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 relationship between hypothalamic-pituitary-adrenal (HPA) function and the noradrenergic system was examined in patients with affective and with schizophrenic disorders. In response to the Dexamethasone Suppression Test (DST), serum cortisol, plasma catecholamine levels, and serum creatine kinase (CK) activity were measured. Among patients with major depression, those with higher post-DST cortisol levels had higher plasma catecholamine levels and lower serum CK activity. Among acute schizophrenic patients, those with higher serum CK activity had higher baseline and post-DST cortisol levels. These results indicate that in both major depression and in acute schizophrenia, there is a dysfunction of the HPA axis and the noradrenergic system, but the noradrenergic dysfunctions are different in the two disorders.
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PMID:Dexamethasone suppression test and noradrenergic function in affective and schizophrenic disorders. 370 36

Newly admitted psychotic patients often have elevations of serum creatine kinase (CK) enzymatic activity. Previous studies indicate that this increase consists of the muscle (MM) isozyme, and increases in the brain (BB) isozyme have not been observed. Using sensitive and specific radioimmunoassays that detect both active and inactive enzyme, we measured CK-MM and CK-BB in the serum and CSF of 100 patients with schizophrenia who were not newly admitted but whose conditions varied from acute to chronic to determine whether CK-MM or CK-BB appears in the CSF and whether CK-BB can be found in the serum of these patients. We found no unusual concentrations of either isozyme in CSF. We did observe a few elevations in serum CK-BB levels, but this test does not appear to be of diagnostic value for schizophrenic patients who are not newly admitted.
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PMID:Creatine kinase isozymes in the serum and CSF of schizophrenic patients. 729 65

Studies in adults have indicated a significant relationship between high serum creatine kinase levels on admission and acute psychosis. However, data on children are sparse. The files of 183 hospitalized children and adolescents (93 boys, 90 girls) with severe psychiatric disorders were reviewed for serum creatine kinase activity on admission, psychomotor agitation, Clinical Global Impression Score, need for intramuscular injection, number of neuroleptic medications and presence of neuroleptic malignant syndrome. Serum creatine kinase levels > 201 IU/ml were considered abnormal. Boys had significantly higher creatine kinase activity than girls. Division of the cohort by diagnosis yielded significantly higher levels in those with schizophrenia, affective disorders and mental retardation. Higher levels were also associated with higher Clinical Global Impression score on admission, use of injections and physical restraint, and nonresponse to neuroleptic medication. There were no cases of neuroleptic malignant syndrome. This first large-scale investigation of serum creatine kinase activity in young psychiatric inpatients shows a significant association between high creatine kinase activity and acute psychosis, similar to that in adults. Furthermore, high creatine kinase levels on admission are predictive of the severity of the psychosis, but are not associated with neuroleptic malignant syndrome. Because psychotic adolescents with high admission creatine kinase levels tend to be nonresponders, clinicians should consider the early use of atypical antipsychotics in this subgroup.
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PMID:Elevated serum creatine kinase activity in adolescent psychiatric inpatients on admission. 986 77

The paper analyzes the authors' own findings and the data available in the literature on the intensity, site, and possible causes of impairment of the creatine-creatine phosphate system of brain energy metabolism in mental diseases, such as Alzheimer's disease (AD) and schizophrenia. Examining the level of cytosolic BB creatine kinase in postmortem AD and schizophrenic's brain structures showed a significant decrease in BB creatine kinase as compared with the similar control brain structures. There was the maximum decline in AD cases. It was considerable as compared with both the control and schizophrenic groups (p < 0.01). The decrement was revealed by various techniques, including the determination of activity, immunological responsiveness and the analysis of two-dimensional protein maps. Immunocytochemical investigation indicated a decrease in responses to BB creatine kinase, mainly in astrocytes. The reduction in cytosolic BB creatine kinase levels is not a result of age, postmortem delay, or psychotic therapy. The causes of lower BB creatine kinase levels in the cell cytosol of the postmortem brain in mental pathology are discussed. The decrement in cytosolic BB creatine kinase in AD and schizophrenia occurs not only in the brain, but also in the peripheral tissues which contain BB creatine kinase. In all cases, it is greater in AD than in schizophrenia. Using immunosorbents with monoclonal antibodies to M-creatine kinase and to B-creatine kinase subunits makes it possible detect BB-creatine kinase in the extracts of human peripheral lymphocytes and platelets. A study of whether there is a relationship between the clinical data of mental patients and the level of BB creatine kinase in their blood elements is assumed to be useful in evaluating BB creatine kinase as a prognostic/diagnostic marker of mental diseases.
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PMID:[Brain isoforms of creatine kinase in health and mental diseases: Alzheimer's disease and schizophrenia]. 1007 58

Olanzapine, a new atypical antipsychotic drug, has been prescribed in the treatment of schizophrenia and psychotic mood disorders for approximately 2.3 million patients worldwide. Considering the increase in olanzapine prescriptions and the increased risk of suicide in this patient population, the number of reported cases of olanzapine overdose may be expected to increase. This report describes the clinical course and serum concentrations in a patient who consumed an olanzapine overdose (800 mg). Profound central nervous system depression and tachycardia without arrhythmia occurred within 2 hours after the ingestion. Additional clinical findings (ie, fever, mutism, agitation, dystonia, akathisia, elevated creatine kinase, and increased leukocyte count) were similar to those of neuroleptic malignant syndrome. After intubation, gut decontamination, and supportive care, the patient recovered and was discharged.
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PMID:Olanzapine overdose with serum concentrations. 1042 35

