OBJECTIVE
To study the association of cortisol level, clinical features of depression, its nosological type, and the therapeutic response in female patients.
MATERIAL AND METHODS
69 females aged 18 to 50 were examined; clinical-psychopathological, clinical-prospective, psychometric, laboratory, and statistical methods were used.
RESULTS
17 patients were included in the group with depression without signs of resistance, and 52 in the group of therapeutically resistant depression (TRD). Hypercortisolemia at baseline was observed in 23% of patients, and hypocortisolemia in 6%. The absence of cortisol inhibition in a low-dose dexamethasone suppression test (LDDST) was found in 42% of patients. Patients with hypercortisolemia were more likely to be diagnosed with paroxysmal schizophrenia compared to patients with normal cortisol: 3/16 (19%) vs. 1/49 (2%), respectively (p=0.043). There were no differences in the clinical and psychopathological structure of depression and its formal severity in patients with hypercortisolemia and normal cortisol levels. In psychometric assessment, patients with hypercortisolemia had significantly higher scores of psychomotor retardation (HAMD, case report form) than those with normal cortisol levels (p=0.009). In the group with negative LDDST, significantly higher agitation (p=0.045) and adynamia (p=0.017) scores were found than those with positive LDDST. In patients with abnormal circadian rhythm of cortisol secretion, significantly higher anhedonia scores were noted than in patients with normal daily cortisol secretion (p=0.02). The state of patients with negative LDDST was significantly worse at follow-up examination than in those with positive LDDST (p=0.04). In patients with a good response to treatment, the cortisol level in LDDST upon repeated examination was significantly lower than in non-curable patients: 34.1 [22.8—65.3] and 80.2 [66.8—120.8] nmol/L, respectively (p=0.02).
CONCLUSIONS
In patients with depression, the prevalence of hypothalamic-pituitary-adrenal (HPA) axis dysfunction is higher than in the general population. HPA axis dysfunction appears to be associated with psychomotor retardation, adynamia, agitation, and anhedonia. The lack of cortisol inhibition in LDDST is the most reliable laboratory marker of a low-curable depressive state. Absolute treatment resistance in depression is associated with HPA axis dysfunction.
