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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

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

Biological studies of the relationships between the schizoaffective disorders, the affective disorders, and schizophrenia suggest that no simple reductionist model is supported by currently available data. Thus, both affective and schizoaffective patients but not schizophrenics, manifest abnormalities such as decreased platelet serotonin (5-HT) uptake, blunted clonidine-induced increase in serum growth hormone, shortened latency of rapid eye movement (REM) sleep, and increased REM density. However, there are some types of studies which show greater similarity between schizoaffective and schizophrenic patients than between schizoaffectives and affectives--e.g., increased cerebrospinal fluid (CSF) norepinephrine levels, increased platelet 5-HT content, and decreased prostaglandin E1-stimulated adenylate cyclase activity. Other types of studies show abnormalities common to all three groups of psychoses--e.g., eye tracking dysfunction, elevated CSF concentration of gamma-aminobutyric acid, and neuromuscular abnormalities. There are also abnormalities that have been reported to be present in only one type of the psychoses. Although none of these findings have been so unequivocally demonstrated that they can be considered to be firmly established, they do suggest that it is premature to conclude that the schizoaffective disorders are subtypes of the affective disorders. The possibility of a continuum model of the psychiatric psychoses of unknown etiology merits further consideration. Further biological studies of a broad range of psychiatric psychoses with inclusion of the schizoaffective categories appear indicated.
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PMID:Biological studies of schizoaffective disorders. 642 46

A marked elevation in human growth hormone (GH) following intravenous infusion of thyrotropin releasing hormone (TRH) was seen in three of seven adolescent male schizophrenic patients receiving neuroleptic drugs, and in one of five controls matched for age, sex, and developmental stage, receiving the same drugs. A positive family history for schizophrenia was noted in all three schizophrenic 'responders' but in only one of the remaining patients. The response patterns of thyroid stimulating hormone (TSH), triiodothyronine (T3), and thyroxine (T4) following TRH infusion were not significantly different in the two groups. No significant correlations were found between T3, T4, TSH, or GH response patterns and age of patient, duration of illness, medication dose or duration, weight change, or hours of sleep preceding testing.
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PMID:TRH response pattern in adolescent schizophrenic males. 643 74

The relationship between DSM-III schizophrenia, major affective disorders, and the psychotic disorders not elsewhere classified (PDNEC) can be explored through studies which attempt to determine whether these disorders can be differentiated from one another and normal controls by biological measures. Preliminary results of an ongoing project which utilizes measures of blood platelet monoamine oxidase (MAO), serotonin (5-HT) uptake, and 5-HT content, and the apomorphine-induced increase in growth hormone (GH) to accomplish these goals are reported here. DSM-III major affective disorders (bipolar disorder and major depression) can be differentiated from normal controls by the V max of platelet 5-HT. Platelet 5-HT V max of bipolar disorder, depressed type, is significantly different from that of schizophrenia and PDNEC. Elevated platelet 5-HT content is present in black schizophrenic patients compared to black normal controls. Platelet MAO was increased in a small group of schizophreniform female patients. There was no difference in the apomorphine-induced GH response between any of the diagnostic groups. If confirmed in a larger series of patients, these results tend to identify the PDNEC more closely with schizophrenia than the major affective disorders.
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PMID:Biological studies of DSM-III psychotic disorders. I. Platelet measures and apomorphine-induced growth hormone response. 675 71

The authors previously found a high correlation between lithium response and clinical diagnostic criteria in a subgroup of schizophrenic-like patients who responded favorably to lithium therapy. In the present study the authors extend this research by using biological markers to predict and identify such patients. They examined growth hormone (GH) response to apomorphine administration and the in vitro lithium ratio in 31 patients before and after a 2-week lithium trial. Peak GH levels (greater than or equal to 20 ng/ml) and lithium ratios (greater than or equal to .39) were correlated with a positive response to lithium therapy. The authors discuss 1) the use of these two biological markers to predict the success of lithium therapy in schizophrenia and 2) biological abnormalities characteristic of lithium-responsive schizophrenic patients.
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PMID:Growth hormone levels and lithium ratios as predictors of success of lithium therapy in schizophrenia. 680 97

The hypothesis that increased central cholinergic neurotransmitter function may be present in schizophrenic illness and may underlie negative symptoms was tested using a neuroendocrine challenge approach. The cholinergic challenge used was the anticholinesterase pyridostigmine, thought to cause the release of growth hormone (GH) from the anterior pituitary by diminishing inhibitory somatostatin tone. Eleven patients, six neuroleptic-naive and five neuroleptic-free, satisfying DSM-III-R criteria for schizophrenia and 11 matched controls took part. Subjects received pyridostigmine (120 mg orally) and blood was sampled at 0, 60, 90, 120, and 180 min for GH estimation. Peak GH responses were significantly increased in the schizophrenic group compared to controls. There was no relationship between individual peak GH values and negative symptom ratings (Scale for the Assessment of Negative Symptoms). Neither could a relationship be established between other aspects of psychopathology or dyskinesias and GH responses. An increased pyridostigmine/GH response is also found in affective disorders and could be related to nonspecific symptoms common to all these diagnostic groups. This study suggests that schizophrenia may be associated with increased cholinergic neurotransmitter function but the relationship between this cholinergic dysfunction and schizophrenia may involve psychopathology not specific to schizophrenia.
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PMID:Growth hormone responses to pyridostigmine in schizophrenia: evidence for cholinergic dysfunction. 783 22

Growth hormone has been investigated in numerous studies involving patients with schizophrenia but has been measured only by radioimmunoassay (RIA). There have been no consistent abnormalities differentiating patients with schizophrenia from normal controls. In the current study, growth hormone (GH) variants were measured by Western blotting techniques, which resulted in the quantitation of 4 GH size variants: 27K (27,000 Daltons), 22K, 20K, and 17K. In the entire sample of 17 schizophrenic subjects, all GH variants were significantly higher than in the 14 normal controls. While there were no significant differences between the 2 groups in RIA GH values, the RIA values were generally higher in the schizophrenic group. In a subset of 12 schizophrenic patients whose RIA values were approximately equal to the controls, both the 27K and 22K GH variants remained significantly higher in the patient group. In the schizophrenic group, none of the GH variants or RIA GH changed significantly after 1 week of treatment with neuroleptic medication. These preliminary results suggest that certain GH forms may be elevated in schizophrenia, but further studies are needed.
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PMID:Potential abnormalities in molecular forms of growth hormone in schizophrenia: a pilot study. 790 55


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