2001
DOI: 10.1176/appi.ajp.158.4.641
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Urinary Free Cortisol in Chronic Fatigue Syndrome

Abstract: There is mild hypocortisolism in chronic fatigue syndrome. Whether a primary feature or secondary to other factors, hypocortisolism may be one factor contributing to the symptoms of chronic fatigue syndrome.

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Cited by 80 publications
(55 citation statements)
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“…It has been proposed that with time, longstanding strain on the HPA axis may lead to hypocortisolism [15][16][17][18]. Although the mechanisms underlying this type of dysregulation in humans are not well understood, data indicate that such conditions as posttraumatic stress disorder (PTSD), CFS, fibromyalgia, and VE are characterised by excessively low levels of cortisol [19][20][21][22][23][24][25][26][27][28][29][30][31]. Some studies, however, have failed to demonstrate differences in cortisol levels between CFS patients and controls [32], and others [33] have even reported the opposite pattern, i.e., raised salivary cortisol in CFS.…”
Section: Introductionmentioning
confidence: 99%
“…It has been proposed that with time, longstanding strain on the HPA axis may lead to hypocortisolism [15][16][17][18]. Although the mechanisms underlying this type of dysregulation in humans are not well understood, data indicate that such conditions as posttraumatic stress disorder (PTSD), CFS, fibromyalgia, and VE are characterised by excessively low levels of cortisol [19][20][21][22][23][24][25][26][27][28][29][30][31]. Some studies, however, have failed to demonstrate differences in cortisol levels between CFS patients and controls [32], and others [33] have even reported the opposite pattern, i.e., raised salivary cortisol in CFS.…”
Section: Introductionmentioning
confidence: 99%
“…Hypothyroid patients also have clear evidence of CRH hyposecretion. [8][9][10][11] Finally, the hypothesis that antidepressants exert their clinical effects through direct modulation of the glucocorticoid hormones and their receptor is one of the most striking and innovative models of the mechanism of action of this class of drugs. [12][13] We will review the evidences supporting that: 1) HPA axis hyperactivity plays an important role in the pathogenesis of major depression; 2) this hyperactivity is mainly due to an impaired feedback inhibition by circulating glucocorticoid hormones on the HPA axis; 3) this impaired feedback inhibition is related to a decreased function of the glucocorticoid receptors (GR), which mediate the effects of glucocorticoid hormones, including the negative feedback on the HPA axis; and 4) antidepressants act by reversing these changes in the GR function and thus normalising HPA axis hyperactivity in patients with major depression.…”
Section: Introductionmentioning
confidence: 99%
“…Furthermore, neurobiological investigations have repeatedly shown hypothalamo-pituitary-adrenal axis functioning to be perturbed in CFS as well as FM, implying a lack of reactivity of this axis and resulting in decreased cortisol secretion [24, 25, 26]. …”
Section: Introductionmentioning
confidence: 99%