What is the pathogenesis of pseudo-Cushing’s syndrome?

Many of the conditions mentioned above have underlying defect in HPA axis or other physiological mechanism which leads to pseudo-Cushing’s state. Depression: It is hypothesized that endogenous CRH is elevated in depression. The adrenal glands would then hypertrophy leading to the increased response of cortisol to ACTH. Cortisol feedback to the corticotroph would remain present, although also blunted. Most of these changes are reversible after recovery from depression. Alcoholism: There is a hypersecretion of CRH in chronic alcohol abuse and chronic liver disease. Also, in alcoholism, there appears to be impaired binding of cortisol to cortisol-binding globulin (CBG), leading to elevated levels of free cortisol. Another possible explanation for pseudo-Cushing’s syndrome in patients with alcohol abuse is impaired hepatic metabolism of cortisol. Lastly, AVP levels are elevated in patients with decompensated liver disease which may stimulate cortisol secretion. Obesity: In obesity, there is an activation of HPA axis, probably attributed to increased metabolism of cortisol. The other causes of pseudo–Cushing’s are less likely to have clinical features of Cushing’s syndrome but only have biochemical hypercortisolism.