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)

Prolactin, FSH, LH and TSH were determined in repeated samples of serum from 16 unmedicated male patients with chronic schizophrenia. Changes in the mental states between the 2 occasions were related to changes in hormone levels. Significant inverse correlations were established between prolactin and incoherence of speech, between prolactin and total positive symptoms and between FSH and poverty of speech. A significant positive correlation was established between FSH and delusions. These findings are discussed in the context of evidence concerning the role of monoamines in the control of anterior pituitary function, and of the dopamine and other monoamine hypotheses of schizophrenia. Although prolactin secretion was not as low, as would be predicted on the basis of the dopamine overactivity hypothesis of schizophrenia, the relationship between symptom change and change in prolactin secretion was consistent with the hypothesis that increasing symptom severity is associated with increasing dopamine release from the tubero-infundibular system.
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PMID:Anterior pituitary hormone secretion in chronic schizophrenia--an approach to neurohumoral mechanisms. 87 85

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

The thyrotrophin (TSH) response to thyrotrophin-releasing hormone (TRH) 300 micrograms intravenously was studied in 25 patients with schizophrenia, 14 with depression, and 8 with mania. The rate of blunted TRH test results was zero in healthy controls, 64.3% in depression, 62.5% in mania, and 28.0% in schizophrenia. These differences of the rates between depression or mania patients and controls were significant, whereas the difference of rates between schizophrenias and healthy controls was not significant by X2 test. These results seemed to support the view that TRH stimulation test can be used as a biological marker to distinguish affective disorder and that both depression and mania is correlated with the decreased function of serotonin.
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PMID:[Thyrotrophin-releasing hormone (TRH) stimulation test in psychiatric patients]. 211 64

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

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

The thyrotropin (thyroid-stimulating hormone; TSH) response to thyrotropin-releasing hormone (TRH) was studied in 64 age-matched healthy volunteers, 44 patients with endogenous depression, and 21 patients with schizophrenia. A significant negative correlation between delta TSH and age was found both in healthy subjects and in depressed patients. We based our comparison on normal ranges for delta TSH calculated from the delta TSH values in the healthy subjects related to age. It was then seen that blunted TSH response to TRH does not occur significantly more often in depression (13.6%) than in healthy controls (4.7%). Blunted TRH test results were also found in a considerable number of severely ill schizophrenic patients (19%). Application of an improved radioimmunoassay revealed a highly significant correlation between TSH values at baseline and after stimulation, and showed decreased baseline TSH levels in subjects with blunted TRH test results.
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PMID:Effects of age and diagnosis on thyrotropin response to thyrotropin-releasing hormone in psychiatric patients. 308 11

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

Two patients with familial dysalbuminaemic hyperthyroxinaemia (FDH) are described in whom the albumin variant resulted in raised total T4 levels, and artefactually raised free T4 using a 'single-step' technique employing an analogue of T4 as tracer. The first patient was clinically euthyroid and presented with relapse of schizophrenia and abnormal thyroid function tests (total T4 336 nmol/L, total T3 4.2 nmol/L, TSH 1.8 mU/L, free T4 73 pmol/L). These results led to diagnostic confusion and the patient was treated with a short course of anti-thyroid drugs. The second patient had signs and symptoms of thyrotoxicosis at her first visit but was clinically euthyroid 5 months later when she was 10 weeks pregnant. Thyroid function tests were total T4 259 nmol/L, total T3 3.6 nmol/L, TSH 3.8 mU/L, free T4 46 pmol/L. Further studies showed both patients to be biochemically euthyroid. A variant albumin was confirmed in both patients by a screening test for FDH and by reverse-flow electrophoresis. Family studies on 10 relatives of the first patient identified eight with FDH. A simple screening procedure for the indentification of FDH is described and the use of laboratory tests in suspected cases is discussed.
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PMID:Thyroid function tests in patients with familial dysalbuminaemic hyperthyroxinaemia (FDH). 376 54

Somatostatin-like immunoreactivity was measured in the cerebrospinal fluid (CSF) of 85 inpatients with current or recent episodes of major depressive disorders, diagnosed according to Research Diagnostic Criteria (RDC) as assessed with the Schedule for Affective Disorders and Schizophrenia (SADS). Several biopsychiatric tests were run during the same week of investigation. Results indicate low levels of CSF somatostatin to be a state marker for episodes of depression characterized by sad appearance, feelings of tiredness, insomnia, and subjective inability to acknowledge any external precipitants for the depression. CSF somatostatin was negatively related to platelet monoamine oxidase (MAO) activity; MAO activity appeared to account better for the degree of melancholic features than did somatostatin. The ratio between 3-methoxy-4-hydroxyphenylglycol (MHPG) and homovanillic acid (HVA) in CSF also correlated negatively with somatostatin. A positive relationship was noted between CSF xanthine and somatostatin. There was a highly significant curvilinear correlation between CSF somatostatin and serum TSH concentrations, but no correlations between CSF somatostatin and serum GH or prolactin, or with plasma cortisol before or after dexamethasone.
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PMID:Low levels of somatostatin in human CSF mark depressive episodes. 614 88


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