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Intragastric carcinogenic N-nitrosamines and gastric acid suppressive therapy with omeprazole

The effect of long-term gastric acid suppressive therapy with omeprazole on intragastric levels of carcinogenic N-nitrosamines has been evaluated in a study published in the September issue of Gastroenterology.

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Ingrid T.M. Vermeer and colleagues from the University of Maastricht and the Maasland Hospital, in Maastricht and Sittard, Netherlands, enrolled 45 patients on long-term omeprazole medication (mean, 35 months), and 13 control patients without medication, onto the study.

The researchers determined volatile N-nitrosamines in gastric juice and urine. Intragastric pH, nitrate, nitrite, and Helicobacter pylori status were also determined.

In addition, DNA isolated from gastric biopsy specimens was analyzed for precarcinogenic alkyl-DNA adducts.

The research team found intragastric pH in subjects on omeprazole medication to be significantly higher compared with controls. Gastric nitrite levels however were not significantly higher.

Long-term omeprazole treatment does not raise intragastric nitrite and N-nitrosamines
Gastroenterology

No differences in the levels of intragastric volatile N-nitrosamines were observed between patients and controls, although urinary N-nitrosodimethylamine excretion was significantly higher in the omeprazole group.

In omeprazole-medicated patients, those that were H. pylori-positive were found to have a non-significantly higher intragastric nitrite level, and higher urinary N-nitrosodimethylamine excretion, when compared to H. pylori-negative patients.

No alkyl-DNA adducts could be detected in gastric epithelium.

The research team concludes that increased gastric pH caused by long-term treatment with omeprazole does not result in increased intragastric levels of nitrite and volatile N-nitrosamines.

They suggest that the significantly higher urinary N-nitrosamine excretion implies the risk of increased endogenous formation of N-nitrosamines during long-term omeprazole treatment and add that this risk may be higher in H. pylori-positive patients.

Gastroenterology 2001; 121 (3): 517-25
30 August 2001

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