Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was undertaken to determine the utility of the Dexamethasone Suppression Test (DST) for diagnosing depression in institutionalized mentally retarded persons. Depressed and nondepressed institutionalized mentally retarded persons were given 1 mg dexamethasone for an overnight DST. Serum cortisol concentrations greater than 4 micrograms/dl at both 8:00 AM and 4:00 PM provided discrimination of depressed from nondepressed groups. Also, using the criteria of serum cortisol concentrations greater than 4 micrograms/dl at 8:00 AM and 4:00 PM, at 4:00 PM and 10:00 PM, or at 8:00 AM, 4:00 PM, and 10:00 PM differentiated these groups. These results suggest that the DST may be useful for detecting melancholia among institutionalized retarded persons.
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PMID:The dexamethasone suppression test in depressed retarded adults: preliminary findings. 402 99

The authors studied the Dexamethasone Suppression Test (DST) in chronic pain patients with and without major depression, using items from a modified version of the Hamilton Depression Scale, the Hamilton Anxiety Scale, and the Montgomery-Asberg Depression Rating Scale. The purpose of the study was to identify the factor or factors which discriminated DST suppressors from nonsuppressors. The data suggest that depression and its profile are efficient discriminators of suppressors and nonsuppressors. Anxiety-related items were not as good as discriminators. The items that identified nonsuppression were the items that are often seen in combination in endogenous depression.
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PMID:What does the dexamethasone suppression test identify? 402 15

Previous reports of cognitive and social improvement in the mentally retarded after administration of MSH/ACTH fragments suggested disregulation of the hypothalamic-pituitary-adrenal (HPA) axis. The current study examined the integrity of this system with the Dexamethasone Suppression Test (DST). The DST is a biological index of HPA integrity and recently has been used as a diagnostic aid for endogenous depression. Thirty-five mentally retarded patients were administered 1 mg of dexamethasone just after a sample of blood was taken. Blood samples were analyzed for cortisol by RIA at 11:00 p.m. (basal), 8:00 a.m., 4:00 p.m., and 10:00 p.m. Between 40% and 48% (depending on sampling) of the patients failed to suppress cortisol (greater than 4 micrograms/dl), after the DST challenge. The results suggested that a significant proportion of mentally retarded patients have a DST index reflecting a disordered HPA axis and complements earlier studies of cognitive enhancement observed after treatment with MSH/ACTH fragments. The possibility that the stress of hospitalization was related to a disordered HPA was suggested. The possible co-existence of depression in the mentally retarded invites further study.
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PMID:Disregulation of hypothalamic-pituitary-adrenal axis in the mentally retarded. 403 19

Fourteen of 64 alcoholic inpatients (22%) showed a nonsuppression postdexamethasone response when tested between the second and fifth days of admission. No association with alterations of hepatic enzymes (GGT, SGOT, SGPT) was observed. At retest (in the fourth week of abstinence), no abnormal response to the Dexamethasone Suppression Test (DST) was detected. The nonsuppressor alcoholics did not meet the criteria for major depression according to the Research Diagnostic Criteria (RDC). The data indicate a lack of specificity of the DST for the diagnosis of depression in alcoholics during the first days of withdrawal.
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PMID:Reversal of abnormal dexamethasone suppression test in alcoholics abstinent for four weeks. 405 17

Although the platelets of the mouse are refractory to the direct effects of platelet-activating-factor (PAF), tail vein injection of 10-150 micrograms/kg PAF produces lethal anaphylactic shock. Sensitivity varies with strain and source: Swiss Webster mice show a range of sensitivity and DBA/2 (complement C5-deficient) mice are very resistant. At lethal doses of PAF, animals show labored respiration and general depression; death occurs within 15-45 min. Dexamethasone administered at least 1.5 hr prior consistently protects, whereas the cyclooxygenase inhibitors do not. Antihistamines, adrenergic antagonists, and methysergide have no effect, but cyproheptadine is partially protective at near lethal doses. Calcium entry blockers and calcium chelators, tetracycline and chlortetracycline are partially protective at very high doses consistent with non-specific effects on calcium dependent processes. The arachidonic acid lipoxygenase inhibitors BW755c, phenidone, nordihydroguaiaretic acid and diphenyldisulfide provide nearly complete protection after oral administration of 50-200 mg/kg. Phosphodiesterase inhibitors and dapsone are also effective orally. The leukotriene antagonist FPL55712 administered intraperitoneally (10 mg/kg) 5 min. prior to PAF challenge provides almost complete protection. PAF-induced mortality in the mouse represents a small animal model of systemic anaphylaxis particularly useful for the systemic testing of arachidonic acid lipoxygenase inhibitors and leukotriene antagonists.
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PMID:Pharmacological investigation of the mechanisms of platelet-activating factor induced mortality in the mouse. 408 Oct 60

The applicability of the Dexamethasone Suppression Test (DST) with 39 mentally retarded individuals was examined. Subjects were assigned to one of three groups based upon the presence of zero, one, or two (or more) primary behaviors: unprovoked aggressive/assaultive behavior, self-injurious behavior, and severely withdrawn behavior. Chi-square analysis revealed that individuals exhibiting two or more of these types of behavior were more likely to obtain a positive DST result than were individuals exhibiting only one behavior. Results support the hypothesis that retarded persons can become depressed (as defined by the DST) and may express the depression through these behaviors. Furthermore, these results suggest that the current diagnostic criteria for depression in the retarded population need to be revised.
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PMID:Use of the dexamethasone suppression test to detect depressive disorders of mentally retarded individuals. 408 5

