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 endocrine response to thyrotropin-releasing hormone (TRH) was studied in severely endogenously depressed patients during illness (n = 21) and after recovery (n = 18). The thyroid-stimulating hormone (TSH) response to TRH was blunted (deltaTSH less than 5 microIU/ml) in over one third of depressives during illness and remained blunted in most even after recovery. There was no correlation between multiple measures of cortisol secretion (the mean 24-hour plasma cortisol, dexamethasone suppression test, and plasma cortisol during the TRH procedure) and the TSH response during illness and after recovery. The TSH and prolactin (PRL) responses to TRH, as well as the baseline PRL, were significantly lower during illness. The role of possible abnormalities in dopamine and/or serotonin in depression contributing to these endocrine disturbances is discussed.
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PMID:Endocrine responses to thyrotropin-releasing hormone in major depressive disorders. 611 98

Plasma prolactin, growth hormone, cortisol, luteinising-hormone-releasing hormone (LHRH), thyrotropin-releasing hormone (TRH), and nicotine and oestrogen stimulated neurophysin (NSN and ESN) were measured before and for 6 min after electroconvulsive therapy (ECT) in eight women with severe electroconvulsive therapy (ECT) in eight women with severe depression. Plasma concentrations of NSN and ESN had increased significantly (as much as 10-fold for NSN) within 1 min of the seizure, and concentrations of prolactin had increased within 2-4 min after the seizure. Whereas plasma prolactin and ESN either continued to increase or remained raised throughout the 6 min after seizure, the concentrations of NSN fell to reach a value at 6 min that was approximately 50% of the maximum. There were no increases in any of the other hormones or peptides within the 6 min period under study. Thus ECT has selective effects on hormone release which cannot be attributed simply to a generalised release of pituitary or hypothalamic hormones in response to brain stimulation and/or stress.
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PMID:Immediate increases in plasma prolactin and neurophysin but not other hormones after electroconvulsive therapy. 612 44

Low levels of cerebrospinal fluid 5-hydroxyindoleacetic acid and a blunted thyroid-stimulating hormone response to thyrotropin-releasing hormone have been reported in depressed patients--in particular in those who have made violent suicide attempts. There are at least two conceivable explanations for these findings: The biological abnormalities relate to (1) disturbed aggression regulation or to (2) disturbed mood regulation (either type or severity). The second alternative presupposes that violent suicide attempts occur differentially in a particular depression type or differentially in severe depression. This study demonstrated that violent suicide attempts are "depression-specific," i.e., they relate to a particular depressive syndrome, that of vital depression, but not to the severity factor. Therefore, it is impossible to decide whether the biological abnormalities in depressed, violent suicide attempters relate to a particular type of mood disorder or to a distorted regulation of aggression.
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PMID:Depression type and depression severity in relation to risk of violent suicide attempt. 620 40

Blunted responses to thyrotropin-releasing hormone (TRH) stimulation have been found consistently in depressed patients, and have been reported in other affective disorders as well. In a smaller number of schizophrenic subjects, TRH tests have generally been normal. Thus, it has been suggested that this test may have diagnostic utility in distinguishing schizophrenia from affective disorders. In the present study the TRH test was performed upon a sample of 51 subjects that included 17 schizophrenics in order to further study the diagnostic or symptom specificity of this endocrine test. Abnormal TRH tests were present in both schizophrenic and affectively disturbed patients. There were no correlations with ratings of depression or other aspects of psychopathology. Factors which may have previously obscured abnormal TRH tests in schizophrenia are discussed.
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PMID:TRH test abnormalities in psychiatric disorders. 623 58

Forty-four consecutive outpatients referred to a psychiatric hospital for evaluation of depression and anergia were assessed by means of the protirelin (thyrotropin-releasing hormone) test. Nineteen patients (43%) had a blunted thyrotropin (TSH) response to protirelin, while six patients (13.5%) had augmented TSH responses indicating some degree of hypothyroidism. One patient had a low thyroxine level, while three patients had elevated basal TSH levels. Five of the six patients with augmented TSH responses were found to have antithyroid antibodies. These results suggest that a majority of depressed outpatients have abnormalities on the protirelin test and that the TSH response to protirelin is useful in both confirming a diagnosis of major depression and assessing thyroid status.
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PMID:Thyroid failure and protirelin (thyrotropin-releasing hormone) test abnormalities in depressed outpatients. 640 17