Some recent studies have shown that clozapine (CLZ) has myopathic side effects and causes alterations in motor force control. The aim of this study was to evaluate the neurologic and electrophysiologic characteristics of patients with schizophrenia who are undergoing long-term CLZ treatment. Ninety-four patients with schizophrenia treated with CLZ for 18.2 +/- 15.5 months were studied retrospectively and prospectively (40% and 60%, respectively) for serum creatine kinase (CK) levels before and after initiation of CLZ treatment. An electrodiagnostic study was performed on patients with CK elevation above normal limits, complained of general weakness or muscle pains, and/or had abnormal clinically significant findings. In 13 patients (13.8%), abnormal CK levels were found. Six patients complained of some muscular weakness. In two patients, clinical assessment revealed mild general muscular weakness; one revealed decreased tendon reflexes and, in both, CK levels were above 1,750 IU/L. On electrophysiologic examinations performed in the six patients with abnormal neurologic findings, the motor and sensory nerve conduction velocity were within normal range in all but one patient, who exhibited some prolongation of distal latency in the lower limbs. In two patients, the electromyography demonstrated a myopathic pattern. In 2.1% of medically healthy patients with schizophrenia treated with clozapine on a long-term basis, signs of myotoxicity were found. It seems warranted to discontinue CLZ therapy in patients who exhibit abnormal CK levels and myopathic features during treatment. Further studies are needed to provide more objective data on the impact of CLZ treatment on muscle tissue.
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PMID:Myotoxicity and neurotoxicity during clozapine treatment. 1115 96

There is evidence for the occurrence of psychopathological symptoms in the adult form of myotonic dystrophy such as disturbance of concentration and memory, chronic depression, disturbed social behaviour, mental retardation, and hypersomnia. In this report we present a patient suffering from multisystemic myotonic myopathy without a cytosine-thymine-guanine [corrected] repeat expansion on chromosome 19q13.3 and schizophrenia. In this patient, a severe increase of creatine kinase (CK) occurred during treatment with olanzapine and amisulpride. The following risperidone medication was well tolerated without side effects. Susceptibility for malignant hyperthermia was detected by a positive in vitro contracture test. The occurrence of elevated muscle enzymes during treatment with atypical neuroleptics is suspicious as a possible side effect of neuroleptic medication and muscle disease.
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PMID:[Incompatibility of olanzapine and amisulpride in multisystemic myotonic myopathy]. 1157 7

We report a patient with proximal myotonic myopathy who was treated with neuroleptics because of exacerbating schizophrenia. Under therapy with fluanxol, the patient developed muscle stiffness and oculogyric cramps. Treatment with both amisulpride and olanzapine lead to markedly elevated serum creatine kinase levels. An in-vitro contracture test was positive for halothane. Thus, in patients with all kinds of multisystemic myotonic myopathies, a susceptibility for malignant hyperthermia and intolerance towards neuroleptics should be taken into account.
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PMID:Intolerance to neuroleptics and susceptibility for malignant hyperthermia in a patient with proximal myotonic myopathy (PROMM) and schizophrenia. 1173 Dec 82

A 30-year-old white man with schizophrenia developed anorexia and nausea, and was admitted to hospital for confusion and delirium. He was on olanzapine, 10 days prior to admission. On admission, typical neuroleptic malignant syndrome (NMS) developed with elevated body temperature (39.7 degrees C), obtundation, tremor, rigidity, diaphoresis, fluctuating pupillary diameter, tachycardia, labile hypertension, elevated serum creatine kinase and severe hypernatremia (190 meq/l). Olanzepine was stopped few days after admission to the hospital and the NMS manifestations resolved by hospital day 12. The patient had all of the major manifestations of NMS. There was no other likely explanation for his illness. This is the first case reported in which NMS was associated with olanzapine and extremely elevated levels of serum sodium. Copyright 2001 John Wiley & Sons, Ltd.
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PMID:Neuroleptic malignant syndrome with olanzapine associated with severe hypernatremia. 1240 81

cDNA microarrays and two-dimensional gel-electrophoresis in combination with mass spectrometry, were used to screen alterations in mRNA and protein levels, respectively, in cerebral cortex of MK-801-treated rats. The rats were divided in two groups; group 1 (short-term treated) and group 2 (long-term treated). In group 1, four genes were up-regulated and five down-regulated. In group 2, seven genes were up-regulated and six down-regulated. In group 1, the levels of one protein was increased and eight proteins reduced. In group 2, the levels of two proteins were increased and four proteins reduced. Several of the altered genes (casein kinase 2, glutamic acid decarboxylase, synaptotagmin, gamma aminobutyric acid [GABA] transporter, creatine kinase, and cytochrome c oxidase) and proteins (superoxide dismutase, hsp 60, hsp 72 and gamma-enolase) have previously been connected to schizophrenia. Alterations of the genes (microglobulin, c-jun proto-oncogene, 40S ribosomal protein S19, adenosine diphosphate (ADP)-ribosylation factors, platelet-derived growth factor, fructose-bisphophate aldolase A, and myelin proteolipid) and the proteins (stathmin, H+-transp. Adenosine triphosphate (ATP) synthase, pyruvate dehydrogenase, beta-actin and alpha-enolase), have not, to our knowledge, earlier been implicated in schizophrenia pathology. Overall, these results with a combined approach of genomics and proteomics add to the validity of subchronic N-methyl-D-aspartate (NMDA)-receptor antagonist treatment as an animal model of schizophrenia.
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PMID:Comparative genome- and proteome analysis of cerebral cortex from MK-801-treated rats. 1254 8


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