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 role of free radicals (FR) in the pathogenesis and in the progression of many diseases has been often discussed, but not widely investigated. However, the total antioxidant capacity in the serum seems to be of great evidence. Total antioxidant capacity was determined using oxygen absorbance capacity assay (ORAC) in serum of patients suffering from depression, schizophrenia, Alzheimer's disease (AD), anorexia nervosa, Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), Aids-encephalopathy, diabetic polyneuropathy (PNP), cardiomyopathy (CM), renal disease, and healthy individuals as controls (C). The results showed that the total antioxidant capacity in serum decreased significantly (p < 0.01) by 24, 20, 13, and 17% for anorexia nervosa, Aids-encephalopathy, PNP and CM respectively. In serum of patients with renal disease significantly elevated antioxidant capacity was found. The data indicated that increased oxidative stress can be involved in the pathogenesis or in the progression of PNP and CM. Decrease of serum antioxidant capacity in patients with anorexia nervosa and Aids-encephalopathy are probably due primarily to malnutrition and secondly to insufficient antioxidant and immune system. In renal disease, the accumulation of urea in serum seems to be responsible for high antioxidant capacity. In contrast, there were no changes in PD, AD, depression syndrome and schizophrenia.
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PMID:Serum antioxidant capacity in neurological, psychiatric, renal diseases and cardiomyopathy. 1211 62

A 71-year old woman with schizophrenia was admitted to our hospital on November 26, 2002 under a diagnosis of acute myocardial infarction because of ST segment elevation in leads V2-V5 and positive serum cardiac troponin T level. Emergent coronary angiography showed no significant stenosis, but left ventriculography demonstrated apical ballooning and basal hyperkinesis. The final diagnosis was ampulla cardiomyopathy. Myocardial contrast echocardiography during the acute phase revealed an echocontrast defect consistent with the area of apical ballooning. The condition improved gradually as determined by disappearance of the abnormal wall motion. The coronary flow reserve in the left anterior descending artery measured by transthoracic Doppler echocardiography was decreased at 1.5 in the acute phase and gradually recovered over a period of 3 months (23 days, 1.9; 96 days, 2.9). Microvascular stunning defined as decreased coronary flow reserve was observed and recovery was delayed in this case compared with cases of myocardial stunning. These findings are of interest in evaluating the pathophysiology of ampulla cardiomyopathy.
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PMID:[Ampulla cardiomyopathy with delayed recovery of microvascular stunning: a case report]. 1459 20

Clozapine is an atypical antipsychotic agent that is more effective than the standard neuroleptics currently used for treating refractory schizophrenia. In addition, clozapine is a drug with few extrapyramidal side effects. However, clozapine is also associated with potentially serious adverse effects, such as cardiac complications as well as agranulocytosis. Clozapine-related cardiomyopathy has not been previously reported in East Asia. This report describes a 31-year-old Korean male patient with schizophrenia who developed dilated cardiomyopathy on treatment with clozapine. The removal of clozapine caused subsequent physical improvement. However, the readministration of clozapine for managing relapse of psychosis caused a recurrence of dilated cardiomyopathy in this patient. Therefore, this is the 1st report showing that the 2nd trial of clozapine caused recurrence of cardiomyopathy associated with clozapine. Thus, this report adds important support for a causal relation between clozapine and cardiac complications. In conclusion, this report attempts to raise awareness of clozapine-related cardiomyopathy.
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PMID:Cardiomyopathy associated with clozapine. 1650 9

Since the first mitochondrial dysfunction was described in the 1960s, the medicine has advanced in its understanding the role mitochondria play in health, disease, and aging. A wide range of seemingly unrelated disorders, such as schizophrenia, bipolar disease, dementia, Alzheimer's disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson's disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis, have underlying pathophysiological mechanisms in common, namely reactive oxygen species (ROS) production, the accumulation of mitochondrial DNA (mtDNA) damage, resulting in mitochondrial dysfunction. Antioxidant therapies hold promise for improving mitochondrial performance. Physicians seeking systematic treatments for their patients might consider testing urinary organic acids to determine how best to treat them. If in the next 50 years advances in mitochondrial treatments match the immense increase in knowledge about mitochondrial function that has occurred in the last 50 years, mitochondrial diseases and dysfunction will largely be a medical triumph.
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PMID:Mitochondrial dysfunction and molecular pathways of disease. 1723 70

Clozapine is contraindicated in patients who experienced cardiac adverse effects during therapy. A young male (34 years old) with clozapine-responsive schizophrenia developed hypokinetic cardiomyopathy during treatment. The decision to resume clozapine therapy and to treat cardiac problems with carvedilol and captopril was made due to the failure of other antipsychotics to control symptoms. He was followed up for 5 years. Significant improvement of psychiatric conditions and persistence of normal left ventricular function were obtained with combination treatment. beta-Blockers and ACE inhibitors may allow resumption of clozapine in refractory schizophrenia in whom it was withdrawn for cardiotoxicity. A large-scale investigation may be useful to confirm the present observations.
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PMID:Beta-blocker and angiotensin-converting enzyme inhibitor may limit certain cardiac adverse effects of clozapine. 1843 62

