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PubMed2003

Troglitazone induces CYP3A4 activity leading to falsely abnormal dexamethasone suppression test.

After evaluating a patient who appeared to have a falsely abnormal response to the dexamethasone suppression test while taking troglitazone, we examined the effects of troglitazone on the activity of hepatic CYP3A4 and the screening tests for Cushing's syndrome. We studied five healthy women and three healthy men, aged 25 +/- 2 yr, before and after treatment with troglitazone (600 mg daily) for 28 d. Baseline 0800 h cortisol and corticosterone were similar before and after troglitazone treatment. Before troglitazone treatment, all subjects suppressed 0800 h cortisol below 1.8 micro g/dl (mean, 0.66 +/- 0.08 micro g/dl) during the 1-mg overnight dexamethasone suppression test (DST), whereas during troglitazone treatment none of the subjects suppressed 0800 h cortisol below 1.8 micro g/dl (mean, 9.0 +/- 1.8 micro g/dl). Serum dexamethasone levels decreased by 66 +/- 4%, and the erythromycin breath test measurements increased by 27 +/- 8%, indicating increased CYP3A4 activity during troglitazone treatment. The hydrocortisone suppression test (HST) was performed by administering 50 mg hydrocortisone at 2300 h. Using the criterion of suppression of 0800 h plasma corticosterone by more than 50%, the specificity of the HST was 100% both before and after troglitazone treatment. In conclusion, troglitazone induced the activity of CYP3A4 leading to falsely abnormal DST. HST is a useful alternative to the DST in patients taking medications that increase the activity of CYP3A4.

Adult↗

PubMed1992

In vivo assessment of pituitary volume with magnetic resonance imaging and systematic stereology: relationship to dexamethasone suppression test results in patients.

The relationship between dexamethasone suppression test (DST) results and in vivo pituitary volume was studied in 24 psychiatric inpatients. The principles of systematic stereology were used to measure pituitary volume from 3-mm contiguous sagittal spin-echo magnetic resonance (MR) images of the brain. There was no correlation between pituitary volume and 3 p.m. or 10 p.m. postdexamethasone (post-DEX) plasma cortisol concentrations. However, when multiple regression analysis was performed to relate pituitary volume to gender, age, and post-DEX plasma cortisol concentrations, there was a significant relationship between pituitary volume and age, gender, and 10 p.m. post-DEX cortisol plasma concentration. This is the first study to demonstrate a method that directly measures, rather than estimates, in vivo pituitary volume. Furthermore, it suggests that activation of the hypothalamic-pituitary-adrenal axis in psychiatric patients, as manifested by elevated post-DEX cortisol concentrations, may influence pituitary volume.

Adult↗

PubMed1992

Depressive attributional style and the dexamethasone suppression test: relationship to the endogenous/melancholic distinction and to each other.

The dexamethasone suppression test (DST) and the depressive attributional style questionnaire (ASQ) were administered to 105 depressed patients prior to participation in a double-blind outpatient study and to 29 normal controls. The depressed patients were classified into three groups (1) met criteria for both research diagnostic criteria for definite endogenous depression and DSM III melancholia; (2) met criteria for neither, and (3) met criteria for one but not both. The group that met criteria for both RDC endogenous depression and DSM-III melancholia had a statistically greater frequency of abnormal DST versus the group that met neither criteria and the normal controls. With regard to ASQ, patients who met both criteria had statistically higher bad event internality scores but statistically lower bad event stability and globality scores as opposed to the group that met neither criteria. In general, normal controls had significantly lower bad event ASQ scores than the three depressive groups. There was no correlation between ASQ and DST, as both DST suppressors and nonsuppressors had similar ASQ scores and there was no correlation between ASQ bad event attributions and initial severity of depression.

Adult↗

PubMed1987

Serial Dexamethasone Suppression Tests and Clinical Outcome in ECT.

Serial dexamethasone suppression tests (DST), obtained during a course of electroconvulsive therapy in 43 severely depressed patients, did not exhibit relationships between the initial DST, final DST, or the change in DST with clinical outcome measures at the time of discharge. In 37 patients reviewed six months after discharge, no relationship with the continuation of improvement, rehospitalization, or suicide was found. We are unable to confirm a clinical application for the DST in the management of patients during a course of convulsive therapy.

