Serum gastrin and chromogranin A levels in patients with fundic gland polyps caused by long-term proton-pump inhibition

Abstract

Objective. Use of proton-pump inhibitors (PPIs) causes hypergastrinemia, and it is well known that gastrin has a trophic effect on the oxyntic mucosa. Some PPI users develop fundic gland polyps. The purpose of this study was to determine whether patients developing fundic gland polyps have a more pronounced gastric hypoacidity, hypergastrinemia or increased serum chromogranin A (CgA), which is an enterochromaffin-like (ECL) cell marker. Material and methods. Five PPI users who developed multiple fundic gland polyps during PPI use were included in the study. PPI users without fundic gland polyps (n=6) as well as healthy individuals (n=6) were used as controls. In PPI users, we measured 24-h gastric pH, serum gastrin and CgA during one day, with standardized meals, whereas only gastrin and CgA were measured in the healthy individuals. Helicobacter pylori status was determined. Results. Gastric pH, serum gastrin and CgA did not differ significantly between PPI users with and those without fundic gland polyps. All patients with fundic gland polyps were H. pylori negative, whereas 4 out of 6 PPI users without fundic gland polyps were H. pylori positive. Fasting CgA levels were elevated in all PPI users, and CgA more than doubled during the day in all groups. Conclusions. Fundic gland polyps induced by PPIs are not related to the level of hypergastrinemia. Serum CgA is markedly affected by meals and should be measured in samples from fasting patients.

• Chromogranin A
• fundic gland polyps
• gastrin
• Helicobacter pylori
• proton-pump inhibitors