Plasma and gastric tissue selenium levels in patients with Helicobacter pylori infection

Goals: We investigated plasma and gastric mucosal selenium levels in patien ts with Helicobacter pylori (HP)-associated histopathologic findings in the ir gastric antral mucosa. Study: Before and after a successful HP eradicati on therapy, we quantitated the plasma and antral selenium levels in patient s with HP-associated chronic antral gastritis using atomic absorption flame emission spectrometry. The same measurements were done in patients with dy speptic complaints who had normal antral histology and negative urease test . Results: Thirty-four patients were studied, of whom 24 had HP-associated chronic antral gastritis confirmed by histology and positive urease test; t he control group included 10 healthy patients. There was no difference betw een the groups with regard to age, gender, and number of smokers. All patie nts with HP infection were diagnosed with diffuse antral gastritis. Histopa thology showed that 11 (49%) had some degree of atrophy. Of the 11 patients , 7 were classified as having chronic atrophic gastritis (CAG) without inte stinal metaplasia (IM), 4 had IM, and none had dysplasia. The plasma concen trations of selenium were found to be very similar in controls and HP-infec ted subjects (68.0 +/- 25.97 mug/L and 71 +/- 32.9 mug/L, respectively; p > 0.05). The antral biopsy samples of the patients with HP-associated gastri tis contained significantly higher levels of tissue selenium than the contr ols (20.17 +/- 19.74 mug/g and 2.83 +/- 1.42 mug/g, respectively; p < 0.05) . Also, it was shown that antral tissue selenium levels decrease after succ essful HP eradication therapy (20.17 +/- 19.4 mug/g and 7.4 +/- 4.56 mug/g, respectively; t < 0.05). The patients with HP gastritis were assigned to m ild, moderate, and severe gastritis groups, according to the histopathologi c degree of inflammation present. The antral gastric selenium levels were s ignificantly higher in patients with moderate and severe HP gastritis (21.1 3 +/- 22.5 mug/g and 22.81 +/- 17.35 mug/g, respectively) than in patients with mild gastric inflammation (9.53 +/- 10,3 mug/g; p < 0.05). The seleniu m concentrations in the biopsies of patients with CAG were significantly lo wer than in those with HP gastritis who did not have CAG (9.45 <plus/minus> 6.44 mug/g vs. 19.13 +/- 22.48 mug/g, respectively; p < 0.05). Conclusions : Selenium accumulates in gastric tissue when it is needed, as is the case in HP-related antral inflammation. This reactive increase in gastric mucosa l selenium seems to disappear in the presence of precancerous gastric lesio ns in the setting of HP-associated gastritis.