Thromb Haemost 1999; 81(01): 71-75
DOI: 10.1055/s-0037-1614421
Review Article
Schattauer GmbH

A Longitudinal Study of the Relationships between Haemostatic, Lipid, and Oestradiol Changes during Normal Human Pregnancy

Naveed Sattar
1   From the University Departments of Pathological Biochemistry,Glasgow, UK
,
Ian A. Greer
2   Obstetrics and Gynaecology, and, Royal Infirmary, Glasgow, UK
,
Ann Rumley
3   Medicine, Royal Infirmary, Glasgow, UK
,
Grace Stewart
1   From the University Departments of Pathological Biochemistry,Glasgow, UK
,
James Shepherd
1   From the University Departments of Pathological Biochemistry,Glasgow, UK
,
Chris J. Packard
1   From the University Departments of Pathological Biochemistry,Glasgow, UK
,
Gordon D. O. Lowe
3   Medicine, Royal Infirmary, Glasgow, UK
› Author Affiliations
Further Information

Correspondence to:

Dr. Naveed Sattar
Department of Pathological Biochemistry
Macewen Building
Royal Infirmary NHS Trust
Glasgow G4 0SF, UK
Phone: +44-141-211-4490   
Fax-Number: +44-141-553-1703

Publication History

Received25 February 1998

Accepted after resubmission09 September 1998

Publication Date:
08 December 2017 (online)

 

Summary

Increased activation of both blood coagulation and fibrinolysis occurs during normal pregnancy. The responsible mechanisms are unclear, but may include increases in both oestradiol and blood lipids. We, therefore, studied the associations between fasting serum oestradiol, plasma cholesterol and triglyceride, and Factor VII activity, PAI activity, t-PA antigen, fibrin D-dimer, and vWF antigen in 10 women, each sampled on 6 occasions between 10 weeks and 35 weeks during normal pregnancy. Strong and similar individual correlations were observed between increases in FVII, PAI, t-PA and D-dimer (but not vWF) and increases in both oestradiol and triglyceride. Associations between increments in plasma cholesterol and haemostatic factors (except for FVII), were somewhat weaker. We, therefore, suggest that oestradiol-induced hypertriglyceridaemia may be a cause of elevations in plasma Factor VII activity, PAI and t-PA, and fibrin turnover (D-dimer) during normal pregnancy, but is poorly related to the increase in vWF antigen.


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  • References

  • 1 Greer IA. Haemostasis and thrombosis in pregnancy. In: Bloom AL, Forbes CD, Thomas DP, Tuddenham EGD. (eds) Haemostasis and Thrombosis. 3rd edn. Edinburgh: Churchill Livingstone; 1994: 987-1016.
  • 2 Hellgren M, Blombäck M. Studies on blood coagulation and fibrinolysis in pregnancy, during delivery and in the puerperium. 1. Normal condition. Gyn Obstet Invest 1981; 12: 141-54.
  • 3 Beller FK, Ebert C. The coagulation and fibrinolytic enzyme systems in normal pregnancy and the puerperium. Europ J Obstet Gynecol Repro Biol 1982; 13: 177-97.
  • 4 Stirling Y, Woolf L, North WRS, Seghatchian MJ, Meade TW. Haemo-stasis in normal pregnancy. Thromb Haemost 1984; 52: 176-82.
  • 5 Ballageer V, Mombaerts P, Declerk PJ. et al. Fibrinolytic response to venous occlusion and fibrin fragment D-dimer levels in normal and complicated pregnancy. Thromb Haemost 1987; 58: 1030-2.
  • 6 Kruithof EKO, Chien TT, Gudinchet A. et al. Fibrinolysis in pregnancy: a study of plasminogen activation inhibitors. Blood 1987; 69: 460-6.
  • 7 Kluft C, Lansink M. Effects of oral contraceptives on haemostasis variables. Thromb Haemost 1997; 78: 315-26.
  • 8 Meade TW. Hormone replacement therapy and haemostatic function. Thromb Haemost 1997; 78: 765-9.
  • 9 Mitropoulos KA. Lipid-thrombosis interface. Br Med Bull 1994; 50: 813-32.
  • 10 Sattar N, Greer IA, Louden J. et al. Lipoprotein subfraction changes in normal pregnancy: threshold effect of plasma triglyceride on appearance of small, dense low density lipoprotein. J Clin Endocrinol Metab 1997; 82: 2483-91.
  • 11 Montelongo A, Lasuncion MA, Pallardo LF, Herrara E. Longitudinal study of plasma lipoproteins and hormones during pregnancy in normal and diabetic women. Diabetes 1992; 42: 1651-9.
  • 12 Silliman K, Shore V, Forte TM. Hypertriglyceridaemia during late pregnancy is associated with the formation of small dense low-density lipo-proteins and the presence of large buoyant high-density lipoproteins. Metabolism 1994; 43: 1035-41.
  • 13 Juhan-Vague I, Alessi MC. Plasminogen activation inhibitor 1 and athero-thrombosis. Thromb Haemost 1993; 70: 138-43.
  • 14 Lowe GDO. Coagulation, fibrinolysis and hormone replacement therapy. In: Shaw RW. (ed) Oestrogen deficiency. Causes and consequences.. Carnforth, UK: Parthenon; 1996: 29-44.
  • 15 Thorsen S, Philips M, Selmer J, Lecander I, Astedt B. Kinetics of inhibition of tissue-type and urokinase-type plasminogen activator by plasminogen-activator inhibitor type 1 and type 2. Eur J Biochem 1988; 175: 33-9.
  • 16 Miller GJ. Lipids and Coagulation. In: Poller L, Ludlam CA. (eds). Recent advances in blood coagulation, 7.. Edinburgh: Churchill Livingstone; 1997: 125-40.
  • 17 Lowe GDO. Haemostatic risk factors for arterial and venous thrombosis. In: Poller L, Ludlam CA. (eds). Recent advances in Blood Coagulation, 7.. Edinburgh: Churchill Livingstone; 1997: 69-96.
  • 18 Lowe GDO, Rumley A, Woodward M, Morrison CE, Phillippon H, Lane DA, Tunstall-Pedoe H. Epidemiology of coagulation factors, inhibitors and activation markers: the third Glasgow MONICA survey I. Illustrative reference ranges by age, sex and hormone use. Br J Haematol 1997; 97: 775-84.
  • 19 Green F, Humphries S. Genetic determinants of arterial thrombosis. Ballieres Clin Haematol 1994; 7: 675-92.