The levels of neurotensin and thyrotropin-releasing hormone (TRH) in normal post mortem human amygdala have been compared with those in cases of schizophrenia, Alzheimer's disease and depression. Amongst various factors which can influence post mortem human brain biochemistry (including age, sex, post mortem delay, time of death, disease status and severity), sex difference appeared to be responsible for the most extensive variation. The levels of both peptides were nearly doubled in males compared with females and this increase was significant in the case of neurotensin. There was also a positive correlation between neurotensin and TRH levels. Although levels of neurotensin and TRH tended to be lower in the disease groups these trends did not reach significance.
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PMID:Post mortem levels of thyrotropin-releasing hormone and neurotensin in the amygdala in Alzheimer's disease, schizophrenia and depression. 640 15

Eighty-eight depressed patients who had received a dexamethasone suppression test (DST) and thyrotropin-releasing hormone (TRH) test were divided into four subgroups based on family history of psychiatric illness. Nonsuppression on the DST was found in 46% of familial pure depressive disease (FPDD) patients, 38% of sporadic depressive disease (SDD) patients, 38% of depressive spectrum disease (DSD) patients, and 50% of mixed depressive disease patients (patients with both a first degree relative with alcoholism and one with depression). A blunted thyroid-stimulating hormone response to TRH was found in 50% of FPDD patients, 56% of SDD patients, 47% of DSD patients, and 56% of mixed depressive disease patients. Neither the DST nor TRH test was found to distinguish significantly among the four familial subgroups of depression.
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PMID:The thyrotropin-releasing hormone and dexamethasone suppression tests in the familial classification of depression. 641 61

The influence of synthetic thyrotropin-releasing hormone (TRH) on locomotion, on the effects of analgetics, learning and memory, electrical activity of hypothalamic neurons, blood pressure, and cerebral circulation have been studied. TRH increases the spontaneous motility and potentiates the stimulating effect of amphetamine and apomorphine. It also antagonizes the decrease of motility induced by tetrabenazine in all these tests. TRH exhibits the similarity to antidepressants. TRH antagonizes the effects of morphine and Tyr-D-Ala-Gly-Phe-(NO2)-NH2, especially in respect of respiratory depression experiments made on rats and rabbits. TRH facilitates the learning in active avoidance paradigme, diminishes the degree of retrograde amnesia evoked by maximal electroconvulsive shock. The latter effect suggests that TRH can be considered as a substance having some signs of nootropic activity. TRH seems to interact with central M-cholinergic system. This is evidenced by the ability of atropine to diminish the excitatory effect of TRH applied microiontophoretically to single neurons of the lateral hypothalamus. TRH elevates blood pressure and volume velocity of the cerebral circulation in normotensive animals and recovers the hemodynamics during hemorrhagic hypotension. The spectrum and mechanism of TRH pharmacological activity are discussed. The data suggest that TRH may be of interest for clinical trials.
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PMID:[Pharmacology of thyroliberin]. 641 82

Fifteen patients with a primary diagnosis of borderline personality disorder were studied with the thyrotropin-releasing hormone (TRH) test. Twelve carried the additional diagnosis of depression, substance abuse, or both. A blunted thyroid-stimulating hormone (TSH) response to TRH was found in seven patients, two of whom were neither depressed nor had the additional diagnosis of depression and/or substance abuse. TSH blunting was unrelated to such factors as thyroid status, serum cortisol, weight, height, or body surface. Since TSH blunting occurs in about 25% of patients with major depression but not in schizophrenia, the findings suggest that some patients with borderline personality disorder share a neuroendocrine abnormality with some affective disorder patients.
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PMID:The TRH test in patients wih borderline personality disorder. 641 92

The authors examined dexamethasone suppression test (DST) and thyrotropin-releasing hormone (TRH) test results in 32 chronic alcoholics without depression or hepatic disease to see if alcoholism alone might lead to positive test results. After 3 weeks of sobriety there were no DST abnormalities, but blunted TRH test results were observed in eight of the 32 alcoholics. More of the 15 patients also tested during alcohol withdrawal than of the 20 normal subjects or the 32 alcoholics without alcohol withdrawal had DST and TRH test abnormalities. When performed after 3 weeks of sobriety, the DST but not the TRH test has potential as a specific laboratory adjunct in the diagnosis of depression in alcoholics.
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PMID:Specificity of the DST and the TRH test for major depression in alcoholics. 642 82


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