Journal Article↗

PubMed1992

Urine free cortisol in the high-dose dexamethasone suppression test for the differential diagnosis of the Cushing syndrome.

OBJECTIVE: To develop criteria for interpreting the high-dose dexamethasone suppression test using urine free cortisol as an end point for the differential diagnosis of the Cushing syndrome. DESIGN: Retrospective review. SETTING: Inpatient research ward. PATIENTS: Patients (118) with surgically confirmed causes of the Cushing syndrome: 94 with pituitary disease, 14 with primary adrenal disease, and 10 with ectopic adrenocorticotropic hormone (ACTH) secretion. MAIN OUTCOME MEASURES: The sensitivity, specificity, and diagnostic accuracy were determined for the high-dose dexamethasone suppression test using urine free cortisol and using 17-hydroxysteroid excretion. For each analysis, patients with pituitary disease were considered to be "diseased" and patients with nonpituitary disease were considered to be "non-diseased". The level of suppression that gave 100% specificity was determined for each steroid. RESULTS: The accuracy of urine free cortisol when used as an end point in the high-dose dexamethasone suppression test was equivalent to that of 17-hydroxysteroid excretion. At all levels of sensitivity and specificity, however, the degree of suppression of urine free cortisol used for the diagnosis of pituitary disease was greater than that of 17-hydroxysteroid excretion. The likelihood ratios for pituitary disease based on urine free cortisol suppression of greater than 50%, of greater than 80%, and of greater than 90% were 4.2, 10.1, and "infinite," respectively. Suppression of urine free cortisol greater than 90% or suppression of 17-hydroxysteroid excretion greater than 64% was associated with 100% specificity. When these criteria were combined, the percentage of correct predictions (102 of 118 [86%; 95% CI, 78% to 92%]) was higher than that obtained using either steroid alone (89 of 118 [75%; CI, 65% to 83%]) (P = 0.009) and higher than that obtained using the traditional criterion of 50% suppression for 17-hydroxysteroid excretion (95 of 118 [80%; CI, 71% to 87%]) (P = 0.016). CONCLUSIONS: In the high-dose dexamethasone suppression test, the degree of suppression of urine free cortisol used for the diagnosis of pituitary disease is greater than that traditionally used for 17-hydroxysteroid excretion. The diagnostic performance of the test is improved by measuring both urine free cortisol and 17-hydroxysteroid excretion and by requiring greater suppression of both steroids.

17-Hydroxycorticosteroids↗

PubMed1986

Dexamethasone suppression testing in chronic renal failure: pharmacokinetics of dexamethasone and demonstration of a normal hypothalamic-pituitary-adrenal axis.

The status of the hypothalamic-pituitary-adrenal axis in chronic renal failure (CRF) was examined by dexamethasone suppression testing (DST) using oral overnight, oral and iv 8-h daytime, and standard 48-h oral dosage protocols. Based on data obtained after iv administration of dexamethasone, the daytime study was used to calculate pharmacokinetic parameters for dexamethasone (clearance, volume of distribution at steady state, and terminal t1/2). None of a group of seven uremic patients had suppressed plasma cortisol concentrations after administration of 1 mg dexamethasone, orally, the night before. Six normal subjects and six patients with CRF participated in the pharmacokinetic study. There was no significant difference between the groups with respect to clearance, volume of distribution at steady state, or t1/2 of dexamethasone, indicating that patients with CRF metabolize dexamethasone in a fashion similar to that of normal subjects. Daily patterns of plasma cortisol determined between 0800-1600 h on a day when dexamethasone was not administered were similar in normal subjects and CRF patients. However, the degree of suppression of plasma cortisol after dexamethasone was significantly greater in the normal subjects (P less than 0.01), possibly due to a prolonged cortisol t1/2 in CRF. Nevertheless, the CRF patients did have decreased plasma cortisol levels from 4-8 h after iv and from 4-7 h after oral dexamethasone. The bioavailability of dexamethasone was not significantly different between the groups. When 48-h oral DSTs were performed in the CRF group, four of five patients had normal responses. The one patient who did not suppress had low levels of plasma dexamethasone, presumably due to decreased gastrointestinal absorption of dexamethasone. These results indicate that the metabolism of dexamethasone is similar in CRF patients and normal subjects, that normal suppression of plasma cortisol can be achieved in uremia if the duration of dexamethasone administration is prolonged sufficiently to compensate for the prolongation of cortisol t1/2 in CRF, and that it is essential to measure plasma dexamethasone as well as cortisol levels to interpret the results of a DST in CRF patients.

