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Glucocorticoid receptors, fibromyalgia (FM) & low back pain

  [ 17 votes ]   [ Discuss This Article ]
By Lentjes EG, Griep EN, Boersma JW, Romijn FP, de Kloet ER • www.ProHealth.com • November 5, 1997


Recently, fibromyalgia (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 dissociation
constant (Kd) of the FMS (14.5 +/- 0.9 nmol/l) and LBP (14.7
+/- 1.3 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 ED50 (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.




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