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Medical Journal of Cairo University [The]. 2008; 76 (Supp. 4): 239-248
in English | IMEMR | ID: emr-88967

ABSTRACT

Cryptogenic stroke [CS] is a stroke of unexplained aetiology, in 1/3 the of cases, the cause of stroke remains undetermined inspite of full investigations. Patient with CS are thought to have a state of hypercoagulablity. To unmask some of the pathogenic mechanisms underlying cryptogenic stroke through assessment of some genetic disorders including C6[77]T mutation methyl-enetetrahydrofolate reductase gene, activated protein C [APC] resistance and role of thrombin anti-thrombin complex concentration [TAT] in plasma as indicators of hypecoagulable state. The study was conducted on 20 Egyptian patients divided into 2 groups, group I included 10 patients [6 males and 4 females] with cryptogenic stroke aged less than 50 years and group II included 10 age and sex matched patients with non-cryptogenic stroke. All of the 20 cases studied were subjected to panel of investigations including routine laboratory tests and imaging studies in orders to exclude any risk factors for stroke in group I patients and to determine risk factor of stroke in group II. Both groups were investigated for C6[77]T mutation in methylenetetrahydrofolate reductase gene, activated protein C [APC] resistance and thrombin anti-thrombin complex concentration [TAT] in plasma. No statistical significant difference was found between the two groups as regard C6[77]T mutation in methylenetetrahydrofolate reductase gene, [APC] resistance and TAT concentration in plasma [p value >0.05]. However, TAT level was found to be positively correlated with the clinical severity in non-cryptogenic stroke [p value <0.05]. C6[77]T mutation in methylenetetrahydrofolate gene, [APC] resistance and TAT concentration in plasma are not independent risk factors for cryptogenic stroke. TAT could be used as indicator of clinical severity and prognosis in patient with non-cryptogenic stroke


Subject(s)
Humans , Male , Female , Thrombophilia/blood , Protein C/blood , /blood , Protein S/blood , Polymorphism, Genetic , Stroke/genetics
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