KIDS HAVE STROKES
Clotting Disorders Associated with Infant Stroke
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Among several factors involved in the origin of pediatric stroke, the role of an inherited promthrombotic state is currently under investigation. Some researchers suggest that a detailed search for mutations in inherited thrombophilia is necessary in all cases of pediatric stroke.
Antiphospholipid syndrome (APS):currently recognized as a common risk factor for arterial or venous thromboembolic disease. These antibodies have also been associated with a range of clinical conditions including fetal loss, endocarditis, stroke, heart attack, and hemolytic anemia.
Arterial embolism: a blood clot in an artery. Results in a sudden interruption of blood flow to an organ or body part.
Artery: blood vessel carrying oxygen rich blood to the tissues. A thrombosis in an artery can cause stroke, heart attack, or peripheral vascular disease.
Blood clots: clumps that result when blood coagulates.
Disseminated intravascular coagulopathy: This occurs when the body's blood clotting mechanisms are activated throughout the body instead of being localized to an area of injury. Small blood clots form throughout the body, and eventually the blood clotting factors are used up and not available to form clots at sites of real tissue injury. Clot dissolving mechanisms are also increased.
Embolism: a blood clot (or a piece of plaque that acts in the same manner as a clot) that travels from the site where it was formed to another location in the body. The embolism can lodge in an artery at the new location and block the flow of blood there.
Factor V Leiden is an inherited disorder that can lead to abnormal blood clotting (coagulation) or thrombophilia. The Factor V Leiden is the most common hereditary blood coagulation disorder in the United States. The name Factor V Leiden means that there's a mutation in the DNA in the gene used to make the Factor V protein.
Hyperhomocysteinaemia: elevated homocysteine plasma levels have been found in children with stroke
Infarction: lack of blood and oxygen
Reductase Mutation (MTHFR): One of the most common genetic defects of
homocysteine metabolism is a mutation in the enzyme MTHFR. Increased
plasma homocysteine is a risk factor for arteriosclerotic vascular disease
and deep-vein thrombosis.
Plasminogen deficiency: an uncommon cause of inherited thrombosis.
Protein C and Protein S: involved in regulation of coagulation (blood clotting); they inactivate factors V and VIII.
Protein C deficiency: can result in excessive clotting. These clots tend to form in veins, not arteries. This disorder can be either inherited or acquired
Protein S deficiency: can result in excessive clotting tendencies. These are usually vein clots, such as deep vein thrombosis, but occasionally this disorder can be associated with arterial clots
ProthrombinGene mutation 020210: an inherited mutation that can result in blood clots. A mutation in the prothrombin gene makes the body produce too much of the prothrombin protein, resulting in an increased tendency for the blood to clot.
Thrombophilia means an increased tendency for the blood to clot. There are several reasons why the blood by have this increased tendency to clot and these include problems with proteins in the blood. Proteins are needed to help the blood clot. If a protein has an odd shape or there isn't enough or there's too much of a it, then there may be problems with clotting. Sometimes inherited conditions from one or both parents may cause problems with these clotting proteins. Sometimes a genetic mutation can cause thrombophilia. A person who has inherited thrombophilia is at increased risk of developing a blood clot and this blood clot can cause a stroke.
Thrombosis: The formation, presence or development of a blood clot.
Inherited causes of thrombophilia include: deficiencies of antithrombin, protein C and protein S; elevated Factor VIII; Factor V Leiden (activated protein C resistance); Factor II 20210A; and dysfibrinogenemia. Most of these are autosomal dominantly inherited. Hyperhomocysteinemia may be inherited or acquired and non-inherited factors influence Factor VIII levels.
Tests for Hypercoagulable State: CBC, PT, PTT, Proteins C and S, Antithrombin, Factor V Leiden (and/or APC resistance), Factor VIII C, Factor II 20210 A, Fasting homocysteine, Lupus Anticoagulant, and anticardiolipin antibody.
Vein: blood vessel carrying blood away from the tissues (without oxygen)
The risks and safety of clopidogrel in pediatric arterial ischemic stroke. March 2006. Canada.
Study of Abnormal Blood Clotting in Children with Stroke sponsored by National Institute of Neurological Disorders and Stroke (NINDS)
Clotting Disorders - Children's Healthcare of Atlanta
Thrombophilia Support includes information on Factor V Leiden, Prothrombin 20210 mutation, Activated Protein C resistance, Protein C & S Deficiency, and other clotting disorders
Thrombophilia information from Children's Healthcare of Atlanta
Effect of factor VIIIc levels in pediatric stroke patients. April 2004. Turkey.
Hyperhomocysteinemia and other inherited prothrombotic conditions in young adults with a history of ischemic strokePlasminogen activator inhibitor-1 4G/5G polymorphism in Turkish children with cerebral infarct and effect on factor V 1691 A mutation 2001 hyperhomocysteinaemia reductase are risk factors of spontaneous ischemic stroke in childhood 1999
Factor V Leiden and prothrombin gene G20210A mutation in children with cerebral thromboembolism. June 2003. Argentina.Factor V Leiden and Antiphospholipid Antibodies Are Significant Risk Factors for Ischemic Stroke in Children 2000
Hyperhomocysteinemia and other inherited prothrombotic conditions in young adults with a history of ischemic strokeischemia with elevated maternal and infant anticardiolipin antibodies 2000 Neonatal middle cerebral artery infarction: association with elevated maternal anticardiolipin antibodies 1998
Anti-beta2-glycoprotein I antibodies in pediatric systemic lupus erythematosus and antiphospholipid syndrome, August 2002
The significance of antiphospholipid antibodies in ischemic stroke in children in light of the most current studies 2001. Conclusions: These preliminary results invite further investigations on the role of anticardiolipid antibodies in the pathogenesis of cerebral vascular diseases in children.High prevalence of antiphospholipid antibodies in children with idiopathic cerebral ischemia. 1994. Italy. Study Conclusions: Results show a very high prevalence of antiphospholipid antibodies in children with idiopathic cerebral ischemia. Because the presence of these antibodies has relevant therapeutic implications, their determination in children with cerebral ischemia is recommended.
risk factors of thrombophilia in ischaemic childhood stroke of cardiac
origin. A prospective ESPED survey
I Antibodies and Ischemic Stroke in a 20-Month-Old Boy. July 2003;
Anti-beta2-Glycoprotein I Antibodies and Ischemic Stroke in a 20-Month-Old Boy. July 2003; Greece.
mutations at the homocysteine metabolism pathway and pediatric stroke
stroke and beta-2-glycoprotein 1 antibodies.
Oct. 2003. Finland. Ebeling, Petaja, Alanko.
Infant stroke and beta-2-glycoprotein 1 antibodies. Oct. 2003. Finland. Ebeling, Petaja, Alanko.Arteriovenous malformations of the brain in children: A forty year experience. Lipoprotein (a): Its role in childhood thromboembolism 1997
Links to information on Genetic Causes of Strokes - adults
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