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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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By Riedel W, Layka H, Neeck G • • March 6, 1998

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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