Role of endogenous cortisol on Helicobacter pylori colonization

Helicobacter pylori infects the gastric mucosa and can lead to chronic gastritis, gastric ulcer and gastric cancer. Colonization of H. pylori in the gastric mucosa is influenced by a variety of host, bacterial and environmental factors. Host defense mechanisms have been affected by endogenous glucocorticoids. We aimed to investigate the relationship between H. pylori and endogenous glucocorticoid. Forty cases with endoscopically and histologically proven H. pylori and 26 patients who did not have H. pylori on gastric biopsy samples were enrolled in our study. Cortisol was tested from 24-h collected urine samples. H. pylori (+) and H. pylori (−) groups consisted of 40 (28 women, 12 men; aged 44.85 ± 12.52 years) and 26 (22 women, 4 men; aged 52.27 ± 15.15 years) patients, respectively. Age and gender were similar in both groups. Body mass index, C-reactive protein and erythrocyte sedimentation rate were not statistically different between the two groups ( p > 0.05). 24-h urine cortisol amount was lower in patients with H. pylori (+) than H. pylori (−) cases. Present study demonstrates that patients with gastric H. pylori colonization have significantly lower cortisol levels when compared with H. pylori negative cases. There is a negative correlation between H. pylori colonization and urine cortisol output.