Administration, Oral↗

PubMed1983

The dexamethasone suppression test in depressed patients: clinical and biochemical aspects.

Endogenous depression (ED) is regarded as a psychiatric disease with a biological pathogenesis. Consequently patients with ED respond favourably to somatic treatment, whereas for non-endogenously depressed patients drug-treatment would be often inappropriate. Until now, psychopathologists have failed to define precisely the endogenous subtype of depression on clinical features alone. It is well established that a subgroup of depressed patients shows hypersecretion of cortisol and consequently inadequate suppression of cortisol after a test dose of dexamethasone. This dexamethasone suppression test (DST) was introduced as a laboratory marker, specifically identifying endogenously depressed individuals. This survey illustrates the present dispute about the diagnostic confidence and clinical value of the DST in a psychiatric population, and related biochemical aspects. The following conclusions are stated: (a) use of the DST to validate a theory of nosology is premature. (b) Influence of psychoactive drug medication, diet and weight loss have to be established. (c) Preliminary data suggest that abnormal DST results frequently normalize before clinical recovery and abnormal DST results may be observed before a relapse into depression is clinically apparent. From this it was concluded that the DST might be useful as predictor of clinical outcome. (d) From the association of depressive episodes with disinhibited HPA-activity, a causative role of corticotropin and glucocorticoids in the development of psychiatric illness can be hypothesized. Beside some pharmacological data no supportive evidence for this hypothesis is available. (e) Multisteroid analysis after dexamethasone has provided promising results indicating increased sensitivity of the test when based upon cortisol/11-deoxycortisol ratios and disturbed mineralocorticosteroid secretion in endogenously depressed patients.

Adjustment Disorders↗

PubMed1982

[ACTH in the dexamethasone suppression test].

Despite the great clinical importance of the low-dose dexamethasone suppression test (determination of cortisol after dexamethasone 2 mg p.o. at 11.00 p.m. in the evening before) and of the determination of ACTH in plasma, so far only little is known about the ACTH response to dexamethasone in normal subjects. In the present study cortisol and ACTH were determined by radioimmunoassay in normal subjects at 8.00 a.m., 10.00 a.m. and noon before and after dexamethasone. Additionally the cortisol response to ACTH was tested under both conditions. The ACTH concentrations in the morning show a periodicity quite similar to the well-known circadian rhythm of cortisol secretion. Dexamethasone blocks this periodicity without decreasing ACTH significantly. The cortisol response to ACTH after dexamethasone is normal. In the morning only a basal and presumably biologically inactive ACTH is secreted which can not further be suppressed by dexamethasone. Therefore it is advisable for the diagnosis of hypercortisolism to measure ACTH only in stimulation tests, e.g. insulin-induced hypoglycemia.

Adrenocorticotropic Hormone↗

PubMed1982

[ACTH response in the dexamethasone suppression test].

Adrenocorticotropic Hormone↗

PubMed1996

Overnight dexamethasone suppression test: comparison of plasma and salivary cortisol measurement for the screening of Cushing's syndrome.

