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Function of the hypothalamic-pituitary-adrenal axis in patients with fibromyalgia (FM) & low back pain

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By Griep EN, Boersma JW, Lentjes EG, Prins AP, van der Korst JK, de Kloet ER • www.ProHealth.com • July 5, 1998


OBJECTIVE: We suggested fibromyalgia (FM) is a disorder
associated with an altered functioning of the stress-response
system. This was concluded from hyperreactive pituitary
adrenocorticotropic hormone (ACTH) release in response to
corticotropin-releasing hormone (CRH) and to insulin induced
hypoglycemia in patients with FM. In this study, we tested the
validity and specificity of this observation compared to
another painful condition, low back pain.

METHODS: We
recruited 40 patients with primary FM (F:M 36:4), 28 patients
(25:3) with chronic noninflammatory low back pain (LBP), and
14 (12:2) healthy, sedentary controls. A standard 100 microg
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 ACTH1-24. At 9 AM, the patients divided
in 2 groups, received either 0.025 or 0.100 microg ACTH/kg
body weight to test for adrenocortical sensitivity. Basal
adrenocortical function was assessed mainly by measurement of
24 h urinary excretion of free cortisol.

RESULTS: Compared to
the controls, the patients with FM displayed a hyperreactive
ACTH release in response to CRH challenge (ANOVA interaction
effect p = 0.001). The mean ACTH response of the patients with
low back pain appeared enhanced also, but to a significantly
lesser extent (p = 0.02 at maximum level) than observed in the
patients with FM. The cortisol response was the same in the 3
groups. Following dexamethasone intake there were 2 and 4
nonsuppressors in the FM and LBP groups, respectively. The
very low and low dose of exogenous ACTH1-24 evoked a dose and
time dependent cortisol response, which, however, was not
significantly different between the 3 groups. The 24 h urinary
free cortisol levels were significantly lower (p = 0.02) than
controls in both patient groups; patients with FM also
displayed significantly lower (p < 0.05) basal total plasma
cortisol than controls.

CONCLUSION: The present data validate
and substantiate our preliminary evidence for a dysregulation
of the HPA axis in patients with FM, marked by mild
hypocortisolemia, hyperreactivity of pituitary ACTH release to
CRH, and glucocorticoid feedback resistance. Patients with LBP
also display hypocortisolemia, 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.




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