CRH challenge test in anxious depression.

Recently, renewed interest has developed in the concept of anxious depression. Using an operational definition of "anxious depression" based on the SADS interview, 25 patients with major depressive disorder were separated into anxious (n = 14) and nonanxious (n = 11) subtypes. These two patient groups and normal control subjects received an intravenous corticotropin-releasing hormone challenge test. Adrenocorticotropic hormone (ACTH) and cortisol responses were compared among the three groups. Patients with anxious depression had significant attenuation of ACTH response when compared to nonanxious patients and normal control subjects.

Pituitary-adrenal axis response to arginine vasopressin in patients with major depression.

Arginine vasopressin (AVP) was administered to 21 patients with major depression and 20 normal control subjects. Thirty-two subjects also underwent an overnight dexamethasone suppression test. The patient group did not differ significantly from the control group in adrenocorticotropic hormone (ACTH) or cortisol response. Dexamethasone suppression status did not affect ACTH or cortisol response. This study supports the hypothesis that unlike the response to corticotropin releasing hormone, the ACTH response to AVP is not attenuated in depression.

Blunted ACTH response to hypoglycemic stress in depressed patients but not in patients with schizophrenia.

In this study, 7 hospitalized patients with major depression (MD), 5 hospitalized patients with schizophrenia (S), and 13 control subjects (C) were administered 0.15 units/kg of regular insulin at 1600 h by intravenous bolus infusion. ACTH, cortisol, and glucose levels were measured intermittently for 2h following infusion. Baseline ACTH, cortisol and glucose levels were similar in Cs, MDs, and Ss. The mean glucose nadir was equivalent for Cs, patients with MD, and patients with S. Patients with MD had a blunted ACTH response (F = 3.28; df = 12,126; p = .0004) and cortisol response (F = 4.20; df = 12,132; p = .0001) to hypoglycemia when compared to Cs and patients with S. Carroll Depression Rating Scale scores in patients with S (23 +/- 10) were similar to patients with MD (30 +/- 8) and significantly higher than in controls (1 +/- 2) (F = 55.2; df = 2.22; p = .0001). These findings suggest that patients with MD show different ACTH and cortisol responses to hypoglycemic stress which are not explained by negative feedback of baseline ACTH or cortisol, glucose nadir, or the number of depressive symptoms per se.

Comparison of time-integrated measurement of salivary corticosteroids by oral diffusion sink technology to plasma cortisol.

We report preliminary data on the standardization of a device used in the recently developed "Oral Diffusion Sink" (ODS) technology for the time-integrated measurement of salivary corticosteroids. The concentrations of corticosteroids collected with the ODS devices were compared to plasma cortisol and saliva corticosteroid levels measured simultaneously. Six volunteers installed the ODS devices into their mouths during unstimulated and ACTH (250 micrograms) stimulated periods. Blood and saliva samples were also collected during these periods. The integrated plasma cortisol response and saliva corticosteroid levels were strongly correlated with the time-integrated total corticosteroid measurement of the ODS devices as well as with the cortisol and cortisone fractions. This preliminary data suggests that the accuracy of assessing adrenocortical activity by the measurement of salivary corticosteroids collected with the ODS device is high in both normal and stimulated conditions in normal volunteers. Continued standardization and studies in the practical use of this technology could lead to an important tool in assessing adrenocortical abnormalities. The use of such technology would increase the convenience while reducing the cost and invasiveness of current provocative testing of adrenal functioning.

Human anterior pituitary response to exogenous arginine vasopressin.

The adrenocorticotropin-releasing effect of arginine vasopressin is well known. The effects of AVP on other anterior pituitary hormones remain confusing, with few in vivo human data available. Two human studies of exogenous AVP effects on ACTH, GH, TSH and prolactin are described. In the dosage and route of administration used, AVP was found to be a specific ACTH secretagogue.

Multiple steroid hormone levels in depressed patients and normal controls before and after exogenous ACTH.

