| Theme | PPI Therapy | |
|---|---|---|
| Title | Clinical Problems with Long-Term PPI Therapy with Special Reference to Growth of Gastric Endocrine Cells | |
| Publish Date | 2002/02 | |
| Author | Satoshi Okahara | Department of Internal Medicine, Doto Hospital / First Department of Internal Medicine, Sapporo Medical University |
| Author | Takahiro Matsunaga | Department of Internal Medicine, Doto Hospital / First Department of Internal Medicine, Sapporo Medical University |
| Author | Asako Takaoka | Department of Internal Medicine, Doto Hospital |
| Author | Shigeo Aoki | Department of Internal Medicine, Doto Hospital |
| Author | Naoaki Nakagawa | Department of Internal Medicine, Doto Hospital |
| Author | Tsuyoshi Yabana | Department of Internal Medicine, Doto Hospital |
| [ Summary ] | PPIs (proton pump inhibitors), strongly inhibit the secretion of gastric acid from parietal cells, subsequently resulting in the production of hypergastrinemia. ECL-cells with CCK-2 (CCK-B/gastrin) receptors on their plasma membrane, which are densely distributed in the corpus and are mainly controled by endogenous gastrin released from G cells in the antrum, have been suspected of causing morphological and functional changes, namely hyperplasia, dysplasiaand gastric carcinoid tumors in humans. It has been reported that excessive dosages of PPI cause the development of gastric carcinoid tumors from ECL cells in female rats (Carlsson, et al; 1986), but the occurrence of gastric carcinoid tumors has not been reported in humans, as yet. The reasons are likely to be that serum gastrin levels induced by clinical doses of PPI are not very high, so dysplasias and carcinoid tumors may not occur and that the ratio of ECL cells to other gastric endocrine cells is lower in humans than in rats. | |