Relationship between thrombomodulin promoter-33G/A polymorphism and cerebral infarction
10.3969/j.issn.1672-5921.2011.05.002
- Author:
Ling WU
1
Author Information
1. Department of Neurology
- Publication Type:Journal Article
- Keywords:
Brain infarction;
Genes;
Polymorphism, restriction fragment length;
Thrombomodulin
- From:
Chinese Journal of Cerebrovascular Diseases
2011;8(5):230-234
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the correlation between cerebral infarction and thrombomodulin (TM) promoter-33G/A (TM-33G/A) mutation. Methods: A total of 130 patients with cerebral infarction in the First People's Hospital in Kunming area, Yunnan province from December 2009 to July 2010 and 120 controls (patients with depression, anxiety, dizziness, and encephalitis) admitted to the hospital at the same time period were included in the study. A polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay was used to detect the TM-33G/A polymorphism of the included subjects. Multivariate Logistic Regression was used to analyze the correlation between cerebral infarction and TM-33G/A polymorphism. Results: Circled digit oneIn 130 patients with cerebral infarction, GG genotype was 99, GA genotype was 30, AA genotype was 1, and the G/A point mutation rate was 23. 85%. In 120 patients in the control group, GG genotype was 106, GA genotype was 13, AA genotype was 1, and the G/A point mutation rate was 11.67%. There was significant difference between the two groups (P < 0.05). Circled digit twoMultivariate Logistic Regression analysis revealed that, in addition to history of smoking, hypertension, increased low-density lipoprotein cholesterol, and increased fasting glucose, the TM-33G/A polymorphism was also an independent risk factor for cerebral infarction (OR, 2.175, 95% CI: 1.049-4.511, P = 0.037). Conclusion: TM-33 G/A polymorphism may be one of the risk factors for cerebral infarction.
