Parietal cells in duodenal ulcer disease: a histochemical study of the effects of omeprazole and ranitidine on mitochondrial activities.

H2-Receptor antagonists and omeprazole, a H-K ATPase inhibitor, inhibit acid secretion from the parietal cells. The ultrastructural changes of the parietal cells after treatment have been described, but the changes in the mitochondrial activity which reflect the energetic metabolism were not well defined. To study the effect of omeprazole and H2-receptor antagonists on the mitochondrial activity of the parietal cells, endoscopic biopsies were taken from nine patients with duodenal ulcer before and after treatment with either 10 mg or 20 mg omeprazole each morning, or 150 mg ranitidine twice daily for 2 weeks, given in a double-blind randomized manner. Three patients with healed duodenal ulcer who were on maintainence treatment with 150 mg ranitidine nightly for 1 year had an endoscopy performed after 4 and 12 months and two non-ulcer dyspeptic patients were recruited as controls. Three biopsies were taken during each endoscopy from the body of the stomach. The mitochondrial activity was assessed by the reaction of succinic dehydrogenase with nitroblue tetrazolium and of cytochrome oxidase with naphthoic acid mixed with N-phenyl-p-phenylenediamine, according to the intensity of the staining reaction. After treatment with omeprazole or ranitidine, the mitochondrial activity decreased appreciably and returned to the pretreatment level on cessation of treatment. Patients on maintainence ranitidine showed decreased mitochondrial activities after 4 months, which, however, returned to pretreatment levels in two patients. It is concluded that short-term treatment with omeprazole or ranitidine resulted in reversible suppression of mitochondrial activity while long-term treatment with ranitidine resulted in an initial suppression followed by a tendency to return to pretreatment level despite continued treatment.

RCT Entities:   Population Interventions Outcomes