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)

The effect of dopaminergic-related and stimulatory drugs have been studied in chronic hebephrenic schizophrenics untreated with neuroleptic drugs. 6 patients received therapy of 2 g L-dopa + 200 mg carbodopa per day orally for 30 days, then placebo for 30 days. Following that 3 of the same patients received therapy of 2 g L-dopa + 200 mg carbodopa + 300 mg imipramine orally for 30 days, then placebo for 30 days. Following that the same 3 patients received 1 mg apomorphine s.c. for 15 days, then placebo for 15 days, then 1 mg apomorphine s.c. + 2 g L-dopa + 200 mg carbodopa per os daily for 15 days, then placebo for 15 days. The patients were examined psychologically by the Wittenborn Rating Scale, the Weigl Object-Sorting Test, and tests for verbal learning and verbal association, before and after each therapeutic trial. Levels of FSH, LH, testosterone and GH were assayed radioimmunologically before, in the middle of and after each course of therapy. 2 patients showed improvement in the affective-behavioural symptomatology during therapy, while the other 4, who had a more severe degree of mental deterioration and destruction, were unchanged. FSH and LH levels, very low under basal conditions, did not change under therapy. Testosterone was very low before therapy and increased in only 1 subject. Normal basal GH levels increased during therapy in some of the patients, but not constantly. The results obtained are discussed in relation to the catecholamine hypotheses of schizophrenia.
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PMID:Catecholaminergic drugs in chronic schizophrenia. 37 21

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

To evaluate hypothalamic-pituitary-gonadal axis in acute schizophrenia, plasma FSH and LH concentrations were estimated both in basal conditions and after stimulation with gonadotropin releasing hormone (GnRH, 200 micrograms i.v.) in 14 young male patients with acute schizophrenia and in a age-matched group of 14 healthy male controls. Basal plasma PRL and testosterone levels were also measured. The mean basal levels of LH and FSH were slightly lower in schizophrenics, while the mean testosterone and prolactin levels were similar in the two groups. The FSH response to GnRH was significantly reduced in patients with acute schizophrenia, while the response of LH was similar in schizophrenics and in the controls. The possible significance of these findings is discussed in the contest of the complex neuroendocrine regulation of gonadotropin secretion and the overactivity of dopaminergic systems in acute schizophrenia.
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PMID:Gonadotropin response to gonadotropin releasing hormone in acute schizophrenia. 643 79

LH, FSH, PRL and testosterone were estimated by radioimmunoassay in serial venous samples from 20 male chronic schizophrenic patients, 17 age-matched controls, 3 patients in remission from acute schizophrenia, and in single samples from age-sex matched populations. LH and FSH, but not testosterone or PRL, were significantly reduced in patients with chronic schizophrenia. There was an associated reduction in the frequency, but not amplitude, of LH secretory episodes in patients with chronic schizophrenia. No abnormalities of LH secretion were detected in those patients in remission from acute schizophrenia. Fourteen of the chronic schizophrenic patients were retested at a later date with similar results, except in the case of the few patients who had been started on neuroleptic medication. Some relationships were established between hormonal secretion and the clinical features of these patients. The possible significance of these findings is discussed in the context of the complex control of gonadotropin secretion from the anterior pituitary and the natural history and nature of chronic schizophrenia.
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PMID:Gonadotropin secretion abnormalities in chronic schizophrenia. 680 36

This study was a preliminary open clinical trial aimed at exploring the hypothesis that estrogen may provide protection against schizophrenia in women. Eleven women with acute psychotic symptoms, as scored on the BPRS, SAPS and SANS, had 0.02 mg estradiol added to neuroleptic treatment for eight weeks. Their response was compared to seven women with similar symptom severity receiving neuroleptic treatment alone. Both groups had baseline hormonal assays of estrogen, progesterone, LH and FSH and underwent regular psychopathology ratings during the eight weeks. The group receiving the estradiol adjunct showed more rapid improvement in psychotic symptoms compared with the group receiving neuroleptics only. This difference was not sustained for the entirety of the trial. Both groups reached similar levels of recovery by the eighth week. These results suggest that estradiol may have antipsychotic properties and/or act as a catalyst for neuroleptic responsiveness in women with schizophrenia.
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PMID:A clinical trial of the effects of estrogen in acutely psychotic women. 882 50

