Objective: To assess basal function and responsiveness of the hypothalamic-pituitary-adrenal (HPA) axis in patients with ankylosing spondylitis during dynamic testing. Methods: Insulin induced hypoglycaemia (IIH) (Actrapid HM 0.1 IU/kg, as intravenous bolus) was induced in 17 patients and 11 healthy controls matched for age, sex, and body mass index. Concentrations of glucose, adrenocorticotrophic hormone (ACTH), cortisol, insulin, dehydroepiandrosterone sulphate (DHEAS), 17a-hydroxyprogesterone, interleukin 6 (IL-6), and tumour necrosis factor a (TNFa) were determined in plasma. Results: Comparable basal cortisol levels were found in the two groups, with a trend to be lower in ankylosing spondylitis. In the ankylosing spondylitis group, there were higher concentrations of IL-6 (mean (SEM): 16.6 (2.8) pg/ml v 1.41 (0.66) pg/ml in controls; p,0.001) and TNFa (8.5 (1.74) pg/ml v 4.08 (0.42) pg/ml in controls; p,0.01). Glucose, insulin, ACTH, DHEAS, and 17a-hydroxyprogesterone did not differ significantly from control. The IIH test was carried out successfully in 11 of the 17 patients with ankylosing spondylitis, and the ACTH and cortisol responses were comparable with control. General linear modelling showed a different course of glycaemia (p = 0.041) in the ankylosing spondylitis patients who met the criteria for a successful IIH test compared with the controls.
Conclusions:The results suggest there is no difference in basal HPA axis activity and completely preserved responsiveness of the HPA axis in patients with ankylosing spondylitis. The interpretation of the different course of glycaemia during IIH in ankylosing spondylitis requires further investigation.A nkylosing spondylitis is a rheumatic disorder which typically affects the sacroiliac joints and the spine. It belongs to the group of spondylarthropathies with a higher prevalence in men. A strong association with the major histocompatibility complex class I molecule HLA B-27, together with hereditary, environmental, and other factors including endocrine perturbations, may operate in the pathogenesis of ankylosing spondylitis.1 Detailed relations are, however, still unclear.During the past decade data have accumulated suggesting a role for the neuroendocrine system in the pathogenesis of rheumatic diseases. Studies in patients with rheumatoid arthritis broadly support the hypothesis that the hypothalamic-pituitary-adrenal (HPA) axis plays a critical role in counterregulation of immune inflammatory processes. Thus dysregulation of the HPA axis response is likely to predispose individuals to the onset of chronic inflammatory diseases including ankylosing spondylitis, or to affect their severity. In contrast to rheumatoid arthritis, few published reports have addressed HPA axis activity in ankylosing spondylitis.The activity of the HPA axis is regarded as inappropriately normal with respect to the ongoing inflammation in rheumatoid arthritis.4 Decreased HPA axis activity seems to result from relative adrenal insufficiency, as reported in a subset of younger w...