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Inherited prothrombotic states and ischaemic stroke in childhood
V Ganesan1, M A McShane, R Liesner
1Neurosciences Unit, Institute of Child Health, University College London, UK. v.ganesan@umds.ac.uk
Insights
Inherited prothrombotic states were rarely found in children with arterial stroke. Further research is needed to confirm this finding in larger pediatric populations.
Area of Science:
- Pediatric Neurology
- Hematology
- Genetics
Background:
- Arterial stroke in children is a serious condition.
- Inherited prothrombotic states are known risk factors for thrombosis.
Purpose of the Study:
- To determine the prevalence of inherited prothrombotic states in children diagnosed with arterial stroke.
- To compare the prevalence of these states in stroke patients versus a control group.
Main Methods:
- Retrospective analysis of pediatric patients with arterial stroke (1990-1996).
- Investigation for specific inherited prothrombotic states including protein S deficiency, factor V Leiden mutation, and activated protein C resistance.
- Comparison with a control group of children without thrombosis.
Main Results:
- Eight out of 67 children (12%) with arterial stroke had an identified inherited prothrombotic state.
- Factor V Leiden mutation was the most common (6 patients).
- Prevalence of factor V Leiden mutation was not significantly higher in stroke patients (12%) compared to controls (5.2%).
Conclusions:
- Currently recognized inherited prothrombotic states appear rarely associated with childhood arterial stroke.
- Larger studies are required to confirm these findings.
- Interpreting prothrombotic screening requires age-appropriate reference ranges, and acute abnormalities may be transient.
Objective:
To investigate the prevalence of currently recognised inherited prothrombotic states in a population of children with arterial stroke.
Methods:
Children with arterial stroke presenting to a tertiary level paediatric neurology centre between 1990 and 1996 were investigated for inherited prothrombotic states.
Results:
Sixty seven children with arterial stroke were investigated. Abnormalities were initially identified in 16 patients; however, only eight children (12%) had an inherited prothrombotic state. This was type 1 protein S deficiency in one patient, the factor V Leiden mutation in six, and activated protein C resistance (without the factor V Leiden mutation) in one. The prevalence of the factor V Leiden mutation was not significantly higher in children with arterial stroke (12%) than in a control population of children without thrombosis attending the same institution (5.2%; Fisher's exact test, p=0.19; difference in prevalence between patients and controls (95% confidence interval)=6.8% (-2.78% to 16.8%)).
Conclusions:
Currently recognised inherited prothrombotic tendencies were rarely associated with stroke in this group of children, although larger numbers of patients would be needed to confirm this. Age appropriate normal values should be used when interpreting the results of a prothrombotic screen. Prothrombotic abnormalities seen acutely are as often transient as inherited. Longitudinal assessment and family studies are required before low concentrations of an anticoagulant protein found acutely can be attributed to an inherited abnormality.