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)

Forty inpatient volunteers with diagnoses of schizophrenia were randomly assigned to treatment either with trebenzomine or thioridazine in a double-blind study of clinical antipsychotic efficacy following a 1-week placebo treatment. Psychopathology was rated using the Brief Psychiatric Rating Scale (BPRS) and Clinical Global Impression (CGI). There was a significant difference in therapeutic response to the two drugs in that psychopathology decreased significantly for the thioridazine group, but not for the trebenzomine group. Serum prolactin was elevated during treatment with thioridazine, but not with trebenzomine. Side effects were more frequently reported for the thioridazine group. These results fail to confirm previous reports of clinical antipsychotic efficacy for trebenzomine.
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PMID:A double-blind comparison of trebenzomine and thioridazine in the treatment of schizophrenia. 611 18

1. Interpretation of neuroendocrine studies in schizophrenia requires consideration of (a) the large number of variables that affect drug-induced endocrine responses (b) the effect of prior neuroleptic therapy (c) heterogeneity of schizophrenia (d) heterogeneity of receptors (e) uniqueness of the hypothalamic-pituitary axis (f) selectivity and pharmacokinetics of administered drugs. 2. Apomorphine increases growth hormone secretion by an effect on dopamine receptors that are not linked to adenylate cyclase and which are located outside the blood brain barrier. 3. Hypothalamic-pituitary histaminergic H2 and alpha-adrenergic function are unchanged in chronic schizophrenia. 4. Schizophrenic symptoms persist despite complete blockade of dopamine receptors modulating prolactin secretion. 5. Studies on dopamine receptors modulating prolactin secretion are unlikely to shed light on the pathophysiology of schizophrenia. 6. Screening for drugs which block apomorphine-induced growth hormone secretion but do not increase prolactin may provide a way of detecting anti-schizophrenic drugs which are devoid of side effects associated with hyperprolactinemia and which do not induce parkinsonism or tardive dyskinesia.
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PMID:Drug-induced growth hormone and prolactin responses in schizophrenia research. 613 95

Melatonin is produced in the pineal gland. Its involvement in various psychiatric and somatic diseases has been suggested. We investigated melatonin in cerebrospinal fluid of 16 healthy controls, 15 paranoid schizophrenics being treated with neuroleptics, and 13 unmedicated paranoid schizophrenics. There were no significant differences in melatonin concentrations among these three groups. No significant correlations were found between melatonin concentrations and various other biochemical substances such as noradrenalin, cyclic adenosine 3', 5'-monophosphate, prolactin, and cortisol. These negative results do not support the suggestion that melatonin is involved in the etiology of schizophrenia. However, other possibilities, e.g., a change of biological rhythms and its influence on other neuroendocrine functions, may be of importance.
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PMID:Melatonin immunoreactivity in cerebrospinal fluid of schizophrenic patients and healthy controls. 614 34

Previous reports have suggested an inverse relationship between serum prolactin concentrations and psychopathology in schizophrenic patients. One such study noted this relationship to be particularly robust in schizophrenic patients with normal as compared to enlarged ventricles, as determined by computed tomography (Kleinman et al., 1982). Because of the potential implications of these findings for the dopamine hypothesis of schizophrenia, we reexamined this issue in 23 schizophrenic patients diagnosed according to Research Diagnostic Criteria. We could find no significant correlation between serum prolactin concentration and psychopathology assessed by either Brief Psychiatric Rating Scale or the Schedule for Affective Disorders and Schizophrenia, Change Form. The lack of a significant relationship was noted in patients with normal or enlarged ventricles. Possible reasons for the discrepancies between our findings and previous reports are discussed.
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PMID:Serum prolactin, psychopathology, and ventricular size in chronic schizophrenia. 614 69

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

Gamma-Hydroxybutyrate (GHB) inhibits firing of dopaminergic neurons and is thus potentially useful in the treatment of schizophrenia. GHB was administered to 10 schizophrenics concurrently with low-dose fluphenazine in a 6-week double-blind crossover study. No antipsychotic efficacy of GHB was noted. GHB had little if any effect on plasma prolactin levels after a single administration and caused few side effects. Trials with higher doses of GHB may be warranted.
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PMID:Gamma-hydroxybutyrate in the treatment of schizophrenia. 619 48

