Maladjustement or inadequacy of the corticotrope axis in burnout situations
Résumé
The basic dosage of corticotropic system hormones (cortisol, ACTH, SDHEA) does not allow the evaluation of the nonadaptation of the corticotropic response to chronic stress that leads to burnout. Dynamic tests, of the adrenal response by tetracosactide and of corticotropic response by exposure to codified stress (Trier Social Stress Test, TSST), distinguish different response profiles between controls and burnout patients. The function of glucocorticoid receptors (GR) is the central point of regulation of stress adaptation; it is intrinsically determined by the genes of GR and its chaperone protein FKBP5 (genetic polymorphisms) but can be modified by epigenetic changes. Tests such as dexamethasone, dexamethasone-CRH and the study of dexamethasone-induced gene expression are the most sensible tests of GR sensibility. The data support hypersensitivity of GRs in burnout and post-traumatic stress disorder and hyposensitivity (or resistance) to severe depression.