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Factor V Leiden and antiphospholipid antibodies are significant risk factors for ischemic stroke in children
1Institute of Thrombosis and Haemostasis, Sheba Medical Center, Tel Hashomer, Israel.
Insights
Pediatric stroke is linked to thrombophilia risk factors. Antiphospholipid antibodies (APLA) and factor V Leiden (FVL) significantly increase stroke risk in children.
Area of Science:
- Pediatric Neurology
- Hematology
- Genetics
Background:
- The relationship between childhood ischemic stroke and thrombophilia remains debated.
- This study investigated thrombophilia risk factors in children with ischemic stroke.
Purpose of the Study:
- To determine the prevalence of thrombophilia risk factors in children with ischemic stroke.
- To compare these prevalence rates with a control group of healthy children.
Main Methods:
- Tested pediatric stroke patients (n=65) and controls (n=145) for deficiencies in antithrombin, protein C, and protein S.
- Assessed for antiphospholipid antibodies (APLA), factor V Leiden (FVL), FII G20210A, and MTHFR C677T polymorphisms.
Main Results:
- 53.4% of pediatric stroke patients had at least one thrombophilia marker, versus 25.5% of controls.
- Antiphospholipid antibodies (APLA) showed a >6-fold increased stroke risk (OR=6.08).
- Factor V Leiden (FVL) heterozygosity increased stroke risk by almost 5-fold (OR=4.82).
Conclusions:
- Thrombophilia markers are more prevalent in children with stroke.
- FVL and APLA are significant contributors to pediatric stroke occurrence.
Background And Purpose:
The association between ischemic childhood stroke and thrombophilia has been debated. We studied the prevalence of thrombophilia risk factors in 65 unrelated children with ischemic stroke compared with 145 control subjects.
Methods:
Patients and control subjects were tested 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 G20210A), 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 patients 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 prevalence of protein C deficiency was higher among pediatric stroke patients than among control subjects, but the difference was not statistically significant (OR=7, 95% CI 0.75 to 65.1). Heterozygous FII G20210A and homozygous MTHFR 677T were not associated with an increased risk for stroke (OR=1.29, 95% CI 0.2 to 8.2; and OR=1.06, 95% CI 0.4 to 2.7, respectively). In contrast, the presence of APLA was associated with a >6-fold risk of stroke (OR=6. 08, 95% CI 1.5 to 24.3), and the heterozygosity for FVL increased the risk of stroke by almost 5-fold (OR=4.82, 95% CI 1.4 to 16.5). Five patients with pediatric stroke had a combination of > or =2 thrombophilia markers, whereas none of the control subjects had a combination of the 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, specifically, that FVL and APLA contribute significantly to stroke occurrence.