Des-tyr1-gamma-endorphin (DT gamma E) was administered intramuscularly in a dose of 1 mg/day for 10 days to 18 neuroleptic-free schizophrenic patients in a double-blind crossover design. Six patients showed either a slight or no antipsychotic response; seven patients showed a moderate antipsychotic response; and the remaining five patients showed a marked antipsychotic response. DT gamma E led to a decrease of plasma prolactin levels in patients treated with DT gamma E in the first period of experimental treatment as compared to those treated with placebo. Neither plasma levels of growth hormone and cortisol nor cerebrospinal fluid concentrations of homovanillic acid, 5-hydroxyindoleacetic acid, and 3-methoxy-4-hydroxyphenylglycol were affected by DT gamma E. Patients suffering from a hebephrenic or paranoid type of schizophrenia and those presenting relatively fewer negative symptoms were most susceptible to treatment with DT gamma E. These data confirm and extend previous findings that DT gamma E has antipsychotic properties in a number of schizophrenic patients.
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PMID:Clinical, biochemical, and hormonal aspects of treatment with Des-tyr1-gamma-endorphin in schizophrenia. 620 51

Previous studies have variably reported the efficacy of apomorphine in treatment of schizophrenia and tardive dyskinesia. Stimulation of dopamine neuron autoreceptors is the presumed mode of action. Low-dose apomorphine (0.75 mg subcutaneously) and placebo were administered to 25 male schizophrenics to evaluate the drug's effect on psychotic and tardive dyskinetic symptoms. No significant improvement or deterioration was seen. Concomitant measurements of plasma prolactin and growth hormone levels and CSF homovanillic acid level indicated that the dose used was centrally active. These results indicate that an active though nonsedating dose of apomorphine does not ameliorate symptoms of schizophrenia or tardive dyskinesia.
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PMID:Apomorphine and schizophrenia. Treatment, CSF, and neuroendocrine responses. 637 37

Pimozide and haloperidol were found to be equally effective in the treatment of acute schizophrenia in a double-blind clinical trial involving 22 patients. Drug plasma levels measured by radioimmunoassay (RIA) did not correlate with clinical response following either drug. Nor was there any correlation between clinical response and the dopamine receptor blocking activity of either drug as measured by radio receptor assay (RRA). Following pimozide plasma prolactin (PRL) levels correlated with clinical change, although the time courses of response of PRL and clinical response were dissimilar. There was no correlation between PRL and clinical response to haloperidol. RRA and RIA values correlated highly following pimozide but not haloperidol. Our findings lead us to conclude that the RRA technique reflects the plasma level of a drug rather than its central dopamine blocking activity. We also consider that the clinical response to antipsychotic drugs in schizophrenia may be less directly linked to dopamine receptor blockade than has previously been supposed.
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PMID:The relationship of dopamine receptor blockade to clinical response in schizophrenic patients treated with pimozide or haloperidol. 638 5

Venous samples were obtained serially from 18 chronic schizophrenics and nine controls before and after the intravenous administration of protirelin and gonadorelin (gonadotropin releasing hormone [GnRH] ) and by venipuncture from 38 controls. Significant reductions in basal luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were found in the schizophrenic group associated with a reduction in the fluctuation of LH in serial samples. The FSH and prolactin responses to the administration of protirelin and gonadorelin were reduced in the schizophrenic group and abnormal increments of growth hormone secretion were noted in a number of patients, particularly those with reduced basal and stimulated hormone secretion. This pattern of hypothalamic-pituitary dysfunction, which is distinct from that seen in other psychiatric and endocrinological conditions, suggests a reduction in spontaneous GnRH release from the hypothalamus in schizophrenia and may be of potential pathophysiological significance.
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PMID:Anterior pituitary hormone secretion in chronic schizophrenics. 640 55


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