Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, & LH in patients with fibromyalgia (FM) syndrome following systemic injection of the relevant hypothalamic-releasing hormones

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To study the hormonal perturbations in FMS patients we

injected sixteen FMS patients and seventeen controls a

cocktail of the hypothalamic releasing hormones:

Corticotropin-releasing hormone (CRH), Thyrotropin- releasing

hormone (TRH), Growth hormone-releasing hormone (GHRH), and

Luteinizing hormone-releasing hormone (LHRH) and observed the

hormonal secretion pattern of the pituitary together with the

hormones of the peripheral endocrine glands. We found in FMS

patients elevated basal values of ACTH and cortisol, lowered

basal values of insulin-like growth factor I (IGF-I) and of

triiodothyronine (T3), elevated basal values of

follicle-stimulating hormone (FSH) and lowered basal values of

estrogen.

Following injection of the four releasing-hormones,

we found in FMS patients an augmented response of ACTH, a

blunted response of TSH, while the prolactin response was

exaggerated. The effects of LHRH stimulation were investigated

in six FMS patients and six controls and disclosed a

significantly blunted response of LH in FMS. We explain the

deviations of hormonal secretion in FMS patients as being

caused by chronic stress, which, after being perceived and

processed by the central nervous system (CNS), activates

hypothalamic CRH neurons. CRH, on the one hand, activates the

pituitary-adrenal axis, but also stimulates at the

hypothalamic level somatostatin secretion which, in turn,

causes inhibition of GH and TSH at the pituitary level.

The

suppression of gonadal function may also be attributed to

elevated CRH by its ability to inhibit hypothalamic LHRH

release, although it could act also directly on the ovary by

inhibiting FSH-stimulated estrogen production. We conclude

that the observed pattern of hormonal deviations in FMS

patients is a CNS adjustment to chronic pain and stress,

constitutes a specific entity of FMS, and is primarily evoked

by activated CRH neurons.

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