Thromb Haemost 2005; 93(04): 706-709
DOI: 10.1160/TH04-08-0532
Blood Coagulation, Fibrinolysis and Cellular Haemostasis
Schattauer GmbH

Protein Z in normal pregnancy

Katharina C. Quack Loetscher
1   Clinic of Obstetrics, Zurich University Hospital, Zurich, Switzerland
,
Ruth Stiller
1   Clinic of Obstetrics, Zurich University Hospital, Zurich, Switzerland
,
Malgorzata Roos
2   Department of Biostatistics, Institute of Social and Preventive Medicine, University of Zurich, Zurich, Switzerland
,
Roland Zimmermann
1   Clinic of Obstetrics, Zurich University Hospital, Zurich, Switzerland
› Author Affiliations
Further Information

Publication History

Received 22 August 2004

Accepted after resubmission 18 January 2005

Publication Date:
14 December 2017 (online)

Summary

Changes in the coagulation and fibrinolytic systems during pregnancy lead to a higher risk of thromboembolism. These changes include the increase of many clotting factors, as well as a significant fall in activity of fibrinolytic proteins, such as protein C. Protein Z is a vitamin-K-dependent plasma glycoprotein and inhibits the activation of factor X by serving as a cofactor to a plasma proteinase inhibitor. Protein Z deficiency has recently been reported in women with unexplained early fetal losses, and antibodies to protein Z can contribute to adverse pregnancy outcomes. The aim of this study was to determine the range of protein Z in normal pregnancies at different gestational weeks in a cross-sectional and a longitudinal setting. In the longitudinal study we found a 20% increase (p=0.006) of protein Z from first trimester to delivery and a 30% decrease (p<0.0001) 6 to 12 weeks after delivery. In the cross-sectional study these findings were reproducible. In summary, our data show a progressive increase in protein Z levels with gestational age in normal pregnancies and a return to normal levels around 6 to 12 weeks postpartum. The normal increase of protein Z during pregnancy may balance the increase of clotting factors to protect pregnant women from thrombosis.

 
  • References

  • 1 Bremme KA. Haemostatic changes in pregnancy. Best Pract Res Clin Haematol 2003; 16: 153-68.
  • 2 Martius G. Lehrbuch der Gynaekologie und Geburtshilfe. Thieme Verlag. 1994
  • 3 Bellart J. et al. Coagulation and fibrinolytic parameters in normal pregnancy and in pregnancy complicated by intrauterine growth retardation. Am J Perinatol 1998; 15: 81-5.
  • 4 Salafia CM. et al. Preterm delivery: correlations of fetal growth and placental pathology. Am J Perinatol 1992; 9: 190-3.
  • 5 Han X. et al. Characterization of the protein Z-dependent protease inhibitor. Blood 2000; 96: 3049-55.
  • 6 Vasse M. et al. Frequency of protein Z deficiency in patients with ischaemic stroke. Lancet 2001; 357: 933-4.
  • 7 Gris JC. et al. High frequency of protein Z deficiency in patients with unexplained early fetal loss. Blood 2002; 99: 2606-8.
  • 8 Gris JC. et al. Anti-protein Z antibodies in women with pathologic pregnancies. Blood 2003; 101: 4850-2.
  • 9 Ravi S. et al. Protein Z in healthy human individuals and in patients with a bleeding tendency. Br J Haematol 1998; 102: 1219-23.
  • 10 Uszynski M. Generation of thrombin in blood plasma of non-pregnant and pregnant women studied through concentration of thrombin-antithrombin III complexes. Eur J Obstet Gynecol Reprod Biol 1997; 75: 127-31.
  • 11 Kobelt K. et al. Protein Z in ischaemic stroke. Br J Haematol 2001; 114: 169-73.
  • 12 Heeb MJ. et al. Low protein Z levels and risk of ischemic stroke: differences by diabetic status and gender. Blood Cells Mol Dis 2002; 29: 139-44.