Forty depressed patients and 36 age- and sex-matched controls were given 250 micrograms ACTH1-24 by IV bolus. Plasma steroid hormone levels were measured prior to and 60 min after ACTH administration. The depressed patients had significantly greater cortisol (F), 11-deoxycortisol (S), androstenedione (AD), and 17 alpha-hydroxyprogesterone (17 alpha-OHP) responses (delta; p less than 0.05) and a marginally greater 11 beta-hydroxyandrostenedione (11 beta-OHAD) response (delta; p = 0.091) than the controls. There was no significant difference in the corticosterone (B) response between the two groups. With the exception of 11 beta-OHAD, all the steroid hormones were significantly negatively correlated with age in the controls, but only S and AD marginally demonstrated this relationship in the depressed patients. F, S, AD, 17 alpha-OHP, and B, but not 11 beta-OHAD, were significantly positively correlated with each other in the controls, but only F was significantly correlated with AD in the depressed patients. These data suggest that the hypercortisolemia found in some depressed patients involves increased precursor and metabolite levels both at baseline and in response to exogenous ACTH, compared to controls. Furthermore, variability in these precursors is greater in depressed patients, and their relationship to age is lost. These findings are consistent with the hypothesis that adrenal products other than cortisol also could be related to affective symptoms.

Elevated CSF protein in male patients with depression.

Elevation of total protein is the most frequent pathologic finding in the cerebrospinal fluid (CSF) examination. It occurs in a variety of situations, such as inflammation or tumors of the central nervous system (CNS), degenerative disorders, and subarachnoid hemorrhage, or as a result of traumatic taps. It has also been reported, for unknown reasons, in patients with psychiatric disease. In a study of hormone changes in depression, 9 of 24 (38%) patients (13 male, 11 female) were found to have elevated CSF protein levels (greater than 45 mg/dl), whereas no elevations were found in healthy controls (8 male, 9 female). Eight of the patients with the elevated CSF protein levels were male (62%) and one was female (9%). Depressed patients had significantly higher CSF protein levels (44.7 +/- 18.0 mg/dl) than controls (31.5 +/- 6.0 mg/dl) (t = 3.32, df = 30.37, p = 0.002). No relationship was found between CSF protein levels and (1) the use of medication (tricyclic antidepressants, lithium carbonate, or monoamine oxidase inhibitors) or (2) post-dexamethasone suppression test cortisol levels. Female controls, however, tended to have lower protein levels than male controls, whereas female patients had significantly lower levels than male patients. Protein electrophoresis was performed on 21 of the 41 subjects (13 patients, 8 controls). Male patients had nonsignificantly higher absolute concentrations of CSF albumin and the globulin fractions when compared to male controls. These differences in CSF protein do not suggest monoclonal CSF protein production, nor are they the result of this elevated peripheral protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Urinary free cortisol levels in obsessive-compulsive disorder.

Seventeen obsessive-compulsive disorder (OCD) patients and 25 normal control subjects submitted 24-hour urine samples for measurement of urinary free cortisol (UFC). Thirteen of the 17 OCD patients submitted a second 24-hour urine collection after a 10-week trial of either clomipramine (n = 6) or placebo (n = 7). At baseline, the OCD patients had significantly higher UFC levels than the control group. After 10 weeks of clomipramine or placebo, however, the UFC levels for both OCD groups decreased and were comparable with those of the control group. Obsessive-compulsive symptomatology, as assessed by the Yale-Brown and the NIMH Global Obsessive-Compulsive Scales, improved in the clomipramine group but did not improve in the placebo group. There was a relationship between UFC levels and depressive symptoms.

Partial 11 beta-hydroxylase activity suppression after dexamethasone in patients with major depression.

Eleven beta-hydroxylase activity was assessed by measuring the cortisol to 11-deoxycortisol ratio in 20 control subjects, 38 patients with major depression, and five patients with Cushing's disease before and after 1 mg of dexamethasone. The mean levels of 11 beta-hydroxylase activity did not differ among groups before dexamethasone. After dexamethasone patients with Cushing's disease showed a nonsignificant increase in 11 beta-hydroxylase activity while patients with major depression and controls subjects both showed a decrease. Endogenous depressive patients were no more likely to show high 11 beta-hydroxylase activity than neurotic depressive patients; however, depressed patients with cortisol nonsuppression after dexamethasone were. Post-dexamethasone 11 beta-hydroxylase activity is positively correlated with age in both control subjects and patients with depression.