Correspondence to:

Dr. Naveed Sattar
Department of Pathological Biochemistry
Macewen Building
Royal Infirmary NHS Trust
Glasgow G4 0SF, UK
Phone: +44-141-211-4490   
Fax-Number: +44-141-553-1703

  • References

  • 1 Greer IA. Haemostasis and thrombosis in pregnancy. In: Bloom AL, Forbes CD, Thomas DP, Tuddenham EGD. (eds) Haemostasis and Thrombosis. 3rd edn. Edinburgh: Churchill Livingstone; 1994: 987-1016.
  • 2 Hellgren M, Blombäck M. Studies on blood coagulation and fibrinolysis in pregnancy, during delivery and in the puerperium. 1. Normal condition. Gyn Obstet Invest 1981; 12: 141-54.
  • 3 Beller FK, Ebert C. The coagulation and fibrinolytic enzyme systems in normal pregnancy and the puerperium. Europ J Obstet Gynecol Repro Biol 1982; 13: 177-97.
  • 4 Stirling Y, Woolf L, North WRS, Seghatchian MJ, Meade TW. Haemo-stasis in normal pregnancy. Thromb Haemost 1984; 52: 176-82.
  • 5 Ballageer V, Mombaerts P, Declerk PJ. et al. Fibrinolytic response to venous occlusion and fibrin fragment D-dimer levels in normal and complicated pregnancy. Thromb Haemost 1987; 58: 1030-2.
  • 6 Kruithof EKO, Chien TT, Gudinchet A. et al. Fibrinolysis in pregnancy: a study of plasminogen activation inhibitors. Blood 1987; 69: 460-6.
  • 7 Kluft C, Lansink M. Effects of oral contraceptives on haemostasis variables. Thromb Haemost 1997; 78: 315-26.
  • 8 Meade TW. Hormone replacement therapy and haemostatic function. Thromb Haemost 1997; 78: 765-9.
  • 9 Mitropoulos KA. Lipid-thrombosis interface. Br Med Bull 1994; 50: 813-32.
  • 10 Sattar N, Greer IA, Louden J. et al. Lipoprotein subfraction changes in normal pregnancy: threshold effect of plasma triglyceride on appearance of small, dense low density lipoprotein. J Clin Endocrinol Metab 1997; 82: 2483-91.
  • 11 Montelongo A, Lasuncion MA, Pallardo LF, Herrara E. Longitudinal study of plasma lipoproteins and hormones during pregnancy in normal and diabetic women. Diabetes 1992; 42: 1651-9.
  • 12 Silliman K, Shore V, Forte TM. Hypertriglyceridaemia during late pregnancy is associated with the formation of small dense low-density lipo-proteins and the presence of large buoyant high-density lipoproteins. Metabolism 1994; 43: 1035-41.
  • 13 Juhan-Vague I, Alessi MC. Plasminogen activation inhibitor 1 and athero-thrombosis. Thromb Haemost 1993; 70: 138-43.
  • 14 Lowe GDO. Coagulation, fibrinolysis and hormone replacement therapy. In: Shaw RW. (ed) Oestrogen deficiency. Causes and consequences.. Carnforth, UK: Parthenon; 1996: 29-44.
  • 15 Thorsen S, Philips M, Selmer J, Lecander I, Astedt B. Kinetics of inhibition of tissue-type and urokinase-type plasminogen activator by plasminogen-activator inhibitor type 1 and type 2. Eur J Biochem 1988; 175: 33-9.
  • 16 Miller GJ. Lipids and Coagulation. In: Poller L, Ludlam CA. (eds). Recent advances in blood coagulation, 7.. Edinburgh: Churchill Livingstone; 1997: 125-40.
  • 17 Lowe GDO. Haemostatic risk factors for arterial and venous thrombosis. In: Poller L, Ludlam CA. (eds). Recent advances in Blood Coagulation, 7.. Edinburgh: Churchill Livingstone; 1997: 69-96.
  • 18 Lowe GDO, Rumley A, Woodward M, Morrison CE, Phillippon H, Lane DA, Tunstall-Pedoe H. Epidemiology of coagulation factors, inhibitors and activation markers: the third Glasgow MONICA survey I. Illustrative reference ranges by age, sex and hormone use. Br J Haematol 1997; 97: 775-84.
  • 19 Green F, Humphries S. Genetic determinants of arterial thrombosis. Ballieres Clin Haematol 1994; 7: 675-92.