Hypothalamic dopaminergic and serotonergic inputs participate in the regulation of pituitary hormones, and drugs that block central dopamine and serotonin receptors are expected to influence the hypothalamus-pituitary-gonadal (HPG) and -adrenal (HPA) axes. In schizophrenic patients, the switch from neuroleptics to clozapine influences prolactin and cortisol secretion, but there is no information on possible changes on HPG-axis hormones. We measured the plasma levels of testosterone (TST), LH, FSH, as well as of prolactin (PRL) and cortisol (CORT), in a group of male patients with schizophrenia during treatment with classical neuroleptics with no satisfactory therapeutic response (31 pts, age 30.3+/-8.5, range 18-50), and 6 weeks later, after switch to treatment with clozapine (CLZ) in doses from 100 to 600 mg daily (mean 328 mg). Psychopathology was assessed using the Brief Psychiatric Rating Scale. The hormone levels were also compared to those of a control group of 38 healthy males. Treatment with CLZ resulted in a reduction in the BPRS score by 30% in the mean. Plasma PRL was reduced from 39.9+/-26.1 to 8.3+/-5.0 ng/ml (P<0.001), CORT from 150+/-42 to 118+/-39 ng/ml (P < 0.003), while LH, FSH, and TST remained unaltered. Compared to healthy controls, patients had higher PRL and CORT levels while on neuroleptics, and no significant differences to any of the estimated hormones, after switch to clozapine. The results show that switching from classical neuroleptics to treatment with clozapine does not have any substantial effect on the HPG-axis hormone plasma levels, although it reduces substantially the levels of prolactin and cortisol.
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PMID:Switch from neuroleptics to clozapine does not influence pituitary-gonadal axis hormone levels in male schizophrenic patients. 1062 22

A case of Klinefelter's syndrome with schizophrenia-like symptoms is reported. He was given a diagnosis of schizophrenia at the age of 39. After being treated with medication for many years, he stopped taking them at the age of seventy-two and involuntary movements appeared in his limbs and the trunk. Upon admission to our hospital, he was experiencing delusion and psychosocial excitement. A physical examination showed him to be a thin man of 175.5 cm height, suffering from a mild degree of gynecomastia, testicular atrophy. Serum LH and FSH were both high 10.9 and 47.8 mU/ml respectively. Serum testosterone concentration was 0.2 ng/ml, much lower than the normal range (2.7-10.7 ng/ml). On the Wechsler adult intelligence scale (Revision), his total IQ was 103 (performance IQ 100, verbal IQ105). Karyotype analysis revealed an XXY pattern. Although slight auditory hallucinations remained, the delusional symptoms as well as the involuntary movements diminished after the administration of psychotrophics. Personality changes such as apathy and abulia was subsided. The psychological symptoms were very similar to these of cases in other reports of Klinefelter's syndrome associated with schizophrenia-like symptoms. Some reports about the relationships between sex hormones and schizophrenia including other psychotic disorders suggest that the X-chromosome plays an important part in the mechanism of psychosocial symptoms and in the prognosis in Klinefelter's syndrome.
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PMID:[A case of Klinefelter's syndrome with schizophrenia-like symptoms]. 1099 33

