Betty Jo Tricou

Plasma acth and cortisol levels in depressed patients: Relation to dexamethasone suppression test

Blood samples collected from normal subjects and newly hospitalized depressed patients at 8 AM on the day before and at 8 AM and 4 PM the day after receiving dexamethasone, 1 mg orally at 11 PM, were analyzed for ACTH and cortisol. The mean plasma ACTH values of these two groups were not significantly different at any of the times, while the cortisol levels of the depressed patients were significantly higher than those of the normal subjects at 8 AM pre-dexamethasone (P<0.001). There was no correlation between plasma ACTH and cortisol values in either group. The cortisol responses to dexamethasone in depressed patients revealed two subgroups. In one subgroup, the cortisol was suppressed as much as in normal subjects, but in the other, cortisol levels were not suppressed. The post-dexamethasone ACTH rebounded at 4 PM in the latter subgroup to higher values than in the subgroup with suppressed cortisol levels and in the normal subjects. After dexamethasone, the ACTH values were negatively correlated with plasma cortisol only in the normal subjects (P<0.01), not in the depressed patients. These results indicate that ACTH levels do not account for the elevated cortisol and the failure of dexamethasone to suppress cortisol levels in some depressed patients.

Effect of low-dose bromocriptine in treatment of psychosis: The dopamine autoreceptor-stimulation strategy

Bromocriptine (0.5–6.0 mg/day) was administered to seven unmedicated chronic schizophrenic and two schizoaffective patients. Transient slight improvement was noted in four patients and marked improvement in one other. Clinical improvement was associated with nausea and drowsiness. These doses of bromocriptine stimulated serum growth hormone and inhibited serum prolactin levels in some subjects. These results suggest that bromocriptine may stimulate dopamine autoreceptors and, through this mechanism, attenuate symptoms in a small proportion of psychiatric patients.

Serotonin uptake in blood platelets and the dexamethasone suppression test in depressed patients

Two putative biological markers of some forms of depressive illness, the dexamethasone suppression test (DST) and the Vmax of serotonin (5-hydroxytryptamine, 5-HT) uptake in blood platelets, were studied in 40 unipolar, bipolar, and schizoaffective depressed patients. The Vmax levels in those whose cortisol levels suppressed normally after dexamethasone (n = 25) were not significantly different from those of the nonsuppressors (n = 15). When a criterion of Vmax greater than or equal to 8.5 pmoles/10(7) platelets/minute of 14C-5-HT uptake was used as the lower limit of normal, 18 patients had Vmax values lower than normal, only four of whom were nonsuppressors. There was a tendency for the incidence of lower than normal Vmax levels in nonsuppressors (4/15, 26.7%) to be less than that of the suppressors (14/25, 56.0%). These results suggest that the two abnormalities are independent of each other but tend to support the hypothesis that decreased Vmax may be an adaptive response which restores serotonergic function to normal. Twenty-nine of the 40 patients (72.5%) had one or both abnormalities, a finding which suggests that determination of both parameters would significantly increase the proportion of depressed patients who could be diagnosed by these biological tests.

Effect of (des-tyr)-gamma-endorphin in schizophrenia

Des-tyrosine-gamma-endorphin (DT gamma E), a derivative of gamma-endorphin, which has been reported to have some neuroleptic-like properties in man, was administered to eight hospitalized schizophrenic patients (six chronic, one subacute, one acute) in an open study. Following an initial drug-free period, patients were given DT gamma E for 12 days in doses ranging from 1 to 10 mg/day. Two of the patients were markedly improved after receiving DT gamma E. The improvement was sustained for 2 months in one subjects, while the other deteriorated to pretreatment status within 48 hours of the discontinuation of DT gamma E. Of the other six patients, one showed moderate improvement, three showed minimal improvement, and two showed no change. Improvement was mainly in the area of social functioning; change in positive psychotic symptoms was less noticeable. The positive results obtained in this study in some subjects could have been nonspecific effects, rather than pharmacological action, since social functioning, the main area of improvement, may be especially sensitive to expectancy effects in open trials. Nevertheless, further study of DT gamma E in acute schizophrenics for longer periods appears indicated.