It has been hypothesized that psychotic symptoms in depression may be due to increased
dopamine activity secondary to hypothalamic-pituitary-adrenal (HPA) axis overactivity.
To test this hypothesis we examined the cortisol response to dexamethasone suppression
test (DST, 1 mg orally) and multihormonal responses to apomorphine (APO, 0.75 mg SC)—a
dopamine agonist—in 123 drug-free DSM-IV severely-depressed inpatients: 81 without
psychotic features (SD; 35M/46F; mean age ± SD, 38.1 ± 10.6 years) and 42 with psychotic
features (SDP; 19M/23F; mean age 39.1 ± 9.7 years); and 36 hospitalized controls (HC;
15M/21F; mean age 35.8 ± 9.1 years). SDPs showed increased activity of the HPA system
(i.e. higher post-DST cortisol levels) than HCs (p < 0.00001) and SDs (p < 0.00002).
Although APO-induced cortisol stimulation was lower in SDPs than in HCs (p < 0.04)—owing
to a baseline cortisol effect—there were no differences in adrenocorticotropic hormone
(ACTH), prolactin (PRL), and growth hormone (GH) responses to APO between SDPs and
SDs and HCs. Moreover, in the total sample and in each diagnostic group, DST suppressors
and DST non-suppressors showed no differences in hormonal responses to APO. Therefore,
our study indicates that dopaminergic function, as assessed by the APO test, does
not differ between psychotic and nonpsychotic depressed patients, although HPA disinhibition
occurs more frequently in psychotic depressed patients. These results suggest that
there is no causal link between HPA axis hyperactivity and dopamine dysfunction at
the hypothalamic-pituitary level in psychotic depressed patients.
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© 2000 Published by Elsevier Inc.