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)

TRH was shown to be an extremely potent (ED50 = 0.04 mg/kg, IP) antagonist of isolation-induced aggression in male mice. The antifighting activity of TRH was selective in that it did not produce concurrent neurological impairment or significant alterations in spontaneous locomotor activity at antiaggressive doses. This activity of TRH appeared to be a direct affect on CNS structures since neither triiodothyronine nor any of the constituent amino acids of TRH antagonized aggression in isolated mice. The results are discussed in terms of the recent clinical effectiveness of TRH in some cases of mental illness (e.g., depression and schizophrenia).
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PMID:Antagonism of isolation-induced aggression in mice by thyrotropin-relasing hormone (TRH). 82 26

Twenty-six in-patients treated for schizophrenia, were divided in two groups. The first group received haloperidol, 20-40 mg p.d., and the second, clozapine, 150-250 mg p.d. TRH-TSH test was performed by injecting 0.2 mg TRH. Four drug-free schizophrenic patients gave normal TSH response to TRH, as well as the group of patients treated with haloperidol. Contrary to that, the clozapine-treated group showed a blunted TSH response. The results obtained are discussed in terms of the different pharmacological profiles of haloperidol and clozapine, especially regarding their dopaminergic actions, alpha-adrenergic and serotonergic control upon thyroid axis.
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PMID:Neuroleptic actions on the thyroid axis: different effects of clozapine and haloperidol. 180 19

Biological tests may help clarify the relationship of schizoaffective disorder to major depressive disorder (MDD) and schizophrenia (SCZ). Thyrotropin-releasing hormone (TRH), 500 micrograms, was administered intravenously to eight schizoaffective depressed (SD), ten SCZ, 23 MDD patients and 43 healthy controls (HC), all males, ages 20-66 years and drug-free. Research Diagnostic Criteria (RDC) were utilized for establishing diagnoses, Hamilton Rating Scale for Depression (HRSD) total scores were used for assessing depressive symptoms. There were no differences in dmax PRL (post-TRH prolactin peak minus baseline, mean +/- SD) amongst SD, SCZ and HC groups (27.3 +/- 5.2, 28.8 +/- 5.4 and 31.5 +/- 5.6 ng/ml respectively). Mean dmax PRL in MDD was significantly lower than each of the other three groups (17.1 +/- 2.2 ng/ml, P less than 0.05 for all). The essentially normal PRL response to TRH in SD, significantly different from MDD but similar to SCZ parallels our previous observations on the pattern of thyrotropin (TSH) response to TRH in the same diagnostic groups. These biological findings may be taken to indicate that schizoaffective disorder, depressed subtype, is closer to schizophrenia than to major depressive disorder. However, they cannot be considered definitive evidence to that effect since schizoaffective disorders are known to be quite heterogeneous, and since the utilized biological tests lack specificity.
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PMID:Prolactin response to thyrotropin-releasing hormone in schizoaffective depressed compared to depressed and schizophrenic men and healthy controls. 212 54

3,5,3'-Triiodothyroacetic Acid (Triac) is reputed to suppress pituitary secretion of TSH with minimal metabolic effects. Triac has been used successfully to treat eight patients with thyroid hormone resistance. We gave Triac to a woman with selective pituitary resistance for treatment of hyperthyroidism (patient 1) and to a man with generalized resistance and chronic schizophrenia to determine whether it would improve his schizophrenia (patient 2). Patient 1 was given 0.35-3.5 mg Triac/day; patient 2 was given 0.7-4.2 mg/day. Dosages were increased by 0.7 mg/day every 2 weeks. Serum T3, T4, free T4, TSH, TSH response to TRH, systolic time intervals (STI), angiotensin-converting enzyme (ACE), and lipids were monitored bimonthly. In both patients, there was no change in symptoms, weight, lipids, or STI. In patient 1, basal TSH suppressed from 16.3 to 1.5 mU/L; in patient 2, from 2.0 to 0.5 mU/L. The peak TSH response to TRH stimulation decreased from 144 to 12.5 mU/L in patient 1 and from 14.2 to 2.8 mU/L in patient 2. Serum T4 decreased from 160 to 109 nmol/L in patient 1 and from 270 to 192 nmol/L in patient 2. ACE levels were persistently elevated in both patients. Resting energy expenditure, measured by oxygen consumption, was increased by Triac in both patients (12% in patient 1 and 9% in patient 2). Although Triac suppressed TSH and T4 secretion in both patients, it did not reduce peripheral action of thyroid hormone as expressed in STI, resting energy expenditure, and ACE. We conclude that in these two patients with resistance to thyroid hormone, at the doses used to suppress TSH and T4 secretion, the intrinsic peripheral action of Triac offset whatever decrease in thyroid hormone secretion it produced.
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PMID:3,5,3'-triiodothyroacetic acid therapy for thyroid hormone resistance. 275 85