Hyperprolactinaemia is commonly induced by antipsychotic medications that have dopamine-blockade as their main mechanism of action. The purpose of this study was to assess the effect of antipsychotic-induced hyperprolactinaemia on hypothalamic-pituitary-gonadal axis (HPG) function.HPG axis function was assessed in 67 consecutive outpatients who were diagnosed with schizophrenia and stabilized for a period of not less than 2 years on typical antipsychotic medication, by means of clinical history, relevant questionnaires and measurement of plasma prolactin, estradiol, progesterone, testosterone, LH, FSH, sex hormone binding globulin, and TSH levels. Normative laboratory data were used to assess whether hormone levels fell within the reference range for a normal population. There was a significant correlation between dose of medication and plasma prolactin levels for the total group (P<0.001). Prolactin levels were significantly negatively associated with sex hormone levels in females (P<0.05). Males taking antipsychotic medication had a mean prolactin level of 404.1m/IU and mean gonadotrophin and sex hormone levels that fell within normal limits. The results of this study indicate that neuroleptic-induced prolactin secretion is a dose-related side effect and, in females, the level of hyperprolactinaemia is correlated with the degree of suppression of the HPG axis. Women taking long-term prolactin-raising antipsychotic medications are likely to be hyperprolactinaemic and have an associated hypogonadal state. In males, prolactin levels remain within normal limits, but at the upper end, with no apparent disturbance of reproductive hormones.
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PMID:The effects of antipsychotic-induced hyperprolactinaemia on the hypothalamic-pituitary-gonadal axis. 1191 Feb 54

In a double-blind, placebo controlled study, conjugated estrogens (CE) (0.625 mg/day) were added to a fixed dosage of haloperidol (5 mg daily). Forty-four female inpatients with acute schizophrenia were included in the study and randomized to one of the groups; 40 patients completed the trial. They were followed for 28 days and evaluated periodically with the BPRS, Negative Symptoms Rating Scale, Simpson Angus Extrapyramidal Rating Scale and UKU rating scale. Hormonal concentrations (estradiol, estrone, progesterone, FSH, LH and prolactine) were measured at baseline and weekly throughout the trial. Both groups showed similar clinical improvement during the evaluation, although there was a trend for the CE group to show a better improvement than the placebo group (p < 0.10). Side effects and the use of anticholinergics were similar in both groups. Conjugated estrogens caused elevation only of estrone levels in the CE group; estradiol and prolactin showed a similar profile for both groups. Our negative findings regarding the antipsychotic effect of conjugated estrogens does not preclude, however, a possible efficacy of other estrogens, such as 17-beta-estradiol, in schizophrenia.
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PMID:Conjugated estrogens as adjuvant therapy in the treatment of acute schizophrenia: a double-blind study. 1506 Dec 41

A "partial" rodent model for schizophrenia has been used to characterize the regulation of hippocampal genes in response to amygdalar activation. At 96 h after the administration of picrotoxin into the basolateral nucleus, we have observed an increase in the expression of genes associated with 18 different monoamine (ie adrenergic alpha 1, alpha 2 and beta 2, serotonergic 5HT5b and 5HT6, dopamine D4 and muscarinic m1, m2 and m3) and peptide (CCK A and B, angiotensin 1A, mu and kappa opiate, FSH, TSH, LH, GNRH, and neuropeptide Y) G-protein coupled receptors (GPCRs). These latter receptors are associated with three different G protein signaling pathways (Gq, Gs, and Gi) in which significant changes in gene expression were also noted for adenylate cyclase (AC4), phosphodiesterase (PDE4D), protein kinase A (PKA), and protein kinase C (PKC). Quantitative RT-PCR was used to validate the results and demonstrated that there were predictable increases of three GPCRs selected for this analysis, including the dopamine D4, alpha 1b, and CCK-B receptors. Eight out of the nine monoamine receptors showing these changes have moderate to high affinity for the atypical antipsychotic, clozapine. Taken together, these results suggest that amygdalar activation may play a role in the pathophysiology and treatment of psychosis by regulating the activity of multiple GPCR and metabolic pathways in hippocampal cells.
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PMID:Acute amygdalar activation induces an upregulation of multiple monoamine G protein coupled pathways in rat hippocampus. 1517 Apr 62


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