Antithrombotic Therapy in Children: Oral Anticoagulant Therapy in Pediatric Patients

Oral Anticoagulant Therapy in Pediatric Patients
Age-Dependent Features: Oral anticoagulants function by reducing plasma concentrations of the vitamin-Independent proteins. At birth, levels of the vitamin-Independent coagulant factors (FII, FVII, FIX, FX) and inhibitors (protein C, protein S) are approximately 50% of adult values. These levels are similar to those found in adults receiving oral anticoagulants for the treatment of venous thrombotic disease.10 A small number of newborns have evidence of a functional vitamin K deficiency state, indicated by significant levels of descarboxy vitamin-K-dependent proteins at birth. Vitamin K deficiency significantly increases the sensitivity to oral anticoagulants and, potentially, the risk of bleeding. Following the neonatal period, levels of the vitamin-K-dependent proteins rapidly increase and are within the adult range of normal by 6 months.35 However, average values of the vitamin-K-dependent proteins remain approximately 20% lower than adult values until the late teenage years.
Decreased concentrations of the vitamin-K-dependent coagulation proteins, particularly prothrombin, contribute to the delay of and decrease in amounts of thrombin generated in plasmas from newborns and children. www.canadian-familypharmacy.com review The pattern of thrombin generation in newborns is similar to plasma from adults receiving therapeutic amounts of oral anticoagulants. Because of the potential risk of bleeding from further anticoagulation and the presence of borderline vitamin K status, oral anticoagulant therapy is avoided when possible during the first month of life. In older children receiving oral anticoagulants, the capacity of plasmas to generate thrombin is delayed and is decreased by 25% compared to plasmas from adults with similar international normalized ratios (INRs). The latter raises the issue of whether the optimal INR therapeutic range for children will be lower than for adults. This hypothesis is further supported by the observation that plasma concentrations of a marker of endogenous thrombin generation, prothrombin fragment 1.2, is significantly lower in children compared to adults at similar INR values.