Studies describing the CNS distribution of neuropeptides can provide important new insights concerning their possible physiological functions. The rational for studying human post-mortem tissue, as well as some methodological constraints, are reviewed. The localization of NT in normal human brain is presented. Concentrations of NT, TRH, and SRIF were determined in brain tissue from normal controls and patients with schizophrenia or Huntington's chorea. Specific alterations in the levels of these neuropeptides were found in each disease. Appreciable quantities of NT immunoreactivity are present in human CSF. Sub-normal CSF-NT levels were found in a sub-group of unmedicated schizophrenics but were elevated back to normal concentrations following neuroleptic treatment. Although the pathophysiological significance of these findings is unclear, they nevertheless indicate that neuropeptides are important brain constituents which deserve further study.
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PMID:Neuropeptides in CSF and post-mortem brain tissue of normal controls, schizophrenics and Huntington's choreics. 285 37

Biological tests may help clarify the relationships of schizoaffective disorder to both major depressive disorder and schizophrenia. Thyrotropin-releasing hormone (TRH), 500 micrograms i.v., was administered to 14 schizodepressed, 23 schizophrenics, 41 unipolar major depressives (all by RDC) and 45 healthy controls, all males 20-67 years old with no significant differences in age, body height or weight. Results showed no differences in maximal delta TSH (dTSH max) amongst schizoaffective depressed, schizophrenia and healthy control groups (10.1 +/- 1.3, 9.2 +/- 1.1, 9.7 +/- 0.8 microU/ml, means +/- SEM respectively). Mean major depressives' dTSH max was lower than in each of the other three groups (6.2 +/- 0.4 microU/ml, P less than 0.01 for all). Utilizing a less than or equal to 5.0 microU/ml cut-off criterion for blunting, the schizodepressed had 36%, schizophrenics 44%, healthy controls 22% and major depressed 59% blunters (P less than 0.05 from other three groups). Schizodepressed patients appeared significantly different from major depressed but closer to schizophrenics (and healthy controls) on the TRH test.
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PMID:Thyrotropin response to thyrotropin-releasing hormone in RDC schizodepressed men. 297 Apr 96

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

Baseline and TRH-induced changes of thyroid stimulating hormone (TSH), prolactin (PRL), and growth hormone (GH) were measured in 15 healthy control subjects and 63 psychiatric inpatients with DSM-III diagnoses of major depression (n = 19), schizophrenic disorder (n = 20), alcohol dependence (n = 10), and adjustment disorder (n = 14); baseline and postdexamethasone cortisol (CS) were also determined 3-6 days after the TRH-challenge. All patients and controls were women of similar mean age, weight, height, and they were free from interfering illness or drugs. Baseline TSH and PRL were lower in depression, TRH-induced TSH and PRL responses were lower in the whole patient group, but most markedly in depression and alcohol dependence. Postdexamethasone CS was significantly higher in depression, schizophrenia and alcohol dependence. Basal GH did not differentiate the subgroups; TRH-induced pathological GH responses were sometimes found in the patient groups. The differences were most marked quantitatively in major depression: a multivariate analysis of variance showed that delta TSH, postdexamethasone CS and delta PRL were the most important variables in separating patients from controls. A discriminant function derived from these variables classified all controls and 18 of 19 depressed patients correctly; however, 25 of the 44 other patients were also classified with depression. It was confirmed that psychiatric patients show significantly more endocrine disturbances than controls, and this was seen not only in major depression but also in at least three other conditions. Further work is needed to identify other neuroendocrine patterns more specific to depressive disorder.
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PMID:Dexamethasone suppression and multiple hormonal responses (TSH, prolactin and growth hormone) to TRH in some psychiatric disorders. 393 Feb 50

A 47-year-old male schizophrenic with hyperthyroidism was found to have non-neoplastic inappropriate thyrotropin (TSH) secretion. Anterior pituitary function, CT scan and alpha subunit determinations were normal. TSH rose after TRH (7.8 to 22.5 microU/ml) and propylthiouracil (26.1 microU/ml after 3 months) and decreased with oral T3 (Cytomel 25 micrograms po q.i.d.). Cytomel and glucocorticoid infusion blunted but did not completely suppress the TSH response to TRH. Intravenous dopamine infusion (4 micrograms/kg/min) completely suppressed the prolactin but not the TSH response to TRH. The association of schizophrenia and differential thyrotroph sensitivity to dopamine suggests a possible role for dopamine in the pathogenesis of selected cases of non-neoplastic inappropriate TSH secretion.
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PMID:Inappropriate TSH secretion with abnormal thyrotroph sensitivity to dopamine. 393 86

Prolactin (PRL) serum levels in a group of patients with acute schizophrenia (AS) and in a group of patients with chronic schizophrenia (CS) have been investigated in order to differentiate the dopaminergic sensitivity in response to chlorpromazine (CPZ) treatment. AS patients show both a greater dopaminergic sensitivity to CPZ and a stronger response in PRL secretion to TRH stimulation after a 14-day CPZ treatment.
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PMID:Prolactin secretion response to TRH stimulation in acute and chronic schizophrenic patients under neuroleptic treatment. 612 89


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