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Influence of the −675 4G/5G dimorphism of the plasminogen activator inhibitor 1 promoter on thrombotic risk in patients with factor V Leiden
Author(s) -
Visanji J. M.,
Seargent J.,
Tahri D.,
Croft S. A.,
Makris M.,
Preston F. E.,
Peake I. R.,
Daly M. E.
Publication year - 2000
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.2000.02152.x
Subject(s) - factor v leiden , allele , medicine , odds ratio , plasminogen activator inhibitor 1 , risk factor , loss of heterozygosity , plasminogen activator , gastroenterology , thrombophilia , venous thrombosis , factor v , heterozygote advantage , t plasminogen activator , thrombosis , biology , genetics , gene
Elevated plasminogen activator inhibitor 1 (PAI‐1) levels are associated with venous thromboembolism, although their significance is unclear. PAI‐1 levels are influenced by a PAI‐1 promoter dimorphism (4G/5G), the 4G allele being associated with increased PAI‐1 activity. We investigated whether the 4G allele influenced thrombotic risk by studying 99 symptomatic factor V (FV) Leiden heterozygotes and 99 healthy subjects. The 4G allele was more prevalent among cases than among healthy subjects (χ 2 = 8·00, P = 0·005) and the odds ratio (OR) for thrombosis associated with either heterozygosity or homozygosity for the 4G allele was 2·43 ( P = 0·011). We conclude that carriership of the 4G allele was more prevalent in patients who already carried factor V Leiden than in control subjects without factor V Leiden.