2012/09/23 by R. Fiocca, L. Mastracci, S. E. Attwood +7
paper · doi:10.1111/apt.12052
Summary Background Sustained acid inhibition with PPI stimulates gastrin secretion, exerting a proliferative drive on enterochromaffin‐like cells ( ECL cells) of the oxyntic mucosa. It may also accelerate development of gastric gland atrophy in H elicobacter pylori ‐infected individuals. Aims To evaluate gastric exocrine and endocrine cell changes in GERD patients randomised to laparoscopic antireflux surgery ( LARS , n = 288) or long‐term (5 years) esomeprazole ( ESO ) treatment ( n = 266). Methods Antral and corpus biopsies were taken at endoscopy and serum gastrin and chromogranin A levels were assayed, at baseline and after 1, 3 and 5 years’ therapy. Results Biopsies were available at each time point for 158 LARS patients and 180 ESO patients. In H . pylori ‐infected subjects, antral mucosal inflammation and activity improved significantly ( P LARS . Oxyntic mucosal inflammation and activity remained stable on esomeprazole but decreased slightly over time after LARS . Neither intestinal metaplasia nor atrophy developed in the oxyntic mucosa. ECL cell density increased significantly after ESO ( P A . After LARS , there was a significant decrease in ECL cell density ( P Conclusions Antral gastritis improved in H . pylori‐ infected GERD patients after 5 years on esomeprazole , with little change in laparoscopic antireflux surgery patients, who acted as a control. Despite a continued proliferative drive on enterochromaffin‐like cells during esomeprazole treatment, no dysplastic or neoplastic lesions were found and no safety concerns were raised. NCT 00251927.