Factor V leiden and antiphospholipid antibodies are significant risk factors for ischemic stroke in children

Background and Purpose-The association between ischemic childhood stroke an d thrombophilia has been debated. We studied the prevalence of thrombophili a risk factors in 65 unrelated children with ischemic stroke compared with 145 control subjects. Methods-Patients and control subjects were rested for antithrombin protein C and protein S deficiencies, the presence of antiphospholipid antibodies ( APLA), factor V Leiden (FVL), G20210A polymorphism of factor II gene (FII G 20210A) and C677T polymorphism of 5,10-methylenetetrahydrofolate reductase gene (C677T MTHFR). Results-Of 65 children, 7 had a stroke in the neonatal/perinatal period and therefore were analyzed separately. Thirty-one of the remaining 58 patient s with pediatric stroke (53.4%) were found to have at least 1 thrombophilia marker compared with only 25.5% of control subjects. None of the patients or control subjects had protein S or antithrombin III deficiency. The preva lence of protein C deficiency was higher among pediatric stroke patients th an among control subjects, but the difference was not statistically signifi cant (OR=7, 95% CT 0.75 to 65.1). Heterozygous FII G20210A and homozygous M THFR 677T were not associated with an increased risk for stroke (OR=1.29, 9 5% CI 0.2 to 8.2; and OR=1.06, 95% CI 0.4 to 2.7, respectively). In contras t, the presence of APLA was associated with a >6-fold risk of stroke (OR=6. 08, 95% CT 1.5 to 24.3), and the heterozygosity for FVL increased the risk of stroke by almost 5-fold (OR=4.82, 95% CT 1.4 to 16,5). Five patients wit h pediatric stroke had a combination of greater than or equal to 2, thrombo philia markers, whereas none of the control subjects had a combination of t he markers. Most of the patients with neonatal/perinatal stroke were found to have at least 1 thrombophilia marker. Conclusions-These data suggest that the prevalence of thrombophilia markers is increased in children with stroke compared with control subjects and, s pecifically, that FVL and APLA contribute significantly to stroke occurrenc e.