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A common 4G allele in the promoter of the plasminogen activator inhibitor-1 (PAI-1) gene as a risk factor for pulmonary embolism and arterial thrombosis in hereditary protein S deficiency.
Thromb Haemost. 1998 Apr; 79(4):802-7.TH

Abstract

Reduced fibrinolytic capacity due to increased plasminogen activator inhibitor-1 (PAI-1) activity in plasma is a common finding in patients with coronary heart disease or venous thromboembolism, although its clinical significance is debated. Recently, a dimorphism in the PAI-1 promoter (4G-5G) has been reported and homozygosity for the 4G allele is associated with increased transcription and higher PAI-1 levels. Homozygous 4G genotype has been suggested to be a risk factor for myocardial infarction. In the present study, the 4G-5G dimorphism was determined in 349 individuals from 21 thrombophilic families with hereditary protein S deficiency and in 140 unrelated healthy controls. Among the 143 protein S deficient individuals, there was no relationship between deep or superficial venous thrombosis and the PAI-1 dimorphism. However, 26% (12/46) of individuals having protein S deficiency combined with homozygosity for the 4G allele had suffered pulmonary embolism as compared to 7% (7/97) of protein S deficient individuals carrying at least one 5G allele (p = 0.0019). In protein S deficient individuals, arterial thrombosis was found to be associated with smoking and 4G homozygosity. No association was found between the PAI-1 dimorphism and arterial or venous thromboembolism in family members without protein S deficiency. In conclusion, the PAI-1 genotype affects the phenotypic expression of thrombophilia in protein S deficient individuals.

Authors+Show Affiliations

Department of Clinical Chemistry, Malmö University Hospital, Lund University, Sweden.No affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9569196

Citation

Zöller, B, et al. "A Common 4G Allele in the Promoter of the Plasminogen Activator Inhibitor-1 (PAI-1) Gene as a Risk Factor for Pulmonary Embolism and Arterial Thrombosis in Hereditary Protein S Deficiency." Thrombosis and Haemostasis, vol. 79, no. 4, 1998, pp. 802-7.
Zöller B, García de Frutos P, Dahlbäck B. A common 4G allele in the promoter of the plasminogen activator inhibitor-1 (PAI-1) gene as a risk factor for pulmonary embolism and arterial thrombosis in hereditary protein S deficiency. Thromb Haemost. 1998;79(4):802-7.
Zöller, B., García de Frutos, P., & Dahlbäck, B. (1998). A common 4G allele in the promoter of the plasminogen activator inhibitor-1 (PAI-1) gene as a risk factor for pulmonary embolism and arterial thrombosis in hereditary protein S deficiency. Thrombosis and Haemostasis, 79(4), 802-7.
Zöller B, García de Frutos P, Dahlbäck B. A Common 4G Allele in the Promoter of the Plasminogen Activator Inhibitor-1 (PAI-1) Gene as a Risk Factor for Pulmonary Embolism and Arterial Thrombosis in Hereditary Protein S Deficiency. Thromb Haemost. 1998;79(4):802-7. PubMed PMID: 9569196.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A common 4G allele in the promoter of the plasminogen activator inhibitor-1 (PAI-1) gene as a risk factor for pulmonary embolism and arterial thrombosis in hereditary protein S deficiency. AU - Zöller,B, AU - García de Frutos,P, AU - Dahlbäck,B, PY - 1998/5/6/pubmed PY - 1998/5/6/medline PY - 1998/5/6/entrez SP - 802 EP - 7 JF - Thrombosis and haemostasis JO - Thromb Haemost VL - 79 IS - 4 N2 - Reduced fibrinolytic capacity due to increased plasminogen activator inhibitor-1 (PAI-1) activity in plasma is a common finding in patients with coronary heart disease or venous thromboembolism, although its clinical significance is debated. Recently, a dimorphism in the PAI-1 promoter (4G-5G) has been reported and homozygosity for the 4G allele is associated with increased transcription and higher PAI-1 levels. Homozygous 4G genotype has been suggested to be a risk factor for myocardial infarction. In the present study, the 4G-5G dimorphism was determined in 349 individuals from 21 thrombophilic families with hereditary protein S deficiency and in 140 unrelated healthy controls. Among the 143 protein S deficient individuals, there was no relationship between deep or superficial venous thrombosis and the PAI-1 dimorphism. However, 26% (12/46) of individuals having protein S deficiency combined with homozygosity for the 4G allele had suffered pulmonary embolism as compared to 7% (7/97) of protein S deficient individuals carrying at least one 5G allele (p = 0.0019). In protein S deficient individuals, arterial thrombosis was found to be associated with smoking and 4G homozygosity. No association was found between the PAI-1 dimorphism and arterial or venous thromboembolism in family members without protein S deficiency. In conclusion, the PAI-1 genotype affects the phenotypic expression of thrombophilia in protein S deficient individuals. SN - 0340-6245 UR - https://www.unboundmedicine.com/medline/citation/9569196/A_common_4G_allele_in_the_promoter_of_the_plasminogen_activator_inhibitor_1__PAI_1__gene_as_a_risk_factor_for_pulmonary_embolism_and_arterial_thrombosis_in_hereditary_protein_S_deficiency_ L2 - http://www.diseaseinfosearch.org/result/6003 DB - PRIME DP - Unbound Medicine ER -