Prediction, prevention, and treatment of venous thromboembolic disease in pregnancy

被引:26
作者
Zotz, RB
Gerhardt, A
Scharf, RE
机构
[1] Univ Dusseldorf, Inst Haemostaseol & Transfusionsmed, D-40225 Dusseldorf, Germany
[2] Univ Dusseldorf, Ctr Med, Dept Hemostasis & Transfus Med, Dusseldorf, Germany
关键词
pregnancy; venous thrombosis; risk factors; therapy; prevention;
D O I
10.1055/s-2003-38829
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Pregnancy is recognized as an independent risk factor for venous thromboembolism leading to thromboembolic events, particularly in women with prior venous thrombosis, family history of thrombosis, or additional thrombophilic risk factors. To reduce the incidence of venous thromboembolism in pregnancy and improve outcomes, an individual risk stratification on the basis of probability of thrombosis as a rationale for an individual risk-adapted prophylaxis is required. In women without prior thrombosis, the presence of a heterozygous factor V Leiden or heterozygous G20210A mutation in the prothrombin gene is associated with a pregnancy-associated thrombotic risk of approximately 1 in 400. Thus, in pregnant carriers of either one of these mutations the risk of venous thromboembolism is low. For this reason, routine thrombophilia screening of all pregnant women is not recommended. However, a combination of the two genetic risk factors can increase the risk to a modest level (risk 1 in 25). In women with a single episode of prior thrombosis associated with a transient risk factor (such as surgery or trauma) and no additional genetic risk factor, the probability of a pregnancy-associated thrombosis also appears to be low. In contrast, in women with a prior idiopathic venous thrombosis who carry an additional hereditary risk factor or who have a positive family history of thrombosis, a high risk (> 10%) can be expected, supporting the indication for active antepartum and postpartum heparin prophylaxis. In many cases, the absolute magnitude of risk is unknown or estimated, and recommendations are often empiric.
引用
收藏
页码:143 / 153
页数:11
相关论文
共 64 条
[11]   FAMILIAL THROMBOPHILIA DUE TO A PREVIOUSLY UNRECOGNIZED MECHANISM CHARACTERIZED BY POOR ANTICOAGULANT RESPONSE TO ACTIVATED PROTEIN-C - PREDICTION OF A COFACTOR TO ACTIVATED PROTEIN-C [J].
DAHLBACK, B ;
CARLSSON, M ;
SVENSSON, PJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (03) :1004-1008
[12]  
DESTEFANO V, 1994, THROMB HAEMOSTASIS, V71, P799
[13]  
Douketis JD, 1996, THROMB HAEMOSTASIS, V75, P254
[14]  
Elkayam U, 1999, J AM COLL CARDIOL, V33, P1642
[15]  
Emmerich J, 2001, THROMB HAEMOSTASIS, V86, P809
[16]   PLACENTAL TRANSPORT OF HEPARIN [J].
FLESSA, HC ;
KAPSTROM, AB ;
GLUECK, HI ;
WILL, JJ .
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1965, 93 (04) :570-&
[17]   LOW-MOLECULAR WEIGHT HEPARIN (PK-10169) DOES NOT CROSS THE PLACENTA DURING THE 2ND TRIMESTER OF PREGNANCY STUDY BY DIRECT FETAL BLOOD-SAMPLING UNDER ULTRASOUND [J].
FORESTIER, F ;
DAFFOS, F ;
CAPELLAPAVLOVSKY, M .
THROMBOSIS RESEARCH, 1984, 34 (06) :557-560
[18]   Frequency of pregnancy-related venous thromboembolism in anticoagulant factor-deficient women: Implications for prophylaxis [J].
Friederich, PW ;
Sanson, BJ ;
Simioni, P ;
Zanardi, S ;
Huisman, MV ;
Kindt, I ;
Prandoni, P ;
Buller, HR ;
Girolami, A ;
Prins, MH .
ANNALS OF INTERNAL MEDICINE, 1996, 125 (12) :955-+
[19]   Prothrombin and factor V mutations in women with a history of thrombosis during pregnancy and the puerperium. [J].
Gerhardt, A ;
Scharf, RE ;
Beckmann, MW ;
Struve, S ;
Bender, HG ;
Pillny, M ;
Sandmann, W ;
Zotz, RB .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 342 (06) :374-380
[20]  
GHAVARI AE, 1998, LUPUS, V7, P52