Evaluation of the hypothalamic–pituitary–adrenal axis in untreated patients with polymyalgia rheumatica and healthy controls

Abstract

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), 17α‐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 µg) 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 µg 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 µg ACTH stimulation test between peak cortisol levels and disease duration was detected. These findings may indicate hypoactivation in the HPA axis.