The relationship of the endogenous opioid system and the hypothalamic-pituitary-adrenal axis to obesity was studied. Morning levels of plasma cortisol and beta-endorphin immunoreactivity in obese patients before diet treatment were found to be no different from those in matched family members of normal weight. In 32 untreated obese patients, no relationship between weight or body mass index (a measurement of obesity) and plasma levels of beta-endorphin immunoreactivity or cortisol was found. However, plasma cortisol levels were significantly correlated with obese patient ratings on the depression subscale of the General Health Questionnaire. Dexamethasone administration failed to suppress plasma beta-endorphin levels in untreated obese patients, but this finding has been reported in normal subjects in whom a similar assay methodology was used; it suppressed plasma cortisol levels in 29 of 32. The three patients resistant to suppression also suffered from benign essential hypertension. Plasma beta-endorphin immunoreactivity was unchanged, but cortisol levels significantly decreased as weight was lost on a 400-calorie/day modified protein fast. Patients who failed to complete the 6-month diet program had significantly increased plasma beta-endorphin levels compared to those who successfully completed the program.
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PMID:Plasma cortisol and beta-endorphin immunoreactivity in human obesity. 609 83

Nowadays the diagnosis of depression can be made through two neuroendocrine tests, which tend to become common: the TRH test and the Dexamethasone Suppression Test which have a wide diagnostic accuracy. Any abnormal finding could implicate a dysfunction of neurotransmitter systems. They are of diagnostic assistance in endogenous depressions supposed to be responsive to antidepressants. They might also be a practical monitor of treatment response since the test results reverting to normal seems to indicate recovery whereas persisting abnormal results are a possible predictor of relapse.
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PMID:[Biologic diagnosis of depression by the TRH and dexamethasone tests]. 613 96

Neuroendocrine abnormalities present in depressive illness and use of the dexamethasone suppression test (DST) in diagnosing depression are reviewed. The coexistence of neuroendocrine disturbances and depressive illness may be explained by a central nervous system neurochemical abnormality. Norepinephrine appears to inhibit hypothalamic corticotropin-releasing factor, thus decreasing ACTH secretion by the pituitary and, in turn, cortisol secretion by the adrenal glands. Thus, a deficiency in brain norepinephrine may lead to both depressive symptoms and increased adrenal cortisol production. Episodes of cortisol secretion are longer and more frequent in depressed patients, and the circadian rhythm of cortisol release is altered. Dexamethasone does not suppress plasma cortisol levels in depressed patients as compared with normal subjects. Abnormal DST results were obtained in 40-70% of inpatients and 20-50% of outpatients diagnosed as having unipolar primary depression or major depressive illness. The incidence of abnormal DST results in most nondepressed psychiatric patients is comparable with that in normal subjects. DST results do not distinguish between unipolar and bipolar depression but may differentiate primary from secondary depression. Depressed patients with abnormal DSTs responded positively to drug treatment. DST nonsuppressors responded more favorably to norepinephrine-reuptake blockers, while DST suppressors preferentially improved with serotonin-reuptake blockers. Normalization of DST response has been associated with clinical improvement. Certain drugs, a number of psychiatric conditions, and several major physical illnesses may alter DST response. The DST is a commonly used and practical tool in evaluating depressive illness; however, its diagnostic value in depressed outpatients and elderly depressed patients is not clear.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dexamethasone suppression test in diagnosis of depressive illness. 614 96

5-Hydroxyindoleacetic acid (5-HIAA) and homovanillic acid (HVA) were measured in the spinal fluid of 45 women hospitalized in a psychiatric department for major depression (14 cases), schizophrenia (18 cases) and alcohol dependence (13 cases). Dexamethasone suppression tests were performed following CSF examinations in all patients, and TRH stimulation tests were also made in six subjects. All biological examinations were carried out in a drug-free state. The Marke-Nyman Temperament scale was administered to all patients as soon as severe psychotic disturbances subsided and sufficient cooperation was achieved, but no later than 10 days following biological examinations. The MNT was repeated after recovery to check reliability of the test results during an episode of a psychiatric disorder. CSF amine metabolite concentrations did not differ significantly in the three patient groups; postdexamethasone average cortisol levels were above the critical level (5 micrograms/dl) in each group, the highest values being found in major depression. One of the three MNT factors was inhomogeneous among diagnostic groups (validity: low in depression and alcoholism), but the other two also differed from a healthy control population. Correlation structure between biological and psychological variables was homogeneous throughout the diagnoses and a significant inverse correlation was found only between CSF 5-HIAA and the validity factor of MNT. Maximal TSH response to TRH stimulation correlated with both solidity and stability in the MNT scale. Since MNT results proved to be stable even during an illness episode, a possible link is suggested between personality traits and central serotonin metabolism.
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PMID:Relationship between cerebrospinal fluid amine metabolites, neuroendocrine findings and personality dimensions (Marke-Nyman scale factors) in psychiatric patients. 619 Mar 56


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