FUNCTION OF THE HYPOTHALAMIC-PITUITARY-ADRENAL AXIS IN PATIENTS WITH FIBROMYALGIA AND LOW-BACK-PAIN

Objective. We suggested fibromyalgia (FM) is a disorder associated wit h an altered functioning of the stress-response system. This was concl uded from hyperreactive pituitary adrenocorticotropic hormone (ACTH) r elease in response to corticotropin-releasing hormone (CRH) and to ins ulin induced hypoglycemia in patients with FM. In this study, we teste d the validity and specificity of this observation compared to another painful condition, low back pain. Methods. We recruited 40 patients w ith primary FM (F:M 36:4), 28 patients (25:3) with chronic non-inflamm atory low back pain (LBP), and 14 (12:2) healthy, sedentary controls. A standard 100 mu g CRH challenge test was performed with measurement of ACTH and cortisol levels at 9 time points. They were also subjected to an overnight dexamethasone suppression test, followed by injection of synthetic ACTH(1-24). At 9 AM, the patients divided in 2 groups, r eceived either 0.025 or 0.100 mu g ACTH/kg body weight to test for adr enocortical sensitivity. Basal adrenocortical function was assessed ma inly by measurement of 24 h urinary excretion of free cortisol. Result s. Compared to the controls, the patients with FM displayed a hyperrea ctive ACTH release in response to CRH challenge (ANOVA interaction eff ect p = 0.001), The mean ACTH response of the patients with low back p ain appeared enhanced also, but to a significantly lesser extent (p = 0.02 at maximum level) than observed in the patients with FM. The cort isol response was the same in the 3 groups. Following dexamethasone in take there were 2 and 4 nonsuppressors in the FM and LBP groups, respe ctively. The very low and low dose of exogenous ACTH(1-24) evoked a do se and time dependent cortisol response, which, however, was not signi ficantly different between the 3 groups. The 24 h urinary free cortiso l levels were significantly lower (p = 0.02) than controls in both pat ient groups; patients with FM also displayed significantly lower (p < 0.05) basal total plasma cortisol than controls. Conclusion. The prese nt data validate and substantiate our preliminary evidence for a dysre gulation of the HPA axis in patients with FM, marked by mild hypocorti solemia, hyperreactivity of pituitary ACTH release to CRH, and glucoco rticoid feedback resistance. Patients with LBP also display hypocortis olemia, but only a tendency toward the disrupted HPA features observed in the patients with FM. We propose that a reduced containment of the stress-response system by corticosteroid hormones is associated with the symptoms of FM.