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Factor VII deficiency associated with valproate treatment

© 2008 Japan Pediatric Society It has long been known that the anti-epileptic, valproate (VPA), which is used widely in the treatments of generalized and focal seizures, may cause subclinical alterations in both intrinsic and extrinsic coagulation pathways. These changes include thrombocyte dysfunction, thrombocytopenia, von Willebrand disease type 1, defi ciency of vitamin K-dependent coagulation factors II, VII, IX, and X and reduction in serum fi brinogen, protein C and protein S concentrations. In addition macrocytosis, erythrocytopenia, neutropenia, reduction in hemoglobin and hematocrit counts and bone marrow suppression are reported to accompany VPA treatment. The incidence of these disturbances is higher in children than in adults. 1 These side-effects of VPA may either be dose related, or idiosyncratic, but life-threatening hemorrhage in such cases is rare. The aforementioned hematological disturbances are generally identifi ed following chronic VPA treatment and when VPA blood concentrations are >100 /mL; 2 they can be recurring, temporary or permanent. Factor VII is a vitamin K-dependent glycoprotein that initializes the extrinsic coagulation pathway to produce thrombin by binding the tissue factors that are released following vascular damage. Binding of tissue factors activates factor VII; activated factor VII (factor VIIa) causes the activation of factors X and IX, respectively, to start intrinsic coagulation cascade. 3