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)

Researchers have long speculated about the existence of a relationship between physical disease and schizophrenia. Psychodynamic and life-stress theories offer opposing predictions about the nature of this relationship. Unfortunately, the empirical research on this topic is often contradictory and frequently plagued by various methodological inadequacies. Despite the theoretical controversy and methodological problems, the present review of the empirical literature suggests that patients with schizophrenia may be at increased risk for breast cancer and possibly for cardiovascular disease. On the other hand, patients with schizophrenia seem to be at reduced risk for developing either rheumatoid arthritis or lung cancer. The epidemiological investigations are worth pursuing since the convincing demonstration of a relationship between schizophrenia and a particular physical disease would yield valuable information about the pathogenesis of both disorders. Future research on this topic will need to consider the possible mediating effects of third variables, such as smoking habits, which may be associated with schizophrenia and which also are, independently, recognized as risk factors for particular physical disorders.
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PMID:Physical disease and schizophrenia. 329 Oct 96

A common missense mutation of the methylenetetrahydrofolate reductase (MTHFR) gene (C677T) has been shown to be a risk factor for premature cardiovascular disease and neural tube defect. Deficient activity of MTHFR has also been implicated in the pathogenesis of psychiatric conditions such as schizophrenia and affective disorders. Arinami et al found an increased frequency of homozygosity for the mutated type (T677) of the MTHFR gene in schizophrenia and depression. We tried to replicate this finding in a sample of 343 patients with schizophrenia, 143 with bipolar disorder, 71 with unipolar depression, and 258 controls; however, there was no significantly increased frequency of homozygosity for the T677 allele in any of the diagnostic groups, compared to the controls. Our results suggest that homozygosity for the T677 allele of the MTHFR gene is unlikely to play a major role in the pathogenesis of schizophrenia or affective disorders in our sample.
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PMID:C677T polymorphism in methylenetetrahydrofolate reductase gene and psychoses. 1020 43

Olanzapine, a new antipsychotic agent, was approved by the U.S. Food and Drug Administration in 1996 for use in the treatment of schizophrenia. It is structurally similar to clozapine, has a low incidence of extrapyramidal effects, and is effective in treating both the positive and negative symptoms of schizophrenia. This paper describes the determination of olanzapine in biological specimens obtained from the autopsy of a 35-year-old white male found dead in bed at a psychiatric facility. In the months prior to his death, the deceased was prescribed multiple medications, including olanzapine. Olanzapine was identified qualitatively by full scan gas chromatography-mass spectrometry, with quantitative analysis performed by liquid-liquid extraction followed by dual-column gas chromatography. The following concentrations were determined in the specimens analyzed: heart blood, 550 ng/mL; bile, 6346 ng/mL; and gastric contents, 157 ng/mL. Vitreous humor, cerebrospinal fluid, and urine specimens were negative. Although steady-state plasma concentrations of 10-25 ng/mL olanzapine have been reported, effective levels are known to be highly variable and a plasma concentration of 300 ng/mL has been tolerated without adverse effects. Based upon the autopsy, toxicological findings, and case investigation, the cause of death was determined to be intramyocardial arteriosclerosis with severe stenosis of the nodal artery due to hypertensive cardiovascular disease, and the manner was natural.
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PMID:Determination of olanzapine in a postmortem case. 984 13

Genetic factors influence virtually every human disorder, determining disease susceptibility or resistance and interactions with environmental factors. Our recent successes in the genetic mapping and identification of the molecular basis of mendelian traits have been remarkable. Now, attention is rapidly shifting to more-complex, and more-prevalent, genetic disorders and traits that involve multiple genes and environmental effects, such as cardiovascular disease, diabetes, rheumatoid arthritis and schizophrenia. Rather than being due to specific and relatively rare mutations, complex diseases and traits result principally from genetic variation that is relatively common in the general population. Unfortunately, despite extensive efforts by many groups, only a few genetic regions and genes involved in complex diseases have been identified. Completion of the human genome sequence will be a seminal accomplishment, but it will not provide an immediate solution to the genetics of complex traits.
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PMID:The genetics of complex diseases. 1061 74

Side effects of antipsychotic medications are particularly problematic in elderly patients, who experience many age-related changes that may exacerbate medication side effects. Side effects of particular concern in the elderly include anticholinergic reactions, parkinsonian events, tardive dyskinesia, orthostatic hypotension, cardiac conduction disturbances, reduced bone mineral density, sedation, and cognitive slowing. In addition, elderly patients with schizophrenia often have comorbid medical illnesses-such as cardiovascular disease and dementia of the Alzheimer's type-and are thus likely to be taking multiple medications. The effects of polypharmacy must be carefully considered. Patients, caregivers, and family often have different perspectives on side effects. This article addresses the side effects of the currently available antipsychotic medications in light of these concerns.
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PMID:Side effects of antipsychotics in the elderly. 1081 Dec 43

