (PPI) does not increase the risk of esophageal cancer.

Dr. Janusz Jankowski, from Digestive Diseases Centre, Leicester, UK, and colleagues undertook a detailed serologic and tissue assessment of gastrin and its CCK2 receptor in 90 patients with Barrett’s esophagus who were randomly assigned to receive high (80 mg/day) or low dose esomeprazole (20 mg/day) during a 2-year follow-up period.

In an August 2nd online publication in Gut, the researchers report that endoscopic biopsies showed gastrin and CCK2 receptor levels to be highest in the stomach, followed next by Barrett’s esophagus tissue and then squamous esophagus.

The change in Barrett’s esophagus segment length during follow-up was similar for patients given high or low doses of esomeprazole. Prolonged PPI use was not linked to an increase in serum gastrin levels.

In vitro testing showed that gastrin promoted epithelial restitution in Barrett’s esophagus, but not in squamous mucosa. The change in tissue type was induced by 1 ng/mL of gastric, whereas proliferation required at least 100 ng/mL. Moreover, both effects were eliminated with antagonist agents.

“While it has been shown in the short term that PPI therapy and/or hypergastrinemia can increase proliferation and induce COX-2 expression in susceptible cells, this study has also shown conclusively in a large randomized cohort that there is no evidence of longer term harm with surrogate histological biomarkers of proliferation, apoptosis, and surrogates of migration in vivo,” the researchers conclude.

Reference:
Gut 2009.