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

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

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

Distorted biorhythms and altered neuroendocrine function may accompany depressive disorders. Restoration of the above derangements occurs with effective therapy, whereas persistence of the biological abnormalities is found in patients incompletely cured and may be predictive of early relapse. The commonest hormonal abnormalities are: decreased suppressibility of the ACTH-cortisol axis to dexamethasone, subnormal thyrotropin response to TRH and growth hormone release to hypoglycemia; attenuated gonadotropin production and abnormal light-dark entrained melatonin secretion. The observed hormonal derangements seem to be epiphenomena of the primary disorder. The reversibility of the disordered neuroendocrine control with treatment of the depressive syndrome suggests that the hormonal abnormalities represent a state rather than trait disorders. Finally, the lack of similar neuroendocrine derangements in schizophrenia or secondary exogenous depression suggests that different neurochemical alterations underlie these disorders.
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PMID:Depression: biological and neuroendocrine aspects. 614 19

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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