Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malignant melanoma developed in an apparently benign nevus four months after therapy with levodopa in a patient with Parkinson's disease. This case is reported, and previous reports of this possible causal relationship are reviewed. Although this and previously reported cases are not inconsistent with the unpredictable and variable natural history of malignant melanoma, it seems prudent to clinically monitor pigmentary lesions in patients receiving levodopa therapy. Biopsy specimens of suspicious lesions in these patients should be examined histologically, and if malignancy is found, alternate therapies for treatment of parkinsonism should be considered.
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PMID:Development of malignant melanoma after levodopa therapy for Parkinson's disease. Report of a case and review of the literature. 401 96

Acutely administered caffeine modestly increases blood pressure, plasma catecholamine levels, plasma renin activity, serum free fatty acid levels, urine production, and gastric acid secretion. It alters the electroencephalographic spectrum, mood, and sleep patterns of normal volunteers. Chronic caffeine consumption has no effect on blood pressure, plasma catecholamine levels, plasma renin activity, serum cholesterol concentration, blood glucose levels, or urine production. Caffeine does not appear to be useful for increasing the motility of hypomotile sperm in artificial insemination or in the therapy of minimal brain dysfunction, cancer, or Parkinson's syndrome, but it may be effective as a topical treatment of atopic dermatitis and as systemic therapy for neonatal apnea. Caffeine does not seem to be associated with myocardial infarction; lower urinary tract, renal, or pancreatic cancer; teratogenicity; or fibrocystic breast disease. The role of caffeine in the production of cardiac arrhythmias or gastric or duodenal ulcers remains uncertain.
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PMID:The health consequences of caffeine. 634 91

In this cohort study, 16,911 men who had completed a mailed dietary questionnaire were followed for 11 1/2 years with 721 deaths reported from ischemic heart disease (IHD) (excluding those reporting on the questionnaire a prior history of angina or other heart conditions). Although no association was found between coffee consumption and mortality from IHD, a negative association between coffee consumption and mortality from diseases other than IHD was found. This negative association, found exclusively in the first four years of follow-up, was observed in deaths from digestive diseases, other than malignancies, and paralysis agitans, which made the greatest contribution to this observed negative association. The negative association appeared to reflect a reduction in coffee consumption related to the disorders in question and not to a protective effect of coffee. It has been suggested that the positive association between coffee consumption and IHD reported in some case-control studies may reflect a decreased consumption among controls rather than an unusually high consumption among cases.
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PMID:Coffee consumption and mortality from ischemic heart disease and other causes: results from the Lutheran Brotherhood study, 1966-1978. 723 54

In a 16-year mortality followup of some 293,000 insured U.S. veterans, specific causes of death were studied in relation to smoking status. The main results confirmed earlier findings.Mortality ratios for cigarette smokers as compared with nonsmokers were 1.73 for all causes of death, 1.58 for all cardiovascular diseases, 2.12 for all cancers, and 4.31 for all respiratory diseases. The highest ratios (those greater than 5.0) were observed for cor pulmonale, aortic aneurysm, emphysema and bronchitis, cancer of the pharynx, cancer of the esophagus, cancer of the larynx, and cancer of the lung and bronchus. The greatest excess in deaths in terms of observed numbers minus expected was found for the cardiovascular diseases, in particular for coronary heart disease.Mortality ratios for ex-cigarette smokers who had stopped smoking for reasons other than physicians' orders were much lower compared with nonsmokers than the mortality ratios for current cigarette smokers: 1.21 for all causes, 1.15 for all cardiovascular diseases, 1.39 for all cancers, and 2.08 for all respiratory diseases. For most causes of death, the mortality ratios for ex-cigarette smokers who had stopped smoking for reasons other than physicians' orders varied inversely with the number of years of cessation. For some diseases, the mortality risk for the ex-cigarette smoker returned to normal almost immediately after the cessation of smoking, whereas for others, the return to normal was more gradual. The first group included stroke and the combined category of influenza and pneumonia; the second group included cardiovascular diseases as a whole and coronary heart disease. For still other diseases, although the mortality ratio declined with the length of time smoking was discontinued, substantial excess risks remained even after 20 years of cessation. In this third group were aortic aneurysm, bronchitis and emphysema, and lung cancer-diseases with very high mortality ratios for current cigarette smokers. Parkinson's disease remained the one disease that clearly exhibited a negative association with cigarette smoking.
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PMID:Smoking and causes of death among U.S. veterans: 16 years of observation. 738 6

To ascertain whether sleep-disordered breathing (SDB) in the elderly is associated with increased mortality, a prospective cohort study with 4-year follow-up was conducted at a retirement village complex in Sydney, Australia. The subjects were 163 non-demented retirement village residents. Logistic regression was used to assess SDB and co-morbidity as independent predictors of mortality. Respiratory disturbance index (RDI) was measured in the home; those subjects with RDIs > or = 15 were classified as having SDB. Co-morbidity was measured by an index of Burden of Illness based on the medical history obtained at baseline. At 4 years, 27% (4/15) of those subjects with RDIs > or = 15 and 22% (33/148) of those with RDIs < 15 were dead. RDI had an odds ratio (OR) of 1.00 (95% CI: 0.96, 1.04). Burden of Illness had an OR of 1.90 (95% CI: 1.34, 2.71). Adjustment for age and sex did not alter these findings. Significant predictors of mortality from the illness measure were a history of hypertension, Parkinson's disease and other severe illnesses (usually cancer). RDI was not a predictor of mortality in this population of non-demented seniors, where the prevalence of high levels of RDI was low.
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PMID:Four-year follow-up of mortality and sleep-related respiratory disturbance in non-demented seniors. 748 14

