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)

The authors studied 243 inpatients with unipolar depression who had received DSTs. Of 205 patients with primary depression, the 4 who later committed suicide were among 96 with abnormal DST results; 1 patients with secondary depression committed suicide despite a normal DST result. The authors suggest that hypothalamic-pituitary-adrenal dysfunction is associated with a type of primary depressive illness that is more likely to involve suicide than are other types.
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PMID:Suicide and the dexamethasone suppression test in unipolar depression. 725 95

We describe the development of a clinical algorithm to differentiate melancholic from non-melancholic depression, using refined sets of 'endogeneity' symptoms together with clinician-rated CORE scores assessing psychomotor disturbance. Assignment by the empirically developed algorithm is contrasted with assignment by DSM-III-R and with several other melancholia sub-typing indices. Both the numbers of 'melancholics' assigned by the several systems and their capacity to distinguish 'melancholics' on clinical, demographic and a biological index test (the DST) varied across the systems with the algorithm being as 'successful' as several systems that include inter-episode and treatment response variables. Analyses provide information on the criteria set developed for DSM-IV definition of 'melancholia'.
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PMID:Sub-typing depression, III. Development of a clinical algorithm for melancholia and comparison with other diagnostic measures. 748 Apr 61

Psychosocial (sociodemographic characteristics, loss and separation and family atmosphere in childhood, recent life events) and biological (family history, DST, TRH-test) variables were investigated in 180 patients with Major Depression (MD) and Dysthymic Disorder (DD). The aim of the study was to reveal certain differences between the chronic and non-chronic course of MD and the early- and late-onset subtypes of dysthymia. When comparing the two course patterns of MD, a higher rate of malignant tumours among first-degree relatives, a greater number of long-lasting stress situations before the index depressive episode, longer duration of the previous episodes, less frequent DST nonsuppression, and a blunted TSH response to TRH were found in patients with a chronic course of MD. Several factors seem to influence the course pattern of MD, or else the chronic form represents a subgroup within MD. The late-onset dysthymics were mainly women with a low level of education, a lower suicidal tendency, normal suppression in DST, and a lack of blunted TSH responses to TRH administration during the period of double depression. The early-onset dysthymics showed a higher number of persons who had never married, who presented a more traumatic and frustrating childhood background, and who had a higher rate of DST non-suppressors and blunted TSH responses after TRH administration during the period of their double depression. Our data suggest that late-onset dysthymia might be a biologically distinct subgroup of chronic depression.
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PMID:The role of psychosocial and biological variables in separating chronic and non-chronic major depression and early-late-onset dysthymia. 779 61

1. In the present study 63 stroke patients and 23 control patients participated. The presence and degree of depression was defined by the Hamilton Rating Scale for Depression and the Research Diagnostic Criteria. 2. The TRH stimulation test was performed in all the patients. 3. No difference in Delta Max TSH was found between stroke patients and control patients. 4. No difference in Delta Max TSH was found between patients with the lesion in the right or left hemisphere. 5. No correlation was found between the frequency of blunted response to the TRH stimulation test and the presence of depression. 6. No difference in Delta Max TSH was found between suppressors and non-suppressors to the DST.
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PMID:Neuroendocrine tests in depressive stroke patients. 782 55

1. Delta TSH, REM latency, 4 pm and 11 pm post-dexamethasone cortisol values were determined after a wash-out period in a group of 74 non-selected depressed patients who were diagnosed (according to RDC with the SADS) as follows: 46 definite and 10 probable MD, 4 minor and 14 intermittent depression. 2. These biological variables, as well as gender, age and basal TSH were introduced in a principal component analysis. The four first PC scores explaining up to 77% of the data set were further calculated for each patients and used in a cluster analysis. A three clusters solution was retained. 3. DST escape and increased TSH response to TRH each identified subgroups of depressed patients. Conversely, blunted TSH response or REM latency were inefficient to classify patients. 4. Thus, HPA hyperactivity characterized CL-I patients (n = 29). These were more severely depressed, displayed more endogenous features and were reported as being more anxious. 5. Increased TSH response to TRH identified CL-III, exclusively composed of female patients (n = 10) that displayed more apparent sadness and tended to be older. 6. In CL-II, the usual sex-ratio for depressive illness was reversed and patients (n = 35) exhibited the least HPA axis disturbances and the same rate of blunted TSH response than in CL-I. They were also less severely depressed, displayed less endogenous characteristics and were rated as more mood reactive. 7. These results suggest heterogeneity in biological disturbances in depression and further stress the importance for controlling age, gender and severity of illness in studies investigating biological markers in depression.
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PMID:Biological markers as classifiers for depression: a multivariate study. 797 60

