Objective: To explore the hypothalamic-pituitary-adrenal (HPA) axis in polymyalgia rheumatica (PMR).
Subjects and methods: This study was carried out on 13 female patients with PMR who were diagnosed according to the criteria of Chuang et al (Ann Intern Med 1982;97:672-80) and 10 healthy female subjects in the Department of Physical Medicine and Rehabilitation, Erciyes University Medical School. In the patient and control groups, basal cortisol, adrenocorticotrophic hormone (ACTH), 17alpha-hydroxyprogesterone (17-OHP), 11-deoxycortisol (11-S), dehydroepiandrosterone sulfate (DHEAS), androstenedione (A), prolactin (PRL), and thyroid stimulating hormone (TSH) levels were measured. Cortisol, 17-OHP, 11-S and A responses after the low-dose (1 microg) ACTH stimulation test and cortisol and DHEAS responses after the dexamethasone suppression test were detected. We also measured acute phase reactants including C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR).
Results: Age and sex characteristics were similar in both patient and control groups. The levels of basal hormones including cortisol, ACTH, 17-OHP, 11-S, DHEAS, A, prolactin and TSH and cortisol and DHEAS levels after the low-dose dexamethasone suppression test were not significantly different between the patient and control groups. However, cortisol/CRP and ACTH/CRP ratios were significantly lower in the patient group. Cortisol and DHEAS responses after the low-dose dexamethasone suppression test were not significantly different between the patient and control groups. Cortisol response after the 1 microg ACTH stimulation test was significantly lower in the patients than in the control group, but there were no significant differences in 17-OHP, 11-S and A responses between the patients and controls. Correlation analysis showed that there was a negative correlation between peak cortisol levels after the ACTH stimulation test and disease duration, and also a positive correlation between cortisol levels after the low-dose dexamethasone suppression test and acute phase reactants including CRP and ESR.
Conclusion: A significant low cortisol response to ACTH stimulation was detected in the patients with PMR. In addition, a negative correlation after the 1 microg ACTH stimulation test between peak cortisol levels and disease duration was detected. These findings may indicate hypoactivation in the HPA axis.