Traffic accidents (TA) are, after heart disease, cancer and stroke, the fourth death cause among the general population. Although the number of AT caused by diseases-excluding alcoholism- seems to be reduced, interaction between organic pathology and functional ability increases the importance of this problem. This paper revises the literature on the relation between AT and specific neurological diseases: epilepsy, obstructive sleep apnea syndrome (SAS), stroke, dementia and Parkinson disease. Also, the problems and the role of the neurologist in assessing driving ability in patients with brain damage is analyzed, with special reference to the legal condition in Spain. The insufficiency of diagnostic labels as predictors of driving ability is stressed; the group of patients affected by these pathologies does not present greater TA risk than young drivers twice that of the general population. In the cases of epilepsy, SAS and ECV, which can cause episodic driving inability, defining recurrence probabilities and finding regulation formulas is the task of clinical epidemiologists and the regulative authorities. In the case of dementia, Parkinson disease and ECV, causing psychomotor performance deterioration, the basic problem, complicated by the presence of comorbility in these patients, is the development of valid clinical scales for driving ability assessment. The regulative authorities need simple measures which are often difficult to develop. Meanwhile, it is the task of the neurologist, as part of the therapeutic intervention during the medical encounter, to discuss driving risks with each patient.
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PMID:[Neurological diseases and driving]. 749 90

In some facilities, group learning has been used to teach adults who have various disabilities or chronic diseases (e.g., diabetes, cardiac problems, cancer, Parkinson's disease, spinal cord injury). The following literature review discusses the advantages of group learning, which include peer support, individuals' learning and gaining motivation from each other, reduced feelings of isolation, and opportunities to share problems and goals. It appears likely that greater use of group learning could enhance rehabilitation efforts for adults.
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PMID:Group learning for adults with disabilities or chronic disease. 756 5

Polymorphisms in many xenobiotic metabolizing enzymes occur leading to variation in the level of enzyme expression in vivo. Enzymes showing such polymorphisms include the cytochrome P450 enzymes CYP1A1, CYP1A2, CYP2A6, CYP2D6, and CYP2E1 and the phase two metabolism enzymes glutathione S-transferase MI (GSTMI) and arylamine N-acetyltransferase 2 (NAT2). In the past, these polymorphisms have been studied by phenotyping using in vivo administration of probe drugs. However, the mutations which give rise to several of these polymorphisms have now been identified and genotyping assays for polymorphisms in CYP1A1, CYP2A6, CYP2D6, CYP2E1, GSTMI, and NAT2 have been developed. Specific phenotypes for several of the polymorphic enzymes have been associated with increased susceptibility to malignancy, particularly lung and bladder cancer, and Parkinson's disease. These associations are likely to be due to altered activation or detoxication of chemicals initiating these diseases, including components of tobacco smoke and neurotoxins. The substrate specificity and tissue distribution of polymorphic enzymes implicated in disease causation discussed with particular reference to previously described disease-phenotype associations.
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PMID:Genotyping for polymorphisms in xenobiotic metabolism as a predictor of disease susceptibility. 769 86

Antineoplastons are naturally occurring cytodifferentiating agents. Chemically, antineoplastons are medium and small sized peptides, amino acid derivatives and organic acids which exist in blood, tissues and urine. In clinical trials in advanced cancer, in addition to the anticancer activity it was observed that patients suffering from both cancer and Parkinson's disease exhibited marked improvement in parkinsonian symtomatology when treated with antineoplaston A5. The present study was designed to analyse the influence of A5 on central dopaminergic structures. Mice and rats were given A5 intraperitoneally at three different dosage levels. Experiments conducted included spontaneous locomotor activity, amphetamine-induced yawning and erections, catalepsy, the effect on the level and utilization of noradrenaline and dopamine in the brain and the influence of prolonged and chronic treatment on the haloperidol-induced catalepsy. It has been demonstrated that A5 stimulates the central dopaminergic receptors. It diminishes the cataleptic response to haloperidol and enhances the incidence of apomorphine-induced yawning. Biochemical studies demonstrated increased concentration of dopamine and noradrenaline in the brain and diminished utilization of both catecholamines.
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PMID:The influence of antineoplaston A5 on the central dopaminergic structures. 781 88

Cytochrome P450 CYP2D6 polymorphism is an autosomal recessive trait associated with impaired debrisoquine metabolism in 5-10% of caucasian populations. This polymorphism has been associated with susceptibility to Parkinson's disease, bladder cancer, various forms of leukemia and possibly melanoma. In many other cancer forms, the data remained contradictory due to the technical limitations for identifying affected individuals (poor metabolizers). A recently developed polymerase chain reaction-based assay allows convenient screening of approximately 80% of known mutations. We have tested brain tumors correlated with chromosome 22 deviations for genetic polymorphism in the cytochrome P450 CYP2D6 locus localized on chromosome 22q13. Thirty-one meningioma samples were analyzed and the observed frequency of heterozygotes and homozygotes for the G to A mutation did not deviate significantly from the distribution in a normal population. These data are comparable to previous observations in for example breast and colon cancer and indicate that the CYP2D6 locus on chromosome 22q13 is not involved in the pathogenesis of meningiomas.
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PMID:Debrisoquine hydroxylase gene polymorphism in meningioma. 784 77


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