Reduction of high fetal loss rate by anticoagulant treatment during pregnancy in antithrombin, protein C or protein S deficient women

被引:41
作者
Folkeringa, Nienke
Leendert, Jan
Brouwer, P.
Korteweg, Fleurisca J.
Veeger, Nic J. G. M.
Erwich, Jan Jaap H. M.
Holm, Jozien P.
van der Meer, Jan
机构
[1] Univ Groningen, Univ Med Ctr Groningen, Div Haemostasis Thrombosis & Rheol, Dept Haematol, NL-9713 GZ Groningen, Netherlands
[2] Univ Groningen, Univ Med Ctr Groningen, Dept Obstet & Gynaecol, NL-9713 GZ Groningen, Netherlands
[3] Univ Groningen, Univ Med Ctr Groningen, Trial Coordinat Ctr, NL-9713 GZ Groningen, Netherlands
关键词
fetal loss; thromboprophylaxis; antithrombin deficiency; protein C deficiency; protein S deficiency;
D O I
10.1111/j.1365-2141.2006.06480.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Hereditary thrombophilia is associated with an increased risk of fetal loss. Assuming that fetal loss is due to placental thrombosis, anticoagulant treatment might improve pregnancy outcome. In an observational family cohort study, we prospectively assessed the effects of anticoagulant drugs on fetal loss rates in women with hereditary deficiencies of antithrombin, protein C or protein S. The cohort contained 376 women (50 probands and 326 deficient or non-deficient relatives). Probands were consecutive deficient patients with venous tromboembolism. Thromboprophylaxis during pregnancy was recommended in deficient women, irrespective of prior venous thromboembolism, and in non-deficient women with prior venous thromboembolism. Outcome of first pregnancy was analysed in 55 eligible women. Of 37 deficient women, 26 (70%) received thromboprophylaxis during pregnancy, compared with three of 18 (17%) non-deficient women. Fetal loss rates were 0% in deficient women with thromboprophylaxis versus 45% in deficient women without (P = 0.001) and 7% in non-deficient women without thromboprophylaxis (P = 0.37). The adjusted relative risk of fetal loss in women who received thromboprophylaxis versus women who did not was 0.07 (95% confidence interval 0.001-0.7; P = 0.02). Our data suggest that anticoagulant treatment during pregnancy reduces the high fetal loss rate in women with hereditary deficiencies of antithrombin, protein C or protein S.
引用
收藏
页码:656 / 661
页数:6
相关论文
共 22 条
[1]   Elevated levels of FVIII:C within families are associated with an increased risk for venous and arterial thrombosis [J].
Bank, I ;
Libourel, EJ ;
Middeldorp, S ;
Hamulyák, K ;
van Pampus, ECM ;
Koopman, MMW ;
Prins, MH ;
van der Meer, J ;
Büller, HR .
JOURNAL OF THROMBOSIS AND HAEMOSTASIS, 2005, 3 (01) :79-84
[2]   Use of antithrombotic agents during pregnancy [J].
Bates, SA ;
Greer, IA ;
Hirsh, J ;
Ginsberg, JS .
CHEST, 2004, 126 (03) :627S-644S
[3]   MUTATION IN BLOOD-COAGULATION FACTOR-V ASSOCIATED WITH RESISTANCE TO ACTIVATED PROTEIN-C [J].
BERTINA, RM ;
KOELEMAN, BPC ;
KOSTER, T ;
ROSENDAAL, FR ;
DIRVEN, RJ ;
DERONDE, H ;
VANDERVELDEN, PA ;
REITSMA, PH .
NATURE, 1994, 369 (6475) :64-67
[4]  
Brenner B, 2000, THROMB HAEMOSTASIS, V84, P935
[5]   The pathogenesis of venous thromboembolism: Evidence for multiple interrelated causes [J].
Brouwer, Jan-Leendert P. ;
Veeger, Nic J. G. M. ;
Kluin-Nelemans, Hanneke C. ;
van der Meer, Jan .
ANNALS OF INTERNAL MEDICINE, 2006, 145 (11) :807-815
[6]  
Danneberg J, 1998, CLIN CHEM, V44, P349
[7]   IS HYPERHOMOCYSTEINAEMIA A RISK FACTOR FOR RECURRENT VENOUS THROMBOSIS [J].
DENHEIJER, M ;
BLOM, HJ ;
GERRITS, WBJ ;
ROSENDAAL, FR ;
HAAK, HL ;
WIJERMANS, PW ;
BOS, GMJ .
LANCET, 1995, 345 (8954) :882-885
[8]   Hyperhomocysteinemia as a risk factor for deep-vein thrombosis [J].
denHeijer, M ;
Koster, T ;
Blom, HJ ;
Bos, GMJ ;
Briet, E ;
Reitsma, PH ;
Vandenbroucke, JP ;
Rosendaal, FR .
NEW ENGLAND JOURNAL OF MEDICINE, 1996, 334 (12) :759-762
[9]   Factor V Leiden and prothrombin G20210A mutations, but not methylenetetrahydrofolate reductase C677T, are associated with recurrent miscarriages [J].
Foka, ZJ ;
Lambropoulos, AF ;
Saravelos, H ;
Karas, GB ;
Karavida, A ;
Agorastos, T ;
Zournatzi, V ;
Makris, PE ;
Bontis, J ;
Kotsis, A .
HUMAN REPRODUCTION, 2000, 15 (02) :458-462
[10]  
Frezzato M, 1996, AM J EPIDEMIOL, V143, P1257