Glucocorticoid receptors, fibromyalgia and low back pain

Recently, fibromyaglia (FMS) was shown to be a disorder associated with an altered functioning of the stress response system. FMS patients display a hyperreactive pituitary adrenocorticotropic hormone (ACTH) release in response to corticotropin-releasing hormone (CRH) and to insulin-induced hypoglyc...

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Published in:	Psychoneuroendocrinology Vol. 22; no. 8; pp. 603 - 614
Main Authors:	Lentjes, E.G.W.M., Griep, E.N., Boersma, J.W., Romijn, F.P.T.H.M., de Kloer, E.R.
Format:	Journal Article
Language:	English
Published:	Oxford Elsevier Ltd 01-11-1997 Elsevier
Subjects:	Adult Anti-Inflammatory Agents - pharmacology Biological and medical sciences Cortisol Dexamethasone - pharmacology Diseases of the osteoarticular system Female Fibromyalgia Fibromyalgia - metabolism Fibromyalgia - physiopathology Glucocorticoid receptors Humans Hydrocortisone - blood Hypothalamo-Hypophyseal System - physiopathology Hypothalamus-pituitary-adrenal axis Low back pain Low Back Pain - metabolism Low Back Pain - physiopathology Lymphocyte Activation - drug effects Male Medical sciences Middle Aged Miscellaneous. Osteoarticular involvement in other diseases Monocytes - metabolism Receptors, Glucocorticoid - metabolism Thymidine - metabolism Fibromyalgia Hypothalamus-pituitary-adrenal axis Cortisol Glucocorticoid receptors Low back pain Human Urine Plasma Lumbar spine Hypothalamohypophysoadrenal axis Diseases of the osteoarticular system Spine disease Hydrocortisone Glucocorticoid Pain Adrenal hormone Rachialgia Hormonal investigation Hormonal receptor
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Summary:	Recently, fibromyaglia (FMS) was shown to be a disorder associated with an altered functioning of the stress response system. FMS patients display a hyperreactive pituitary adrenocorticotropic hormone (ACTH) release in response to corticotropin-releasing hormone (CRH) and to insulin-induced hypoglycemia. We suggested that negative feedback of cortisol could be deranged. Therefore we investigated the properties and function of the glucocorticoid receptors (GR) in FMS patients and compared the results with those of healthy persons and patients with chronic low back pain (LBP a localized pain condition). Forty primary FMS patients (F:M = 36:4), 28 LBP patients (25:3) and 14 (12:2) healthy, sedentary control persons were recruited for the study. Urinary free cortisol excretion in FMS and LBP patients was lower compared to controls. Only FMS patients displayed lower CBG and basal serum cortisol concentrations when compared to controls. However, plasma free cortisol concentrations were similar in the three groups. There was no difference in the number of GR per cell among the three groups (FMS: 6498 ± 252, LBP: 6625 ± 284, controls: 6576 ± 304), but the dissociationh constant ( K d ) of the FMS (14.5 ± 0.9 nmol/l) and LBP (14.7 ± 13 nmol/l) subjects was significantly higher than that of the controls (10.9 ± 0.8 nmol/l) ( p < .05). The maximal stimulation of the lymphocytes, as measured by the maximal thymidine incorporation (in the absence of cortisol) in the FMS group was approximately 1.5 times higher ( p < .05) than in the control or LBP group. The ED 50 (the cortisol concentration giving 50% inhibition of the thymidine incorporation), however, was identical in all three groups. We conclude that FMS patients have a mild hypocortisolemia, increased cortisol feedback resistance in combination probably with a reduced CRH synthesis or release in the hypothalamus. The role of the GR and mineralocorticoid receptor (MR) in the CRH regulation in the FMS patients remains to be solved.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23
ISSN:	0306-4530 1873-3360
DOI:	10.1016/S0306-4530(97)00061-9