The prevalence of thrombophilia in patients with chronic venous leg ulceration.

BACKGROUND Thrombophilia is increasingly recognized as a risk factor for deep venous thrombosis (DVT), which in turn is a major risk factor for chronic venous ulceration (CVU). However, the relationship between thrombophilia and CVU remains unknown. The aim of this study was to define the prevalence of thrombophilia in patients with CVU and to determine whether this is associated with a history or duplex scan evidence of DVT. METHODS Eighty-eight patients with CVU were prospectively studied. The patients underwent clinical assessment and duplex ultrasound scanning. Blood was drawn for antithrombin, proteins C and S, activated protein C resistance, factor V Leiden, prothrombin 20210A, lupus anticoagulant, and anticardiolipin antibodies. RESULTS The study included 35 men with a median age of 61 years (interquartile range, 45 to 72 years) and 53 women with a median age of 76 years (interquartile range, 69 to 82 years). Thirty-six percent of the patients had either a history or duplex scan evidence suggestive of previous DVT. The following abnormalities were detected: four, five, and six cases of antithrombin, protein C, and protein S deficiencies, respectively; 14 cases of activated protein C resistance; 11 cases of factor V Leiden mutation; three cases of prothrombin 20210A mutation; eight cases of lupus anticoagulant; and 12 cases of anticardiolipin antibodies. Thrombophilia was not significantly related to previous DVT, deep reflux, or disease severity. CONCLUSION Patients with CVU have a 41% prevalence rate of thrombophilia. This rate is two to 30 times higher than the rate of the general population but is similar to that reported for patients with previous DVT. However, in patients with CVU, thrombophilia does not appear to be related to a history of DVT, a pattern of reflux, or severity of disease. Many patients with CVU may have unsuspected postthrombotic disease.

[1]  P. Allan,et al.  The relationship between lower limb symptoms and superficial and deep venous reflux on duplex ultrasonography: The Edinburgh Vein Study. , 2000, Journal of vascular surgery.

[2]  A. Tosetto,et al.  The VITA Project: Prothrombin G20210A Mutation and Venous Thromboembolism in the General Population , 1999, Thrombosis and Haemostasis.

[3]  P. Gloviczki Subfascial endoscopic perforator vein surgery: indications and results , 1999, Vascular medicine.

[4]  Paul,et al.  A prospective coagulation study including resistance to activated protein C and mutations in factors V and II in venous leg ulcers , 1999, The British journal of dermatology.

[5]  M. Woodward,et al.  Activated Protein C Resistance and the FV:R506Q Mutation in a Random Population Sample , 1999, Thrombosis and Haemostasis.

[6]  G. Forzy,et al.  Ulcères de jambes et anticorps anti-phospholipides. Etude prospective de 48 observations. , 1999 .

[7]  P. Belardi,et al.  Regarding "Saphenous surgery does not correct perforator incompetence in the presence of deep venous reflux". , 1998, Journal of vascular surgery.

[8]  R. Hull,et al.  1 Thrombophilia: disorders predisposing to venous thromboembolism , 1998 .

[9]  J. Vandenbroucke,et al.  The Leiden Thrombophilia Study (LETS) , 1997, Thrombosis and Haemostasis.

[10]  A. Tosetto,et al.  The epidemiology of inherited thrombophilia: the VITA Project. Vicenza Thrombophilia and Atherosclerosis Project. , 1997, Thrombosis and haemostasis.

[11]  P. Mannucci,et al.  Inherited Thrombophilia*: Part 2 , 1996, Thrombosis and Haemostasis.

[12]  P. Mannucci,et al.  Inherited Thrombophilia: Part 1 , 1996, Thrombosis and Haemostasis.

[13]  F. Fowkes Epidemiology of Chronic Venous Insufficiency , 1996 .

[14]  S. Munkvad,et al.  Resistance to activated protein C: a common anticoagulant deficiency in patients with venous leg ulceration , 1996, The British journal of dermatology.

[15]  P. Brill-Edwards,et al.  Antiphospholipid antibodies and venous thromboembolism. , 1995, Blood.

[16]  C. Ruckley,et al.  Venous Insufficiency following Deep Vein Thrombosis , 1994 .

[17]  R. Bertina,et al.  Venous thrombosis due to poor anticoagulant response to activated protein C: Leiden Thrombophilia Study , 1993, The Lancet.

[18]  B. Dahlbäck,et al.  Familial thrombophilia due to a previously unrecognized mechanism characterized by poor anticoagulant response to activated protein C: prediction of a cofactor to activated protein C. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[19]  J J Dale,et al.  Chronic ulceration of the leg: extent of the problem and provision of care. , 1985, British medical journal.

[20]  K. Burnand,et al.  THE CAUSE OF VENOUS ULCERATION , 1982, The Lancet.

[21]  T. O'donnell,et al.  RELATION BETWEEN POSTPHLEBITIC CHANGES IN THE DEEP VEINS AND RESULTS OF SURGICAL TREATMENT OF VENOUS ULCERS , 1976, The Lancet.

[22]  E. Thomas,et al.  ANTIBIOTIC SUSCEPTIBILITY OF SHIGELLA IN AUSTRALIA , 1974 .

[23]  K. Hamulýak,et al.  The prevalence of factor V Leiden mutation in patients with leg ulcers and venous insufficiency. , 1999, Archives of dermatology.

[24]  P. Allan,et al.  Popliteal vein reflux reduces the healing of chronic venous ulcer , 1998, The British journal of surgery.

[25]  J. Hafner,et al.  Resistance to activated protein C in patients with venous leg ulcers. , 1997, Dermatology.

[26]  P. Reitsma,et al.  Prevalence of Protein C Deficiency in the Healthy Population , 1995, Thrombosis and Haemostasis.

[27]  W. Laing,et al.  Chronic Venous Diseases of the Leg , 1992 .