Omeprazole-induced pseudohypertrophy of gastric parietal cells.

Paraffin-embedded and haematoxylin-eosin-stained sections of biopsy material obtained from patients taking omeprazole reveal a characteristic "hypertrophy" of the parietal cells; these are taller than the chief cells, and project, with convexly bulging apical cell membrane, into the lumen of the body glands, producing a serrated internal gland profile. We have found this phenomenon in 92.9% of 198 patients with non-operated stomachs. After Billroth I or II resection, this phenomenon was found in the body mucosa of the stomach remnant in only 35.3% of the cases (n = 17). The specificity of the diagnosis "hypertrophy" of the parietal cells under omeprazole therapy was 89.4%, the sensitivity 91.0%. A comparative morphometric analysis in forceps biopsy material investigated after paraffin and epoxide embedding, showed that this "hypertrophy" was a pseudohypertrophy. Apparently, as a result of an increase in intracytoplasmic secretory canaliculi, the gastrin-stimulated parietal cell shrinks less than the non-stimulated parietal cell. This pseudohypertrophy of the parietal cells can readily be used to monitor the compliance of the patient prescribed omeprazole. A question that has yet to be clarified is how quickly pseudohypertrophy develops, and how long it takes to regress after discontinuation of omeprazole. The phenomenon can also be seen in active autoimmune gastritis with no atrophy of the gland, since the parietal cell antibody also binds selectively to the proton pump of the parietal cell.