LAUSR

Sir, Factor (F) VII is essential for the initiation of coagulation, binding to tissue factor (TF) that is exposed to blood following tissue damage to form the activated FVIIa-TF complex that then activates FIX and FX leading to the formation of thrombin [1]. FVII deficiency, which was first identified in 1951, is a rare autosomal recessive bleeding disorder with a variable phenotype resulting in mild-to-severe bleeding [2]. Its prevalence is estimated to be in the range of 1 : 300 000–500 000 individuals. Missense mutations are most frequent and occur in about 70%–80% of patients [2]. Clinically, FVII deficiency usually presents with mild symptoms of epistaxis, easy bruising, gum bleeding, and menorrhagia but severe bleeding can occur in patients with homozygous or double heterozygous mutations [2]. Treatment, if needed, focuses on FVII replacement, using prothrombin complex concentrates (PCCs), fresh frozen plasma (FFP), or recombinant activated FVII (rFVIIa, [NovoSeven; Novo Nordisk, Denmark]) [2]. Factor V Leiden (FVL) is the most common heritable thrombophilic disorder, with a prevalence of 3%–8% in the Caucasian population [3]. In this disorder, activated FV is relatively resistant to degradation by activated protein C, a natural anticoagulant, and this facilitates overproduction of thrombin leading to thrombosis. Factor V Leiden results from a missense mutation, with the adenine substituted for guanine resulting in the replacement of arginine (Arg) by glutamine (Gln) in the FV protein [4]. Heterozygotes have about fourto eightfold increased risk of venous thromboembolism (VTE), whereas this risk is increased to eighty-fold in homozygous mutations [3]. Factor V Leiden should be suspected in patients with a thrombotic event who are below 45 years of age or with a positive family history of VTE [4]. Case