The overnight 1-mg dexamethasone suppression test is a very good screening test for subjects suspected of having Cushing's syndrome. To simplify the procedure, we evaluated the 1-mg dexamethasone suppression test with measurement of salivary cortisol. We performed this test with plasma and salivary cortisol measurements in 27 patients with Cushing's syndrome and 64 normal controls. The sensitivity and specificity of plasma cortisol measurements were 100% and 87%, respectively, for a cut-off point of 100 nmol/l, in accordance with previous studies. The results of salivary cortisol showed the absence of overlap between the two groups, with a sensitivity and specificity of 100% for a cut-off point of 2.8 nmol/l. On a larger series, however, one might occasionally miss the diagnosis of a patient with Cushing's syndrome. Therefore, we favor a cut-off point of 1.9 nmol/l, the sensitivity remaining at 100% and the specificity being 94%. In conclusion we recommend the overnight dexamethasone suppression test with measurement of salivary cortisol as a screening test for Cushing's syndrome.

Adult↗

PubMed1985

Are schizophrenics with abnormal dexamethasone suppression test results a distinct subgroup?

Nonsuppression on the dexamethasone suppression test (DST) in schizophrenics has been reported by three independent groups. To elucidate the significance of this finding a schizophrenic cohort was tested on a wide range of parameters: computed tomography (CT), electroencephalography (EEG), the Halstead-Reitan Neuropsychological Battery (HRB), platelet monoamine oxidase activity (MAO), serum dopamine-beta-hydroxylase levels (DBH), premorbid personality adjustment, response to medication and family history of mental illness. Our results indicate that DST nonsuppressing and DST suppressing schizophrenics are no different on any of these measures, lending support to the notion that DST nonsuppression in schizophrenics is a random and changing event.

Adult↗

PubMed1982

The dexamethasone suppression test in panic disorder and agoraphobia.

Reports that imipramine and phenelzine prevent panic attacks in agoraphobia suggest the possibility that agoraphobia and/or panic disorder might be a clinical manifestation of underlying depression. To test this hypothesis, dexamethasone suppression tests (DSTs) were performed in 10 patients meeting DSM-III criteria for agoraphobia with panic attacks, 6 for panic disorder, and 4 whose diagnosis could have been either panic disorder or agoraphobia except that another axis I disorder precluded such a diagnosis. Abnormal DSTs were observed in only 3 patients and appeared to be attributable to causes other than panic attacks or agoraphobia. The results suggest that panic attacks and endogenous depression are separate disorders and that the antipanic properties of imipramine and phenelzine are separate from their antidepressant actions.

Adult↗

PubMed1987

Diagnostic utility of the dexamethasone suppression test.

This article discusses the current controversy surrounding the diagnostic utility of the Dexamethasone Suppression Test, addresses the questions raised by the recent editorial by Ross in this journal, discusses the general principles behind the development of tests, and estimates their diagnostic utility. This discussion aims to clarify some aspects of the controversy. It presents an operational analysis of the Dexamethasone Suppression Test as utilized at a state hospital. This operational analysis shows that the test may be useful in distinguishing schizophrenia from psychotic depression, and mania from schizophrenia. Furthermore, it shows that the test is not useful as a screening test. These results are compared with those obtained by other investigators. The authors further show how test results can be used rationally by clinicians by so-called threshold analysis. Clinical data from a state hospital are used to illustrate this.

Dexamethasone↗

PubMed1989

The plasma dexamethasone window: evidence supporting its usefulness to validate dexamethasone suppression test results.

Two doses of dexamethasone (DEX) (0.5 and 1.0 mg) were administered in a randomized crossover design to 31 patients with major depression, 9 healthy controls, and 14 nondepressed psychiatric patients. Using this modified Dexamethasone Suppression Test (DST), minimum DEX levels of 6 nmol/liter at 8:00 AM and 2.0 nmol/liter at 4:00 PM were required to achieve reliable suppression of cortisol in healthy controls and nondepressed psychiatric patients. Failure to achieve these minimum plasma DEX levels was associated with similar rates of nonsuppression in both depressed and nondepressed patients, thereby reducing the specificity of the DST. Conversely, high DEX levels greater than 13 nmol/liter at 8:00 AM or 4.0 nmol/liter at 4:00 PM were associated with abnormal "suppressibility" in depressed patients, thereby reducing the sensitivity of the test. Controlling for plasma DEX concentrations by selecting a test result that fell within a plasma DEX window at 8:00 AM and 4:00 PM increased the sensitivity and specificity of the DST. Significant differences in plasma DEX between suppressors and nonsuppressors were no longer evident when comparing patients with adequate DEX levels, thus ensuring that cortisol escape reflected HPA axis changes associated with depression and not peripheral mechanisms responsible for the availability of DEX. These results suggest that the clinical utility of the DST would be significantly enhanced by extending the standard 1.0-mg DST and retesting those patients with levels outside the DEX window with a higher or lower dose. The data also indicate that the measurement of plasma DEX is essential to validly interpret DST status and highlight the need to standardize DEX assays to compare DST results between research centers.