Obesity is common in schizophrenia, and people with schizophrenia appear to be at increased risk for certain obesity-related conditions, such as type 2 diabetes and cardiovascular disease. Antipsychotic drugs, used chronically to control symptoms of schizophrenia, are associated with often-substantial weight gain, a side effect that is a special concern with the latest generation of highly effective "novel" agents. That the most effective (e.g., novel) antipsychotic medications lead to substantial weight gain presents the field with a critical public health problem. Although preliminary data have been reported regarding the beneficial use of behavior therapy programs for short-term weight control in patients with schizophrenia, the available data are quite limited, and there are no data regarding the long-term beneficial effects of these programs in this population. The obesity field recently has developed programs emphasizing "lifestyle changes" (e.g., diet, exercise, and problem-solving skills) to successfully manage weight in patients without schizophrenia. Such programs can be adapted for patients with schizophrenia through the use of highly structured and operationalized modules emphasizing medication compliance, social skills development, and participation in outpatient programs. Moreover, these programs can potentially be combined with the use of adjunctive pharmacotherapy to maximize and maintain weight loss. The field must solve the paradox that some of our most effective medications for schizophrenia produce substantial weight gain and its associated troubling health risks.
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PMID:Weight gain from novel antipsychotic drugs: need for action. 1093 29

A study of mortality for all patients with a first hospital diagnosis of schizophrenia in Stockholm County, Sweden, during 1973 to 1995 was performed, by linking the in-patient register with the national cause-of-death register. Overall and cause-specific standardized mortality ratios (SMR) were calculated by 5-year age classes and 5-year calendar time periods. The number of excess deaths was calculated by reducing the observed number of deaths by those expected. Our results confirmed a marked increase in mortality in schizophrenia both in males and females. Natural (somatic) causes of death was the main cause of excess deaths, with more than half of the excess deaths in females, and almost half of the excess deaths in males. Suicide was the specific cause of the largest number of excess deaths in males, while in females it was cardiovascular disease. SMRs were increased in both natural and unnatural causes of death, with 2.8 for males and 2.4 for females for all deaths, but were highest in suicide with 15.7 for males and 19.7 for females, and in unspecified violence with 11.7 for males and 9.9 for females. SMRs in suicide were especially high in young patients in the first year after the first diagnosis.
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PMID:Mortality and causes of death in schizophrenia in Stockholm county, Sweden. 1097 69

The mortality risk associated with cardiovascular disease is significantly increased in patients with major depression and panic disorder. The mechanism of this phenomenon is unclear. Thrombin is responsible for platelet aggregation and shape change, and it plays a significant role in the development of thromboembolic events. In this study, we examined the platelet second messenger intracellular calcium response to thrombin stimulation in patients with major depression (n = 13), major depression after response to electroconvulsive therapy (ECT; n = 13), subsyndromal depression (n = 16), schizophrenia (n = 15), and control subjects (n = 65). Patients with major depression had significantly higher intracellular calcium responses to thrombin stimulation than control subjects, patients with subsyndromal depression, and patients with schizophrenia (p < 0.05). Electroconvulsive therapy did not significantly change this supersensitivity. This suggests that the platelet response to activation in patients with major depression is supersensitive. This study suggests a possible mechanism for the increased risk of cardiovascular disease that is seen in these two psychiatric disorders. The lack of difference between the control and subsyndromal depression groups appears to validate current diagnostic thresholds in depression. The failure of nonpharmacologic treatment to alter this marker suggests that it may be a trait marker of depression.
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PMID:Platelet supersensitivity to thrombin stimulation in depression: a possible mechanism for the association with cardiovascular mortality. 1102 Jan 20

As a class, the atypical antipsychotics are the first line treatment choice for the psychopharmacologic management of psychotic disorders. Emerging evidence currently suggests that at least two of the atypical antipsychotics, clozapine and olanzapine, and possibly quetiapine may be associated with the risk of new onset diabetes or serum glucose dyscontrol. Computerized Medline and Current Contents searches from years 1966 through June 2000 were undertaken to retrieve all pertinent studies and case reports of typical and atypical antipsychotics and glucose-insulin problems. Historically, both schizophrenia and the older antipsychotics medications have been reported to be associated with a similar risk for causing disruptions in serum glucose control. Additionally, diabetes has well recognized associations with a number of medical disorders such as cardiovascular disease; it is therefore worthy of attention. Hypothesized mechanisms for antipsychotic induced diabetes ranges from the antagonism of several neurotransmitter receptors to insulin resistance. A total of thirty-five cases of induced or exacerbated diabetes are presently available in the published literature; the vast majority of cases implicate clozapine (n=20) and olanzapine (n=15). In multiple cases, diabetic ketoacidosis has been the presenting symptom; daily atypical antipsychotic doses have been within acceptable ranges and were not considered to be excessive.
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PMID:New onset diabetes and atypical antipsychotics. 1122 9

With the completion of the human genome project, micro-array technology offers the potential to open up a whole new vista in assisted reproduction. In the next 10-20 years we will be able to screen each human embryo for all numerical chromosomal abnormalities as well as many genetic diseases. Micro-array analysis may permit the screening of multiple alleles for monogenetic diseases and polygenic diseases, including diabetes, hypertension and schizophrenia. In the near future, it may be possible to assess an individual's genetic predisposition for cardiovascular disease, all types of cancer and infectious diseases. In the distant future, it may even be possible to screen for any genetic trait, e.g. stature, baldness, obesity, hair colour, skin colour or even IQ. Although it is still uncertain what molecular genetic tools may be available, we can be sure that some of these trends will have major consequences on the future of assisted reproduction and society at large.
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PMID:The genetic revolution in artificial reproduction: a view of the future. 1126 33


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