Dear sir, I got stroke two years ago. One was on 29.04.14 (thalamic infarct) and the other was on 7.10.14 (cerebral infarct). Now, can I term those two as two separate strokes. I do not have hypertension, no cholesterol, nothing of any sort. Doctor has quoted me saying Antithrombin III deficiency. Now, I want to know whether there is any cure as I have fear of recurrence. Kindly guide me.

Dr. Sajeev KumarGeneral Physician32yrs exp

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Antithrombin III (ATIII) is a nonvitamin K-dependent protease that inhibits coagulation by lysing thrombin and factor Xa. Antithrombin III activity is markedly potentiated by heparin, the principal mechanism by which both heparin and low molecular weight heparin result in anticoagulation. Congenital antithrombin III deficiency is an autosomal dominant disorder in which an individual inherits one copy of the SERPINC1 (also called AT3) gene on chromosome 1q25. 1, which encodes antithrombin III. This condition leads to increased risk of venous and arterial thrombosis, with an onset of clinical manifestations typically appearing in young adulthood. This form is most commonly diagnosed during childhood by screening after an affected family member has been identified or after a child has had a thrombotic event. Severe congenital antithrombin III deficiency, in which the individual inherits 2 defective genes, is a rare autosomal recessive condition associated with increased thrombogenesis, typically noted in the neonatal period or early infancy. This condition is rarely compatible with life. Most neonates have heterozygous antithrombin III deficiency. Acquired antithrombin III deficiency is a deficiency of antithrombin primarily due to consumption. It is observed in situations in which activation of the coagulation system is abnormal. Common conditions that result in acquired antithrombin III deficiency include disseminated intravascular coagulation (DIC), microangiopathic hemolytic anemias due to endothelial damage (ie, hemolytic-uremic syndrome), and venoocclusive disease (VOD) in patients undergoing bone marrow transplantation. Replacement of antithrombin in neonates with antithrombin III deficiency to treat lung disease has been studied and found to have no benefit. Antithrombin infusion in otherwise asymptomatic neonates found to be deficient is not recommended. Enoxaparin (Lovenox), a low molecular weight heparin (LMWH), is frequently used to prevent thrombi as well as to prevent thrombi that have already occurred from propagating. In antithrombin III deficiency, the activity of LMWH is not as reliable as in an otherwise healthy person. Careful monitoring of the anti-Xa activity in the patient should be performed. Consider alternative anticoagulation medications (eg, warfarin) because the effectiveness of LMWH is likely reduced. Once a patient with congenital antithrombin III deficiency has developed thrombosis, anticoagulation is more strongly indicated. Replacement with recombinant antithrombin is not indicated for the treatment of thrombi. Warfarin (Coumadin) is the principal anticoagulant used. This vitamin K antagonist is administered at a dose to maintain an international normal ratio (INR) on PT of 1.5-2.5. Initially, therapy with LMWH or standard heparin may be administered to decrease the risk of warfarin-associated thrombosis (warfarin-induced skin necrosis) resulting from the inhibition of protein C production, which may occur before inhibition of the synthesis of vitamin K?dependent procoagulant factors (II, VII, IX, X) is reduced adequately for anticoagulation. 

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