Adult↗

PubMed1983

Dexamethasone suppression test and serum prolactin in dementia disorders.

The dexamethasone suppression test (DST) was performed on 21 patients with dementia of the Alzheimer type (DAT), 11 patients with multi-infarct dementia (MI) and 14 healthy controls. Twelve of the DAT patients and eight of the MI patients showed abnormal lack of suppression, compared with just one member of the control group. Abnormal DST was related to dementia as such and not to age or depression, or to levels of CSF monoamine metabolites. Basal serum prolactin concentrations were not increased.

Aged↗

PubMed1985

A modified dexamethasone suppression test for endogenous depression.

In order to simplify the dexamethasone suppression test (DST), we have administered a lower dosage of dexamethasone (DEX) and shortened the sampling time to a single morning blood sample. DEX (in dosage increments from 0.125 to 1.0 mg, p.o.) was administered at 2300 h to normal volunteers in a double-blind randomized fashion, and blood samples were taken at 0700 h the following morning. While significant cortisol suppression occurred after the 0.375 mg, 0.5 mg, and 1.0 mg doses of DEX, the 0.5 mg dose was the smallest that clearly suppressed cortisol in all eight subjects. This dose then was used to test the feedback sensitivity of the central nervous system (CNS)-pituitary-adrenal axis in endogenously depressed patients. Twenty endogenously depressed patients and 20 normal volunteers were given both the standard 1.0 mg DST, with post-DEX serum cortisol determined at 1500 h, and the simplified 0.5 mg DST, with post-DEX serum cortisol determined at 0700 h. Four patients (20%) and one control (5%) were nonsuppressors after the 1.0 mg DST, and nine patients (45%) and one control (5%) were nonsuppressors after the 0.5 mg DST. In addition, nine patients with major depression (nonendogenous subtype) and 15 patients with panic attacks also were studied using the 0.5 mg DST. Only 2 of these 24 patients (8%) were nonsuppressors. The results suggest that the single-sample 0.5 mg DST is more sensitive than the standard 1.0 mg DST, and the specificity of the modified test appears comparable to the standard form of the test.

Adult↗

PubMed1985

Does the dexamethasone suppression test predict antidepressant treatment success?

The 1 mg dexamethasone suppression test (DST) was carried out in patients with a major depressive illness in order to establish whether the results of this test, given before antidepressant or ECT treatment, could predict eventual therapeutic outcome. No significant difference could be detected in overall therapeutic improvement between those patients with a normal or abnormal DST response respectively, based on the 50 ng/ml cortisol cut-off point. However, using 100 ng/ml as a cut-off point it was found that patients with an abnormal DST response (i.e. a post-DST plasma cortisol concentration greater than or equal to 100 ng/ml) responded significantly better than those who had a normal DST response. These observations were statistically significant for those patients receiving antidepressants and in the combined treatment groups of those patients receiving either antidepressants or ECT.

Antidepressive Agents↗

PubMed1986

The dexamethasone suppression test in panic disorder and major depressive episodes.

Dexamethasone Suppression Tests (DST) were performed on 30 patients with panic disorder and on 30 patients treated for major depressive episodes in order to seek an answer to the question of whether or not the two disorders have a common biological background. The hypothesis was based on the results of family studies known from the literature and on the favorable therapeutic response obtained with tricyclic antidepressants. Normal suppressive (i.e., negative in our terminology) DSTs were found in 16.7% of the patients with panic disorder and in 56.7% of patients suffering from major depressive episodes. The anxiety indices of the two groups differed significantly from each other. The results do not suggest the possibility of a close genetic relationship between the two conditions.

Adult↗