Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Male patients suffering from borderline personality disorder (n = 13), major depression (n = 13) or schizophrenia (n = 13) were investigated on several psychopathological (HDRS, BPRS) and neuroendocrinological (DST and TSH, PRL, GH responses to TRH) parameters. Comparisons were made between the borderline group and the other groups of patients. Borderline patients differed from schizophrenics psychopathologically (BPRS) and neuroendocrinologically (DST). Also, borderline patients differed from major depressives in the HDRS, but behaved like them concerning DST. Our findings support the hypothesis that there are neuroendocrinological similarities between borderline personality disorder and major depressive patients, especially on the hypothalamo-pituitary-adrenal axis.
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PMID:Multiple neuroendocrinological responses in borderline personality disorder patients. 312 3

The rate of abnormal dexamethasone suppression test (AbDST, post-dexamethasone cortisol greater than 5.0 micrograms/dl) was analyzed in different psychiatric samples, diagnostic categories and different time points of blood sampling. Differences in the AbDST rate in different samples were largely due to different composition of diagnostic categories and time points of samplings. By standard DST protocol (using 4 PM and 11 PM as sampling time points), melancholics had the highest AbDST rate (58.5%) among all diagnostic groups. DST was not a practical technique for differential diagnosis in psychiatric practice because of low prevalence of melancholia in the total patient population. However, it could be a promising variable for psychopathological study. The rate of AbDST was higher at the sampling time of 4 PM than any others. For one time point sampling, the 4 PM one was suggested. 8 AM and 4 PM sampling times were suggested as a practical 2-time-point sampling for DST. The rate of AbDST in different diagnostic groups had a positive relation with the severity of depressive psychopathology in a global sense. There was not any single item or any cluster of depressive symptomatology consistently related to AbDST among all diagnostic categories. Each diagnostic category had its own specific depressive symptoms in relation to AbDST, either positively or negatively. The severity of hypothalamic-pituitary-adrenal axis dysfunction, as shown in persistent AbDST and a high level of post-dexamethasone cortisol level, showed heterogeneous relation with depressive psychopathology. The relation was positive in schizophrenia and mania, was nill in melancholia, and probably reversed U relation in other psychotics and neurotics. Multiple psychopathological and pathophysiological mechanisms responsible for AbDST were suggested.
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PMID:Dexamethasone suppression test in psychiatric diagnosis and psychopathology for Chinese patients. 361 70

The metyrapone test was applied to patients suffering from major depressive illness with melancholia, from mania, and from schizophrenia. Hypoactivity of the HPA axis as assessed by the test appears to occur infrequently in affective disorders and schizophrenia. High normal or exaggerated responses to metyrapone, as observed in Cushing's disease, appear to be correlated to DST non-suppression in melancholia.
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PMID:The metyrapone test in affective disorders and schizophrenia. 623 55

The promise of an easily administered and highly specific test for depression has produced a rapidly growing literature, which now contains numerous exceptions to the specificity described earlier as well as misgivings about the test's performance when endogenous depression is rare. Due to its modest sensitivity and the effect of prevalence on positive predictive value, the DST is of little use as a screening test. These limitations, however, do not affect its use as a confirmatory test if the suspicion of 'endogenous' depression is strong. According to the large majority of studies, the DST is rarely abnormal in healthy controls or in schizophrenics. Some of the exceptions are probably due to the lack of appropriate exclusion criteria, recruitment bias, nonspecific assays for cortisol, the use of overly broad definitions of schizophrenia. The possibility remains that some schizophrenics, perhaps the ones in which negative symptoms predominate, are truly nonsuppressors. This is certainly true for patients with dementia and the DST now shows little promise as a diagnostic aid when that disorder is suspected. In light of family history, follow-up and sleep studies, the occurrence of abnormal DST results among patients with such diagnoses as schizophreniform disorder and borderline personality is more likely to indicate diagnostic heterogeneity than DST nonspecificity. Nonsuppression is specific to 'endogenous' depression in the large majority of reports despite considerable differences in the 4 most commonly studied definitions. The few studies which applied 2 or more definitions to the same sample found marked specificity for one and very little for another definition, however, and did not find them to be interchangeable. Despite the use of operational criteria, occult rater variance among investigators poses a serious problem for the study of affective disorder. Studies so far suggest that the DST can figure prominently in the solution.
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PMID:The use of laboratory tests in psychiatric diagnosis: the DST as an example. 639 22

In a study of 20 inpatients who met DSM-III criteria for schizophrenia, there was a high incidence of depressed mood (N = 14), DSM-III melancholia (N = 6) and dexamethasone nonsuppression (N = 7). This incidence of positive DSTs (serum cortisol greater than 5 micrograms/dl at 3:30 or 10:00) was significantly higher than the expected rate based on a literature review (35% vs. 4%, p less than .001). A positive DST did not result in all cases in antidepressant pharmacotherapy, nor did a negative result preclude such treatment. Hence, clinicians in the study did not "treat the DST" in the absence of clinical evidence of depression. This study is consistent with others reporting a significant proportion of depressed schizophrenics. However, some studies have claimed no differences in response to dexamethasone between nondepressed and schizophrenic patients. These findings do not support a biological basis for the RDC differentiation of primary and secondary depression and challenge the DSM-III concept of schizophrenia as excluding the diagnosis of major depression. Viewed from a different perspective, the data may support recent reports casting doubt on the specificity of the DST.
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PMID:The dexamethasone suppression test in schizophrenia. 646 27

