Significant changes in both the coagulation and fibrinolytic systems that have been
associated with normal pregnancy are thought to be part of a hemostatic mechanism
that can cope with the physiological stresses associated with delivery [
1
,
2
,
3
,
4
,
5
]. These hemostatic changes, which normally favor coagulation over that of fibrinolysis,
generally revert back to normal values following delivery. Impaired fibrinolysis during
pregnancy has been attributed to increased levels of both plasminogen activator inhibitor-1
(PAI-1) and the placenta-derived plasminogen activator inhibitor-2 (PAI-2) [
- Cerneca F
- Ricci G
- Simeone R
- Malisano M
- Alberico S
- Guaschino S
Coagulation and fibrinolysis changes in normal pregnancy. Increased levels of procoagulants
and reduced levels of inhibitors during pregnancy induce a hypercoagulable state,
combined with a reactive fibrinolysis.
Eur J Obstet Gynecol Reprod Biol. 1997; 73: 31-36
[6]
]. Although somewhat controversial, some reports have demonstrated that plasma levels
of tissue plasminogen activator (tPA) are increased during normal pregnancy [
[3]
], while other reports have found no changes in tPA levels [
7
,
8
]. Impaired fibrinolysis, which has been implicated as a possible cause for venous
thromboembolism (VTE) in both men and women [
[9]
], has also been suggested as a reason for the increased risk of pregnancy associated
VTE [
1
,
2
,
3
,
4
,
5
,
- Cerneca F
- Ricci G
- Simeone R
- Malisano M
- Alberico S
- Guaschino S
Coagulation and fibrinolysis changes in normal pregnancy. Increased levels of procoagulants
and reduced levels of inhibitors during pregnancy induce a hypercoagulable state,
combined with a reactive fibrinolysis.
Eur J Obstet Gynecol Reprod Biol. 1997; 73: 31-36
6
,
7
,
8
].To read this article in full you will need to make a payment
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References
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- Coagulation and fibrinolysis changes in normal pregnancy. Increased levels of procoagulants and reduced levels of inhibitors during pregnancy induce a hypercoagulable state, combined with a reactive fibrinolysis.Eur J Obstet Gynecol Reprod Biol. 1997; 73: 31-36
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- Genetic factors associated with thrombosis in pregnancy in a United States population: the role of factor V Leiden, prothrombin 20210 G to A, angiotensin converting enzyme and methylenetetrahydrofolate reductase in a U.S. population.Am J Obstet Gynecol. 2000; 183: 1271-1277
- Coagulation and fibrinolytic parameters in normal pregnancy and in pregnancy complicated by intrauterine growth retardation.Am J Perinatol. 1998; 15: 81-85
- The incidence of the factor V Leiden mutation in an obstetric population and its relationship to deep vein thrombosis.Am J Obstet Gynecol. 1997; 176: 883-886
- Factor V Leiden mutation as a risk factor for recurrent pregnancy loss.Ann Intern Med. 1998; 128: 1000-1003
- Increased risk for fetal loss in carriers of the factor V Leiden mutation.Ann Intern Med. 1999; 130: 736-739
- Fibrinolysis during normal pregnancy and severe preeclampsia relationships between plasma levels of plasminogen activators and inhibitors.Gynecol Obstet Invest. 1996; 42: 95-101
- A racial difference in the prevalence of the Arg506→Gln mutation.Thromb Res. 1996; 81: 577-581
- The prevalence of the prothrombin 20210 G to A variant in African-Americans: infants, venous thrombosis patients, myocardial infarction patients and controls.J Lab Clin. 1998; 132: 452-455
Article info
Publication history
Accepted:
January 8,
2001
Received in revised form:
January 8,
2001
Received:
March 1,
2000
Identification
Copyright
© 2001 Elsevier Science Ltd. Published by Elsevier Inc. All rights reserved.