Major depression is reportedly characterized by increased activity of the hypothalamic-pituitary-adrenal (HPA) axis and by in vivo immune activation. The present study was carried out in order to investigate the relationships between HPA-axis activity and in vivo immune function in depression. Towards this end the following parameters were measured: 24 h urinary cortisol (UC) excretion; basal and post-dexamethasone (DST) plasma cortisol, beta-endorphin/beta-lipotropin (beta END/beta LPH) and dexamethasone concentrations; and leucocyte subsets (i.e. lymphocytes, neutrophils, monocytes, CD4+, CD4+CD45RA+, CD4+CD45RO+, CD8+, CD8+CD57+, CD8+CD57-, HLA-DR+, CD25+ T cells, HLA-DR+, CD19+, CD20+, and CD21+ B cells) both pre- and post-DST. Dexamethasone administration (1 mg orally) induced leucocytosis, lymphocytopaenia, monocytopaenia and neutrophilia. HPA-axis non-suppressors exhibited a relative resistance to the enhancing (e.g. neutrophils) or depressant (e.g. lymphocytes, CD4+ T cells) effects of dexamethasone. There were significant correlations between UC excretion and the number of percentage of lymphocytes, monocytes, CD4+CD45RA+ and CD8+CD57- T cells (negatively) and neutrophils (positively). It is concluded that multiple and complex intertwined relationships between HPA-axis hyperactivity and systemic immune stimulation participate in the pathophysiology or pathogenesis of major depression.
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PMID:Multiple reciprocal relationships between in vivo cellular immunity and hypothalamic-pituitary-adrenal axis in depression. 820 82

Transient DST non-suppression during disulfiram-treatment was fortuitously observed in a depressed patient. A disulfiram-potentiated DST (DSTd) was constructed by giving 800 mg disulfiram on the dexamethasone and postdexamethasone days. DST and DSTd were compared intraindividually in 21 patients and 14 controls. Disulfiram-potentiation was significant in constantly depressed patients, and in questionable controls due to possible subclinical depression or somatic factors which may cause 'false-positive' results. It did not occur in depressed patients during marked improvement or long-term recovery, and not in accurately screened controls. DSTd was significantly correlated with depression ratings, whereas DST was not.
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PMID:Can disulfiram potentiate the dexamethasone suppression test in depressive patients? 822 60

Increased adrenal cortex responsiveness to adrenocorticotropic hormone (ACTH) has been suggested to contribute to increased cortisol secretion in dexamethasone nonsuppression and melancholia. To further examine this hypothesis, the following variables were examined in 68 patients with unipolar depression (minor, n = 24; simple major, n = 25; melancholic, n = 19): basal or post-Synacthen [ACTH(1-24), 250 micrograms IV] intact ACTH(1-39), beta-endorphin/beta-lipotropin, cortisol, and androstenedione concentrations, as well as the postdexamethasone (DST) plasma ACTH(1-39) and cortisol values. Melancholic subjects showed significantly higher baseline ACTH(1-39), beta-endorphin/beta-lipotropin, and androstenedione values compared with subjects with minor depression. No significant differences in post-Synacthen cortisol or androstenedione secretion between any of the groups or between [ACTH(1-39) or cortisol] DST nonsuppressors and suppressors were found. No significant relationships between DST and ACTH test results were observed. Abnormally increased post-DST cortisol values in melancholic subjects were highly predicted (> 68% of the variance) by post-DST intact ACTH levels. ACTH(1-39) values were significantly lower after Synacthen administration in melancholic subjects than in subjects with minor depression. These results are not consistent with the hypothesis that melancholia is characterized by an increased adrenocortical responsivity to exogenous ACTH compared with minor depression or that DST nonsuppression is due to adrenal hyperresponsiveness.
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PMID:Pituitary and adrenal hormone responsiveness to Synacthen in melancholic subjects versus subjects with minor depression. 839 86

The frequency of depression was assessed in 43 chronic schizophrenic patients during an acute exacerbation phase of schizophrenia. The dexamethasone suppression test was administered to all patients. Depressive symptomatology showed a prevalence from 16.3% for moderate symptoms to 23.3% for mild ones. Depressive symptoms occurred concurrently with the psychotic picture and resolved as the psychosis remitted. Depressive symptoms were not relative to age, sex, duration of illness, DST cortisol levels, drug dosages and extrapyramidal side effects while basal cortisol levels were negatively correlated with basal Hamilton score.
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PMID:Depressive symptoms and schizophrenia a psychopharmacological approach. 852 64

To further examine the association between basal and postdexamethasone (DST) pituitary and adrenal activity in depression, the authors measured intact adrenocorticotropic hormone (ACTH), androstenedione and cortisol, both in baseline and post-DST conditions, in 63 depressed subjects (14 minor, 33 simple major and 16 melancholic subjects). It was found that post-DST androstenedione, cortisol and ACTH values were significantly higher in melancholic than in minor depressed subjects. There were highly significant correlations between plasma androstenedione and ACTH both in baseline and post-DST conditions. The significant intercategory differences in post-DST androstenedione were determined by differences in post-DST ACTH. Basal and post-DST androstenedione values were significantly higher in men than in women and both values were significantly and negatively related to age. There were highly significant, positive relationships between cortisol and ACTH and between cortisol and androstenedione both in baseline and post-DST conditions. The results corroborate our hypotheses that, in depression, pituitary (ACTH) and adrenal (cortisol and androstenedione) hormonal secretion are tightly coupled in post-DST conditions and that the augmented escape of ACTH-target hormones in melancholia is, in part, related to that of pituitary ACTH.
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PMID:An augmented escape of androstenedione from suppression by dexamethasone in melancholia: relationships to intact ACTH and cortisol nonsuppression. 855 Sep 55


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