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

Hypothalamic-pituitary-adrenal system (HPA) function was tested in 24 patients with schizophrenia and compared to 24 age-matched healthy volunteers using the combined dexamethasone-suppression (DST/CRH) corticotropin-releasing hormone stimulation test (DST/CRH). After stimulation with CRH, the dexamethasone-pretreated patients released significantly more cortisol, but a similar amount of adrenocorticotropic hormone (ACTH) in comparison to controls. No association between DST status and degree of severity of illness and/or current medication was found. However, in comparison to unmedicated patients, those patients currently receiving antipsychotics, who were also those with a lesser degree of severity of illness, showed a decreased release of CRH-stimulated cortisol and ACTH. This study demonstrates that schizophrenic patients have a dysregulation of the HPA system as assessed with the DEX/CRH test. Overall, however, the degree of HPA-system dysfunction in schizophrenic patients seems to be of a lesser magnitude than in patients with affective disorders.
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PMID:Combined dexamethasone/corticotropin-releasing hormone test in patients with schizophrenia and in normal controls: II. 887 82

1. It has been hypothesized that psychotic symptoms in depression may be due to increased dopamine activity secondary to hypothalamic-pituitary-adrenal (HPA) axis overactivity. 2. To test this hypothesis, the authors examined the cortisol response to dexamethasone suppression test (DST, 1 mg orally) and multihormonal responses to apomorphine (APO, 0.75 mg s.c.)--a dopamine agonist--in 150 drug-free hospitalized patients with DSM-IV major depressive episode with psychotic features (MDEP, n=35), major depressive episode without psychotic features (MDE, n=74), or schizophrenia paranoid type (SCZ, n=41), and 27 hospitalized healthy controls (HCs). 3. MDEPs showed increased activity of the HPA system (i.e. higher post-DST cortisol levels) than HCs, SCZs and MDEs. However, there were no differences in adrenocorticotropic hormone (ACTH), cortisol, prolactin and growth hormone (GH) responses to APO between MDEPs and MDEs and HCs. On the other hand, SCZs showed lower APO-induced ACTH stimulation and a higher rate of blunted GH than HCs, MDEs and MDEPs, suggesting a functional alteration of the hypothalamic dopamine receptors in SCZs. 4. In the total sample and in each diagnostic group, DST suppressors and non-suppressors showed no differences in hormonal responses to APO. 5. These results suggest a lack of causal link between HPA axis hyperactivity and dopamine dysregulation. In contrast to schizophrenia, psychotic symptoms in depression seem not to be related to dopamine function dysregulation.
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PMID:Dopaminergic function and the cortisol response to dexamethasone in psychotic depression. 1080 Jul 44

It is characterized by mainly depressive mood and psychomotor retardation. Another symptoms are retardation of thought, diurnal change, anxiety, irritability, delusion of belittlement, etc. There are often somatic symptoms as loss of appetite, sleep disturbance, loss of body weight, constipation, etc. Depressive symptoms are often seen in schizophrenia, brain injury, endocrinosis illness and other somatic illness. Diagnosis of depression is carefully carried out by detailed interviews and symptoms. Recently diagnosis of depression is determined mechanically by DSM-IV or ICD-10. Neuro-endocrine tests as DST or Dex-CRH test, are useful strategies in examination of depression.
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PMID:[Symptomatology and diagnosis of depression]. 1151 47

A balanced translocation affecting DISC1 cosegregates with several psychiatric disorders, including schizophrenia, in a Scottish family. DISC1 is a hub protein of a network of protein-protein interactions involved in multiple developmental pathways within the brain. Gene set-based analysis has been proposed as an alternative to individual analysis of single nucleotide polymorphisms (SNPs) to get information from genome-wide association studies. In this work, we tested for an overrepresentation of the DISC1 interacting proteins within the top results of our ranked list of genes based on our previous genome-wide association study of missense SNPs in schizophrenia. Our data set consisted of 5100 common missense SNPs genotyped in 476 schizophrenic patients and 447 control subjects from Galicia, NW Spain. We used a modification of the Gene Set Enrichment Analysis adapted for SNPs, as implemented in the GenGen software. The analysis detected an overrepresentation of the DISC1 interacting proteins (permuted P-value=0.0158), indicative of the role of this gene set in schizophrenia risk. We identified seven leading-edge genes, MACF1, UTRN, DST, DISC1, KIF3A, SYNE1, and AKAP9, responsible for the overrepresentation. These genes are involved in neuronal cytoskeleton organization and intracellular transport through the microtubule cytoskeleton, suggesting that these processes may be impaired in schizophrenia.
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PMID:Role of DISC1 interacting proteins in schizophrenia risk from genome-wide analysis of missense SNPs. 2390 65


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