Thromb Haemost 2004; 92(05): 1025-1031
DOI: 10.1160/TH04-06-0387
Blood Coagulation, Fibrinolysis and Cellular Haemostasis
Schattauer GmbH

Thrombin activatable fibrinolysis inhibitor and its fibrinolytic effect in normal pregnancy

Hatem A. Mousa
1   Departments of Obstetrics and Gynaecology, Thrombosis Centre, Royal Liverpool University Hospital, Liverpool, UK
,
Colin Downey
2   Departments of Roald Dahl Haemostasis and Thrombosis Centre, Royal Liverpool University Hospital, Liverpool, UK
,
Zarko Alfirevic
1   Departments of Obstetrics and Gynaecology, Thrombosis Centre, Royal Liverpool University Hospital, Liverpool, UK
,
Cheng-Hock Toh
2   Departments of Roald Dahl Haemostasis and Thrombosis Centre, Royal Liverpool University Hospital, Liverpool, UK
3   Departments of Haematology, University of Liverpool, Thrombosis Centre, Royal Liverpool University Hospital, Liverpool, UK
› Author Affiliations
Fiancial support: This study was supported by an unrestricted educational grant from NovoNordisk.
Further Information

Publication History

Received 22 June 2004

Accepted after revision 03 September 2004

Publication Date:
04 December 2017 (online)

Summary

We investigated changes in both thrombin activatable fibrinolysis inhibitor (TAFI) antigen levels and its functional effect on in vitro fibrinolysis in normal pregnancy. 152 pregnant women and 31 women in the immediate postpartum period were studied, with pregnancy divided into 6 windows at 4 weekly intervals. As TAFI influences and is in turn influenced by components of the protein C (PC) pathway, its measurements were correlated with levels of soluble thrombomodulin, PC, protein S (PS) and the overall phenotype of activated PC resistance (APCR). Compared with mean TAFI levels at booking gestation (6.6 +1.2 μg/ml), levels peaked at 35-39 weeks gestation (9.6 +2 μg/ml, p = 0.001), followed by a significant drop within 24 hours of delivery (7.2 + 1.1 μg/ml). In functional terms, the mean clot lysis time (CLT) (101 + 13 min at booking) also peaked at 35-39 weeks gestation (141 + 42 min, p = 0.007) and dropped after delivery (99 + 33 min), and was significantly correlated with gestational age (r = 0.410, p = 0.001) and could be abrogated in the presence of an inhibitor to TAFI activation. A significant negative correlation was found between TAFI levels and APCR (r = −0.478, p <0.001), APCRV (r = −0.598; p <0.001), PS (r = −0.490, P <0.001) and PC (r = −0.198, p = 0.02). In summary, there is a significant increase in TAFI levels, which translates into increased CLT during pregnancy. Furthermore, changes in TAFI contribute to the increasing APCR of pregnancy.