Source:http://linkedlifedata.com/resource/pubmed/id/17196621
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2007-1-12
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| pubmed:abstractText |
There was increasing evidence suggesting that angiotensin I-converting enzyme may play an important role in the pathogenesis of PD. Our former study has shown that angiotensin I-converting enzyme gene (ACE) may confer a susceptibility for the risk of Parkinson's disease (PD). Meanwhile, recent studies have emphasized that genetic factors may involve in the occurrence of the adverse effects of chronic L-dopa therapy in PD patients. This study was designed to assess whether genetic polymorphism of the ACE could be a predictor of L-dopa-induced adverse effects in PD. There were 251 patients included in this study and their mean age at onset of disease was 63.3+/-11.4 years. The duration of disease and the treatment with L-dopa was 6.3+/-5.1 and 5.0+/-4.3 years, respectively. The frequency of the homozygote ACE-II genotype of the ACE in PD patients with L-dopa-induced psychosis was significantly higher than that in PD patients without the adverse effect (63.3% vs 43.0%; chi(2)=6.347, OR=1.435, 95%CI=1.105-1.864, p=0.012). However, the ACE polymorphism was not associated with the risk to develop dyskinesia or motor fluctuation induced by L-dopa. Furthermore, a logistic regression analysis confirmed that the ACE-II genotype was an independent risk factor for L-dopa-induced psychosis in PD patients (OR=2.542, p=0.012). In conclusion, results of the study showed that ACE-II genotype might confer a primary predictor for the occurrence of psychosis in L-dopa-treated PD.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Jan
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| pubmed:issn |
0022-510X
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
31
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| pubmed:volume |
252
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
130-4
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| pubmed:meshHeading |
pubmed-meshheading:17196621-Adult,
pubmed-meshheading:17196621-Aged,
pubmed-meshheading:17196621-Aged, 80 and over,
pubmed-meshheading:17196621-Antiparkinson Agents,
pubmed-meshheading:17196621-Dyskinesia, Drug-Induced,
pubmed-meshheading:17196621-Female,
pubmed-meshheading:17196621-Genetic Predisposition to Disease,
pubmed-meshheading:17196621-Homozygote,
pubmed-meshheading:17196621-Humans,
pubmed-meshheading:17196621-Levodopa,
pubmed-meshheading:17196621-Male,
pubmed-meshheading:17196621-Middle Aged,
pubmed-meshheading:17196621-Parkinson Disease,
pubmed-meshheading:17196621-Peptidyl-Dipeptidase A,
pubmed-meshheading:17196621-Polymorphism, Genetic,
pubmed-meshheading:17196621-Predictive Value of Tests,
pubmed-meshheading:17196621-Psychoses, Substance-Induced,
pubmed-meshheading:17196621-Risk Factors
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| pubmed:year |
2007
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| pubmed:articleTitle |
Genetic polymorphism of the angiotensin converting enzyme and L-dopa-induced adverse effects in Parkinson's disease.
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| pubmed:affiliation |
Department of Neurology, Chushang Show-Chwan Hospital, Nantou, 557, Taiwan. jjlinn@tcts.seed.net.tw
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| pubmed:publicationType |
Journal Article
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