Factor V Leiden: should we screen oral contraceptive users and pregnant women?

The factor V Leiden mutation is the most common genetic risk factor for deep vein thrombosis: it is present in about 5% of the white population. The risk of deep vein thrombosis among women who use oral contraceptives is greatly increased by the presence of the mutation. The same seems to be true of the risk of postpartum thrombosis. Several authors have called for all women to be screened before prescription of oral contraceptives and during pregnancy. Such a policy might deny effective contraception to a substantial number of women while preventing only a small number of deaths due to pulmonary emboli. Moreover, in pregnancy the ensuing use of oral anticoagulation prophylaxis might carry a penalty of fatal bleeding that is equal to or exceeds the risk of death due to postpartum thrombosis. It might pay, however, to take a personal and family history of deep vein thrombosis when prescribing oral contraceptives or at a first antenatal visit to detect women from families with a tendency to multiple thrombosis.

[1]  Robert A. Small,et al.  Oral contraceptives and venous thromboembolism: a quantitative discussion of the uncertainties , 1995, Journal of internal medicine.

[2]  G. J. Kloosterman,et al.  Epidemiological observations of thrombo‐embolic disease during pregnancy and in the puerperium, in 56,022 women , 1983, International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics.

[3]  P. Ridker,et al.  Factor V Leiden and risks of recurrent idiopathic venous thromboembolism. , 1995, Circulation.

[4]  B. Dahlbäck.  Factor V gene mutation causing inherited resistance to activated protein C as a basis for venous thromboembolism , 1995, Journal of internal medicine.

[5]  B. Dahlbäck,et al.  Resistance to activated protein C as a basis for venous thromboembolism associated with pregnancy and oral contraceptives. , 1995, American journal of obstetrics and gynecology.

[6]  S. Eichinger,et al.  The Risk of Thromboembolism in Asymptomatic Patients with Protein C and Protein S Deficiency: A Prospective Cohort Study , 1994, Thrombosis and Haemostasis.

[7]  J. Vandenbroucke,et al.  Enhancement by factor V Leiden mutation of risk of deep-vein thrombosis associated with oral contraceptives containing a third-generation progestagen , 1995, The Lancet.

[8]  P. Reitsma,et al.  Increased risk of venous thrombosis in oral-contraceptive users who are carriers of factor V Leiden mutation , 1994, The Lancet.

[9]  N. Dzimiri,et al.  World distribution of factor V Leiden , 1996, The Lancet.

[10]  D. Perry,et al.  Thromboembolism and the combined oral contraceptive pill , 1995, The Lancet.

[11]  C. Carter,et al.  The natural history and epidemiology of venous thrombosis. , 1994, Progress in cardiovascular diseases.

[12]  T. Farley,et al.  Effect of different progestagens in low oestrogen oral contraceptives on venous thromboembolic disease , 1995 .

[13]  H. Jick,et al.  Risk of idiopathic cardiovascular death and rionfatal venous thromboembolism in women using oral contraceptives with differing progestagen components , 1995, The Lancet.

[14]  T. Speroff,et al.  A meta-analysis of methods to prevent venous thromboembolism following total hip replacement. , 1994, JAMA.

[15]  M. Murphy.  Haemostasis and Thrombosis in Obstetrics and Gynaecology , 1992 .

[16]  B. Dahlbäck.  Are we ready for factor V Leiden screening? , 1996, The Lancet.

[17]  P. Reitsma,et al.  High risk of thrombosis in patients homozygous for factor V Leiden (activated protein C resistance) , 1995, Blood.

[18]  J. Laissy,et al.  Fatal Cerebral Venous Sinus Thrombosis Associated with the Factor V Leiden Mutation and the Use of Oral Contraceptives , 1995, Thrombosis and Haemostasis.

[19]  J. Vandenbroucke,et al.  Bleeding complications in oral anticoagulant therapy. An analysis of risk factors. , 1993, Archives of internal medicine.

[20]  P. Majerus.  Bad blood by mutation , 1994, Nature.

[21]  P. Ridker,et al.  Mutation in the gene coding for coagulation factor V and the risk of myocardial infarction, stroke, and venous thrombosis in apparently healthy men. , 1995, The New England journal of medicine.

[22]  B. Dahlbäck.  Resistance to activate protein C, the Arg506 to Gln mutation in the factor V gene, and venous thrombosis. Functional tests and DNA-based assays, pros and cons. , 1995, Thrombosis and haemostasis.

[23]  S. Fihn.  Aiming for safe anticoagulation. , 1995, New England Journal of Medicine.

[24]  J G Weg,et al.  Venous thromboembolism during pregnancy. , 1996, The New England journal of medicine.

[25]  J. Houwing-Duistermaat,et al.  The family history and inherited thrombophilia , 1994, British journal of haematology.

[26]  S. Marsoni,et al.  Fluorouracil and folinic acid in colon cancer , 1995, The Lancet.

[27]  Pieter H. Reitsma,et al.  Mutation in blood coagulation factor V associated with resistance to activated protein C , 1994, Nature.

[28]  D. Hosmer,et al.  A population-based perspective of the hospital incidence and case-fatality rates of deep vein thrombosis and pulmonary embolism. The Worcester DVT Study. , 1991, Archives of internal medicine.

[29]  B. Ransil,et al.  Maternal Mortality in Massachusetts—Trends and Prevention , 1987, The New England journal of medicine.

[30]  D. Bergqvist,et al.  Recurrent thromboembolism in pregnancy and puerperium. Is there a need for thromboprophylaxis? , 1989, American journal of obstetrics and gynecology.