Helicobacter pylori infection and the hypothalamic-pituitary axis: association with cortisol and thyroid-stimulating hormone levels in adults.

BACKGROUND AND

OBJECTIVES

Helicobacter pylori is a common chronic bacterial infection primarily associated with gastrointestinal disease. Increasing evidence suggests that H. pylori may also exert systemic effects beyond the stomach, including possible modulation of neuroendocrine pathways. This study aimed to investigate the association between H. pylori infection and alterations in serum cortisol and thyroid-stimulating hormone (TSH) levels as indicators of hypothalamic-pituitary-adrenal (HPA) and hypothalamic-pituitary-thyroid (HPT) axis activity.

MATERIALS AND

METHODS

In this case-control study, 850 adults were enrolled, including 425 H. pylori-positive cases and 425 H. pylori-negative controls. Active H. pylori infection was determined using a monoclonal stool antigen test (HpSA). Fasting venous blood samples were collected between 08:00 and 10:00 AM under standardized conditions. Serum cortisol and TSH levels were measured using validated immunoassays. Group comparisons, correlation analysis, sex-stratified subgroup analysis, and receiver operating characteristic (ROC) curve analysis were performed.

RESULTS

H. pylori-positive participants had significantly higher serum cortisol levels and lower TSH levels compared with controls (both p < 0.001). A significant inverse correlation between cortisol and TSH was observed only in infected participants (r = -0.41, p < 0.001). These hormonal alterations were evident in both sexes. ROC analysis showed moderate discriminatory performance for cortisol (AUC = 0.71) and fair-to-moderate performance for TSH (AUC = 0.67).

CONCLUSION

H. pylori infection was significantly associated with elevated cortisol levels, reduced TSH levels, and an inverse relationship between both hormones in adults. These findings suggest that chronic H. pylori infection may influence both HPA and HPT axis regulation and support further investigation into its systemic neuroendocrine effects.