Since the first mitochondrial dysfunction was described in the 1960s, the medicine has advanced in its understanding the role mitochondria play in health and disease. Damage to mitochondria is now understood to play a role in the pathogenesis of a wide range of seemingly unrelated disorders such as schizophrenia, bipolar disease, dementia, Alzheimer's disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson's disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis. Medications have now emerged as a major cause of mitochondrial damage, which may explain many adverse effects. All classes of psychotropic drugs have been documented to damage mitochondria, as have stain medications, analgesics such as acetaminophen, and many others. While targeted nutrient therapies using antioxidants or their precursors (e. g., N-acetylcysteine) hold promise for improving mitochondrial function, there are large gaps in our knowledge. The most rational approach is to understand the mechanisms underlying mitochondrial damage for specific medications and attempt to counteract their deleterious effects with nutritional therapies. This article reviews our basic understanding of how mitochondria function and how medications damage mitochondria to create their occasionally fatal adverse effects.
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PMID:Medication-induced mitochondrial damage and disease. 1862 87

Clozapine is a superior agent for treatment-refractory patients with schizophrenia, but is underutilized in the US, likely due to the risk of side effects. This study examined all available autopsy data on cardiac disease and risk factors in people with schizophrenia in a sample of deceased persons with severe mental illness who had received clozapine (N=62) or risperidone (N=42). The mean body mass index (BMI) at the time of death was 31.4+/-8.8 kg/m2 and 27.1+/-8.2 kg/m2 in the clozapine and risperidone groups respectively (t=1.98, df=60, p=0.052). Cardiac related measures examined included: abdominal wall thickness, heart weight, left ventricle thickness, right ventricle thickness, presence of notable cardiac involvement (atherosclerosis, fibrosis and hypertrophy) and number of cardiac arteries occluded. No significant differences in any of the cardiac findings were noted between patients in the clozapine and risperidone groups. Independent of treatment, cardiomyopathy deaths were associated with a higher abdominal wall thickness (p=0.042) and a tendency towards higher BMI (p=0.051) as compared to the other causes of death. The results of this study suggest that while clozapine is associated with weight gain and metabolic abnormalities, there does not appear to be an increased occurrence of cardiac abnormalities in deceased persons who were treated with clozapine as compared to risperidone.
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PMID:Cardiac-related findings at autopsy in people with severe mental illness treated with clozapine or risperidone. 1902 22

Clozapine is a valuable drug for patients with treatment-resistant schizophrenia. Myocarditis is the most publicised cardiac complication of clozapine treatment, but cardiomyopathy and pericarditis have also been reported. Myocarditis has heterogeneous and non-specific presenting features, making it difficult to identify patients with clozapine-related myocarditis clinically. A high index of suspicion is required. The gold standard for diagnosis of myocarditis is an endomyocardial biopsy, but this is not a practical initial approach. Transthoracic echocardiography is a valuable, reproducible and widely available tool to assist in diagnosis of clozapine-induced cardiotoxicity. The level of B-type natriuretic peptide, a hormone secreted in response to ventricular wall stress, may be useful for evaluating patients with clozapine-induced cardiac dysfunction and may in the future be useful for screening asymptomatic patients. The mainstay of treatment of clozapine-induced cardiotoxicity is cessation of clozapine and provision of supportive care.
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PMID:Clozapine-induced cardiotoxicity: a clinical update. 1922 Jan 77

Autopsy records (protocols) and medical histories of 850 patients with schizophrenia (death cases from 1952 to 2007) have been studied using statistical analysis. There were substantial changes of indicators studied which were most distinctly seen over the last two decades: the dramatic increase of frequency of cardiac pathology, in particular, chronic ischemic heart disease; appearance of such diseases as acute myocardial infarction and dilatation cardiomyopathy; increase in the number of cases of chronic obstructive lung diseases and active lung tuberculosis as well as malignant tumors, mainly lung cancer. Some changes may be caused by the long-term treatment of schizophrenic patients with neuroleptics of phenothiazine group. The author suggests a term tanatomorphosis for such changes.
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PMID:[Somatic pathology and causes of death in schizophrenia]. 1949 13

The author considers selected clinical and morphological characteristics of secondary dilatation cardiomyopathy in patients with schizophrenia after long-term treatment with phenotiazine neuroleptics for the purpose of substantiating nosological self-sufficiency of this pathology (PCMP). 65 cases of PCMP (46 in men and 19 in women) were revealed at postmortem examination (2% of all autopsies or significantly higher than the general incidence of idiopathic dilatation cardiomyopathies (DCMP). Analysis of the patients" medical histories, dynamics of clinical conditions, and results of electrocardiography did not show significant differences between patients with schizophrenia and PCMP compared with mentally healthy DCPM subjects DCMP. Slightly lower heart mass was documented in the former group due to cardiovascular hypoplasia. It is concluded that phenothiazine-induced dilatation cardiomyopathy should be regarded as a separate nosological form belonging to a group of secondary DCMPs and designated as PCMP.
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PMID:[Phenothiazine-induced dilatation cardiomyopathy: selected aspects of clinical course and morphology]. 1982 23


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