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Genetic Variations Observed in Arterial and Venous Thromboembolism – Relevance for Therapy, Risk Prevention and Prognosis

Genetic Variations Observed in Arterial and Venous Thromboembolism – Relevance for Therapy, Risk... Abstract 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 methylenetetrahydrofolate 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 genotype (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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Clinical Chemistry and Laboratory Medicine (CCLM) de Gruyter

Genetic Variations Observed in Arterial and Venous Thromboembolism – Relevance for Therapy, Risk Prevention and Prognosis

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References (17)

Publisher
de Gruyter
Copyright
Copyright © 2003 by the
ISSN
1434-6621
DOI
10.1515/CCLM.2003.075
pmid
12747593
Publisher site
See Article on Publisher Site

Abstract

Abstract 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 methylenetetrahydrofolate 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 genotype (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.

Journal

Clinical Chemistry and Laboratory Medicine (CCLM) – de Gruyter

Published: Apr 25, 2003

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