Glucocorticoid receptors, fibromyalgia and low back pain

E. G.W.M. Lentjes; E. N. Griep; J. W. Boersma; F. P.T.H.M. Romijn; E. R. De Kloet

doi:10.1016/S0306-4530(97)00061-9

Glucocorticoid receptors, fibromyalgia and low back pain

E. G.W.M. Lentjes^*, E. N. Griep, J. W. Boersma, F. P.T.H.M. Romijn, E. R. De Kloet

^*Corresponding author for this work

Research output: Contribution to journal › Article › Academic › peer-review

84 Citations (Scopus)

Abstract

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 (K(d)) 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.

Original language	English
Pages (from-to)	603-614
Number of pages	12
Journal	Psychoneuroendocrinology
Volume	22
Issue number	8
DOIs	https://doi.org/10.1016/S0306-4530(97)00061-9
Publication status	Published - 1 Nov 1997

Keywords

Cortisol
Fibromyalgia
Glucocorticooid receptors
Hypothalamus-pituitary-adrenal axis
Low back pain

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10.1016/S0306-4530(97)00061-9

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title = "Glucocorticoid receptors, fibromyalgia and low back pain",

abstract = "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 (K(d)) 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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AU - Lentjes, E. G.W.M.

AU - Griep, E. N.

AU - Boersma, J. W.

AU - Romijn, F. P.T.H.M.

AU - De Kloet, E. R.

PY - 1997/11/1

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N2 - 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 (K(d)) 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.

AB - 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 (K(d)) 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.

KW - Cortisol

KW - Fibromyalgia

KW - Glucocorticooid receptors

KW - Hypothalamus-pituitary-adrenal axis

KW - Low back pain

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DO - 10.1016/S0306-4530(97)00061-9

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VL - 22

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JO - Psychoneuroendocrinology

JF - Psychoneuroendocrinology

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ER -

Glucocorticoid receptors, fibromyalgia and low back pain

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Keywords

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