Journal: Annals of the New York Academy of Sciences. 2006 Nov;1088:41-51.
Authors and affiliation: Johnson EO, Kostandi M, Moutsopoulos HM. Department of Anatomy-Histology-Embryology, University of Ioannina, School of Medicine, Ioannina, Greece. [E-mail: email@example.com ]
To date, evidence suggests that rheumatic diseases are associated with hypofunctioning of the hypothalamic-pituitary-adrenal (HPA) axis. Sjogren’s syndrome (SS), the second most common autoimmune disorder, is characterized by diminished lacrimal and salivary gland secretion.
To examine HPA axis activity in SS patients, the adrenocorticotropin (ACTH) response to ovine corticotropin-releasing factor (oCRH) was used as a direct measure of corticotrophic function, and the plasma cortisol response to the ACTH released during oCRH stimulation as an indirect measure of adrenal function.
Significantly lower basal ACTH and cortisol levels were found in patients with Sjogren’s syndrome and were associated with a blunted pituitary and adrenal response to oCRH compared to normal controls.
Fibromyalgia (FM) patients demonstrated elevated evening basal ACTH and cortisol levels and a somewhat exaggerated peak, delta, and net integrated ACTH response to oCRH.
A subgroup of Sjogren’s syndrome patients also met the diagnostic criteria for FM and demonstrated a pituitary-adrenal response that was intermediate to Sjogren’s syndrome and Fibromyalgia.
These findings suggest not only adrenal axis hypoactivity in Sjogren’s syndrome and Fibromyalgia patients, but also that varying patterns of adrenal and thyroid axes dysfunction may exist in patients with different rheumatic diseases.