Acta Dermato Venereologica · 2002 · 10 citations · 2 references
MedicineClinical SciencesHematologyHematopathologyHemostasisVascular SurgeryAnticoagulant TherapyCoagulation DisordersDeep Vein ThrombosisThromboembolic DiseaseThrombosisVenous ThromboembolismFactor V Leiden ThrombophiliaFactor V MutationGenetic ThrombophiliaThrombosis MechanismsThrombosis PathophysiologyVenous Leg UlcersVenous Thrombus FormationVenous Ulcers
We present a young male patient referred to our hospital with leg ulcers on both legs that were more than 3 years refractory to standard treatment with compression therapy. By thrombophilia screening factor V Leiden mutation, hyperhomocysteinemia and evidence for impaired fibrinolysis were found. Treatment with folic acid in combination with long-term oral anticoagulant therapy was added to non-elastic compression therapy. The leg ulcers showed slow improvement and complete healing within 3 years. During a 6-year follow-up period neither new thrombo-embolic events occurred nor recurrence of ulcerations. This case suggests a potential synergistic pathogenic role of factor V Leiden, hyperhomocysteinemia and impaired fibrinolysis in the development of postthrombotic syndrome and his sequelae. We postulate that increased formation of thrombi in the microcirculation of the skin in combination with ambulatory venous hypertension due to recurrent deep venous thrombosis might explain our observation.
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Risk Factors for Venous Thrombotic Disease
Frits R. Rosendaal · Thrombosis and Haemostasis · 1999 · 377 citations
Coexistence of Hereditary Homocystinuria and Factor V Leiden — Effect on Thrombosis
Hanna Mandel, Benjamin Brenner, Moshe Berant et al. · New England Journal of Medicine · 1996 · 266 citations · Full text
Medicine, Genetics, Hematology +17