期刊
BLOOD COAGULATION & FIBRINOLYSIS
卷 16, 期 2, 页码 135-140出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/01.mbc.0000161567.59140.47
关键词
thromboembolism; venous; arterial; protein S deficiency type III
类别
Free protein S rather than total protein S levels are currently measured to detect inherited protein S deficiency. Because type III (free protein S) deficiency is still not established as risk factor for thrombosis, we assessed the absolute risk of venous and arterial thromboembolism in a family cohort study. Annual incidences in first-degree relatives with and without protein S deficiency type III were compared. Probands had experienced thrombosis and had either the prothrombin G20210A mutation, increased factor VIII:C levels or hyperhomocysteinemia. Relatives were tested for these thrombophilic disorders and factor V Leiden. Levels of antithrombin, protein C, total and free protein S, and factor XI:C were additionally measured. Of 500 relatives enrolled, 105 were excluded from analysis because they could not be classified, due to acquired conditions. Protein S deficiency type III was demonstrated in 60/395 remaining relatives (15%). Other thrombophilic defects were equally distributed among deficient and nondeficient relatives. Annual incidences of venous thromboembolism were 0.28 per 100 person-years [95% confidence interval (CI), 0.09-0.66] in deficient relatives versus 0.20 per 100 person-years (95% Cl, 0.12-0.30) in non-deficient relatives [hazard ratio, 1.4 (95% Cl, 0.4-4.0)]. For arterial thromboembolism these values were 0.16 per 100 person-years (95% Cl, 0.03-0.46) versus 0.10 per 100 person-years (95% Cl, 0.05-0.19) [hazard ratio, 1.5 (95% Cl, 0.3-6.0)]. These results suggest that protein S deficiency type III is not associated with an increased risk of either venous or arterial thromboembolism. (c) 2005 Lippincott Williams & Wilkins.
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