Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, and LH in patients with fibromyalgia syndrome following systemic injection of the relevant hypothalamic-releasing hormones
W. Riedel et al., Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, and LH in patients with fibromyalgia syndrome following systemic injection of the relevant hypothalamic-releasing hormones, Z RHEUMATOL, 57, 1998, pp. 81-87
To study the hormonal perturbations in FMS patients we injected sixteen FMS
patients and seventeen controls a cocktail of the hypothalamic releasing h
ormones: Corticotropin-releasing hormone (CRH), Thyrotropin-releasing hormo
ne (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. W
e found in FMS patients elevated basal values of ACTH and cortisol, lowered
basal values of insulin-like growth factor I (IGF-I) and of triiodothyroni
ne (T-3), elevated basal values of follicle-stimulating hormone (FSH) and l
owered 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 th
e deviations of hormonal secretion in FMS patients as being caused by chron
ic stress, which, after being perceived and processed by the central nervou
s system (CNS), activates hypothalamic CRH neurons. CRH, on the one hand, a
ctivates the pituitary-adrenal axis, but also stimulates at the hypothalami
c 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 rel
ease, although it could act also directly on the ovary by inhibiting FSH-st
imulated estrogen production. We conclude that the observed pattern of horm
onal deviations in FMS patients is a CNS adjustment to chronic pain and str
ess, constitutes a specific entity of FMS, and is primarily evoked by activ
ated CRH neurons.