Can omeprazole induce gastric hyperplasia and/or polyps?/nBackground: A 67-year-old female patient

Fråga: Can omeprazole induce gastric hyperplasia and/or polyps?

Background: A 67-year-old female patient suffering from gastric ulcer and reflux esophagitis has been treated with omeprazole (Losec, 40-20 mg daily) since October 1991. In December 1994, a control gastroscopy was performed and multiple polyps up to 2 cm in diameter were diagnosed in left upper and middle parts of the corpus. Biopsies were taken showing hyperplastic polyps with parietal cell hyperplasia. No signs of malignancy were seen. In January 1995, serum gastrin level was slightly elevated (136 pg/ml).

Sammanfattning: Gastric hyperplastic polyps or glandular cysts have been reported during long-term omeprazole treatment. Their clinical significance and causal relationship to omeprazole treatment is, however, unclear.

Svar: In the published studies assessing long-term treatment with omeprazole, there has been no suggestion of gastric polyp development (1,2). However, gastric polyposis was reported in 4 out of 11 Australian patients receiving omeprazole for 12 months or longer (3,4). Histologically the polyps were hyperplastic or fundic gland polyps, of 1-5 mm in size and located in the body of the stomach. According to a German expert, these small polypoid elevations could just be reversible gastric glandular cysts without hyperplastic, metaplastic or neoplastic characteristics (5,6). In addition, one case of multiple hyperplastic polyps in the antrum of the stomach after 8 + 8 week therapy with omeprazole and famotidine has recently been reported (7). This patient also developed acute gastric lesions after receiving endoscopic sclerotherapy for esophageal varices.

The toxicological concerns of omeprazole raised from early animal experiments and the impact on long-term exposure have recently been reviewed in Drugline (8). Slight increases in the endocrine (enterochromaffin-like) cell volume density and even micronodular hyperplasia of the oxyntic mucosa have been found during long-term omeprazole treatment. The latter change is considered, however, to be related to the severity of corpus gastritis and not to drug-induced hypergastrinemia (2).

It should also be mentioned that probably as a result of increases in intracytoplasmic secretory canaliculi, gastrin-stimulated parietal cells may shrink less than non-stimulated cells during the specimen preparation of biopsy material. The ensuing pseudohypertrophy of gastric parietal cells appears to be common during omeprazole treatment and this artefact has even been suggested to demonstrate patient compliance (9). 1 Brunner GHG, Lamberts R, Creutzfeldt W. Efficacy and safety of omepraxole in the long-term treatment of peptic ulcer and reflux oesophagitis resistant to ranitidine. Digestion 1990; 47 (Suppl 1): 64-68 2 Creutzfeldt W. Risk-benefit assessment of omeprazole in the treatment of gastrointestinal disorders. Drug Safety 1994; 10: 66-82 3 Graham JR, Gastric polyposis: onset during long-term therapy with omeprazole (letter). Med J Aust 1992; 157: 287-288 4 Graham JR. Omeprazole and gastric polyposis in humans (letter). Gastroenterology 1993; 104: 1584 5 Stolte M. Fundic gland polyps: a rare, innocuous, and reversible disturbance (letter). Gastroenterology 1993; 105: 1590 6 Eidt S, Stolte M. Gastric glandular cysts - investigations into their genesis and relationship to colorectal epithelial tumors. Z Gastroenterol 1989; 27: 212-217 7 Tanaka J-I, Fujimoto K, Iwakiri R, Koyama T, Sakata H, Ohyama T, Mizuguchi M, Tokunaga O. Hyperplastic polyps following treatment of acute gastric ulcers (letter). Int Med 1994; 33: 366-368 8 Drugline nr 11067 (year 1994) 9 Stolte M, Bethke B, Ruhl G, Ritter M. Omeprazole-induced pseudohypertrophy of gastric parietal cells. Z Gastroenterol 1992; 30: 134-138