Rebound acid hypersecretion after long-term inhibition of gastric acid secretion
Article first published online: 22 DEC 2004
Alimentary Pharmacology & Therapeutics
Volume 21, Issue 2, pages 149–154, January 2005
How to Cite
Fossmark, R., Johnsen, G., Johanessen, E. and Waldum, H. L. (2005), Rebound acid hypersecretion after long-term inhibition of gastric acid secretion. Alimentary Pharmacology & Therapeutics, 21: 149–154. doi: 10.1111/j.1365-2036.2004.02271.x
- Issue published online: 22 DEC 2004
- Article first published online: 22 DEC 2004
- Accepted for publication 24 August 2004
Background : Rebound acid hypersecretion develops after the use of acid inhibitors.
Aim : To estimate the duration of hypersecretion and to elucidate the role of the enterochromaffin-like (ECL) cell in rebound acid hypersecretion.
Methods : Patients waiting for anti-reflux surgery who had used a proton pump inhibitor daily > 1 year were included. All patients discontinued taking acid inhibiting drugs after the operation. Basal and pentagastrin stimulated acid output was measured at 4, 8, 16 and 26 weeks postoperatively. Oxyntic mucosal biopsies were collected before and 26 weeks after the operation for counting of histidine decarboxylase (HDC) immunoreactive cells. Serum chromogranin A (CgA) and gastrin were measured before and at 4, 8, 16 and 26 weeks after the operation.
Results : Pentagastrin stimulated acid secretion was higher at 4 and 8 weeks than at 26 weeks after the operation. Gastrin and CgA were significantly reduced at 4 and 8 weeks, respectively. The number of HDC immunoreactive cells was reduced by 60% at 26 weeks postoperative.
Discussion : Rebound acid hypersecretion lasts more than 8 weeks, but less than 26 weeks after long-term proton pump inhibition.
Conclusion : The findings indicate that not only the parietal cell mass, but also ECL cell mass and activity are involved in the mechanism of acid hypersecretion.