| Autor: |
Harrington, Dominic J., Malefora, Agata, Schmeleva, Veronika, Kapustin, Sergey, Papayan, Ludmila, Blinov, Mikhail, Harrington, Pip, Mitchell, Mike, Savidge, Geoffrey F. |
| Předmět: |
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| Zdroj: |
Clinical Chemistry & Laboratory Medicine; Apr2003, Vol. 41 Issue 4, p496-500, 5p, 1 Diagram, 3 Charts, 3 Graphs |
| Abstrakt: |
We undertook genetic and biochemical assays in patients with arterial (n = 146) and venous (n = 199) thromboembolism and survivors of pulmonary embolism (n = 58) to study causation and gene-life style interactions. In the clinical material from North Western Russia, factor V Leiden was found to be a risk factor in venous thrombosis (OR = 3.6), while the methylenete-trahydrofolate reductase (MTHFR) C677T mutation was a significant variable in both venous (p = 0.03) and arterial thrombosis (p = 0.004). Homocysteine levels were determined (n = 84) and hyperhomocysteinemia correlated with the T allele of the MTHFR gene, and with smoking and coffee consumption. Vitamin supplementation reduced homocysteine levels dependent on MTHFR genotypes (36% TT, 25% CT, 22% CC). In pulmonary embolism patients, frequency of the -455G/A β-fibrinogen dimorphism was studied. Carriers of this allele were significantly underrepresented (p < 0.02) among pulmonary embolism survivors (34.5%) compared to controls (56.7%). Additionally, -455AA homozygotes were found in 11.7% controls but only 1.7% of pulmonary embolism patients (p = 0.006). In venous and arterial thrombosis cases, MTHFR and homocysteine data led to effective dietary supplementation with a reduced risk of disease progression. Results from the pulmonary embolism study may indicate that screening tests for the -455G/A β-fibrinogen genetic variation could be of prognostic value, and may point the way for novel anticoagulation strategies. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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