Cortisol and treatment of depression: predictive value of spontaneous and suppressed cortisol levels and course of spontaneous plasma cortisol

Abstract

In 72 consecutive depressed hospitalized patients afternoon plasma cortisol was measured in three ways before treatment with antidepressants: 1) Spontaneous (n = 72), 2) 2h after oxazepam suppression (45 mg, n = 28; 60 mg, n = 37) and 3) 16 h after dexamethasone suppression (2 mg, n = 71). In addition, spontaneous cortisol was measured after 3 weeks' treatment (n = 55) and 5 weeks' treatment (n = 36). Both spontaneous and suppressed cortisol levels seemed to have a predictive value in the endogenously depressed patients: complete responders had significantly lower pretreatment cortisol levels compared to poor responders. However, other covarying factors such as distress and age may as well account for the differences in treatment effect. During treatment a significant decrease of spontaneous cortisol was found from about 400 nM in poor responders and 325 nM in complete responders to about 300 nM in all groups. There was a positive correlation between pre- and post-treatment cortisol levels and between pretreatment levels and per cent fall in spontaneous cortisol levels.

Depression and Late Mortality After Myocardial Infarction in the Enhancing Recovery in Coronary Heart Disease (ENRICHD) Study

“…Other potential differences between the patients who improved and those who did not are suggested by studies of treatment-refractory depression. Patients with treatment-refractory depression have evidence of adrenergic and serotonergic disturbances (20), hypothalamic-pituitary-adrenal axis dysregulation (21)(22)(23), elevated inflammatory markers suggesting an immunological acute phase response (24,25), and low plasma folate and high homocysteine levels (26). All of these abnormalities have also been suggested as possible mechanisms underlying the effect of depression on mortality in patients with CHD (27).…”

Treatment-Resistant Depression and Mortality After Acute Coronary Syndrome

“…Elevated inflammatory markers consistent with an acute phase immunological response(28–33), HPA axis and ANS dysregulation(34–37), low thyroid hormone levels(37), and low plasma levels of omega-3 free fatty acids(38), have all been associated with poor response to a variety of antidepressants. In separate studies, they have also been identified as risk factors for cardiac morbidity and mortality.…”

Increased levels of alpha‐1‐acid glycoprotein and interleukin‐6 in refractory depression

“…Other findings suggest hypothalamic-pituitary-adrenal (HPA) axis hyperactivity involvement in the pathogenesis of RD. Christiansen et al (1989) found poor response to antidepressant treatment in major depressed patients with high spontaneous cortisol levels. Others (McLeod, 1972;Amsterdam et al, 1983) observed poor response to tricyclic antidepressants in patients having pathological results on the dexamethasone suppression test (DST).…”