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21/144. Mesenteric venous thrombosis in a patient with prothrombin 20210A mutation and antithrombin iii deficiency: challenges to conventional anticoagulation--a case report.

    Mesenteric venous thrombosis presents as vague abdominal pain in patients with a medical or family history suggestive of a hypercoagulable state. Classic computed tomography findings will often confirm the diagnosis, and the presence of persistent abdominal pain or tenderness will determine the need for surgical intervention. Expeditious anticoagulation is the treatment of choice. This case demonstrates the CT findings for mesenteric venous thrombosis and discusses the challenges of anticoagulation in a patient with 2 hypercoagulable disorders.
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22/144. A case of cortical vein thrombosis with the cord sign.

    BACKGROUND: Computed tomography is performed in suspicious cases of cerebral venous thrombosis. Although an empty delta sign is not uncommonly reported, a cord sign is rarely reported. But this is, if present, pathognomonic, especially in the case of cortical vein thrombosis. CASE DESCRIPTION: A young man with antithrombin iii deficiency sought emergency treatment for headache and seizure. Noncontrast computed tomography showed a typical cord sign in multiple sections. It seemed to be independent from the adjacent pathologic findings in most sections. brain magnetic resonance imaging verified it as a thrombosed vein in conjunction with acute venous infarction. CONCLUSION: The cord sign should be considered for early and accurate diagnosis of cortical vein thrombosis.
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23/144. antithrombin iii deficiency and cerebrovascular accidents in young adults.

    A young man with antithrombin III (AT-III) deficiency sustained a cerebellar venous infarct and recovered following treatment with AT-III concentrate. A family study showed that other members were affected. AT-III deficiency in this family was found to be due to a new variant AT-III TRURO 1. Young patients with strokes should be screened for thrombophilia.
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24/144. cerebral infarction in a heterozygote with variant antithrombin III.

    BACKGROUND: We report a heterozygous case of familial qualitative deficiency of antithrombin III associated with cerebral infarction. CASE DESCRIPTION: A 33-year-old man had a history of recurrent transient ischemic attacks from the age of 28. Cerebral computed tomography at age 29 disclosed a low-density area in the left frontal lobe, and an internal carotid angiogram showed branch occlusion of the right anterior cerebral artery and stenosis of the left middle cerebral artery. Occlusion of the right middle cerebral artery developed thereafter. The plasma antithrombin III antigen concentration and progressive antithrombin activity were normal, but plasma heparin cofactor activity was low in the patient and his father. Nucleotide sequence analysis of the proband's deoxyribonucleic acid showed no mutation in exons II and VI of antithrombin III. CONCLUSIONS: We conclude that abnormal antithrombin III with defective heparin binding, even though heterozygous, may cause ischemic stroke in young adults. We named this antithrombin III variant "Antithrombin III Nagasaki."
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25/144. budd-chiari syndrome due to antithrombin iii deficiency.

    budd-chiari syndrome is a disease complex with varied etiology and is one of the causes of post-hepatic portal hypertension. We report a 2 year-old boy who presented with budd-chiari syndrome due to congenital antithrombin iii deficiency, who was managed with an expandable metal stent placed in the inferior vena cava and oral anticoagulation.
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26/144. Prophylactic antithrombin III administration during pregnancy immediately reduces the thrombin hyperactivity of congenital antithrombin iii deficiency by forming thrombin-antithrombin III complexes.

    We examined the changes of haemostatic molecular markers after antithrombin III (AT III) administration in a 22-year-old woman with congenital AT III deficiency in the third trimester of pregnancy who did not have thrombosis. Various markers including fibrinopeptide a (FPA), thrombin-antithrombin III complex (TAT), prothrombin fragment F1 2 (F1 2), plasmin-alpha 2antiplasmin, D-dimer, beta-thromboglobulin, and platelet factor 4 were measured before and just after 3,000 U of AT III concentrate, which was given three times per week from the 34 week of pregnancy until delivery. Just after AT III administration, F1 2 and FPA levels decreased on most occasions, while TAT sometimes increased. plasma FPA levels were markedly decreased on all 8 occasions when the plasma FPA levels was above 2.0 ng/ml before AT III administration. plasma FPA levels were always greater than or equal to 6.4 ng/ml before AT III administration on the 4 occasions when TAT increased to above 115%. The changes of plasma F1 2 levels were significantly correlated with the AT III level. These results suggest that prophylactic AT III administration in the third trimester immediately inactivates intravascular thrombin to form TAT and reduce the plasma FPA level. Thus, the transient TAT elevation following AT III administration may not only be due to extraction of thrombin from the fibrin clots of thrombi but also to intravascular thrombin which is not attached to thrombi. FPA is the best molecular marker for thrombin hyperactivity and it should be monitored in AT III-deficient pregnant women in the third trimester.
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27/144. Occurrence of arterial thrombosis in a cohort of patients with hereditary deficiency of clotting inhibitors.

    Hereditary deficiency of protein c, protein s or antithrombin III has been associated with an increased incidence of venous thrombosis or pulmonary embolism. The relationship between these deficiencies and the development of arterial thrombosis is a matter of current investigation. We retrospectively studied the occurrence of arterial thrombosis in 92 symptomatic patients belonging to a group of 160 with a confirmed diagnosis of hereditary deficiency of one of the physiologic clotting inhibitors. Seventeen of them experienced at least one arterial thrombotic event. This indicates that about one out of five of the symptomatic patients had experienced arterial thrombosis. The control group consisted of 92 sex and age matched ( /- 5 years) patients with no clotting deficiency who had experienced in the same period at least one episode of deep vein thrombosis or pulmonary embolism. Only one of them had developed arterial thrombosis. Ischemic stroke, myocardial infarction, upper and lower limb arterial thrombosis, and mesenteric artery occlusion occurred regardless of the type of defect taken into account; mean age of about 37.05 /- 23 years (mean /- SD). In some cases, arterial thrombosis was fatal. The overall number of venous thrombotic events in the 92 symptomatic patients of this study was much higher than that of arterial thrombosis, with a ratio of 24 to 1. The use of long-term anticoagulant therapy in our group of patients seemed to be able to prevent recurrences of both arterial and venous thrombosis.
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28/144. Renovascular hypertension due to antithrombin deficiency in childhood.

    Inherited antithrombin deficiency generally causes a predisposition toward vascular thrombus above the age of 15 years. A 1-year-old boy developed renal hypertension caused by renal artery obstruction due to thrombus formation. This thrombus formation was attributed to antithrombin deficiency caused by a novel SERPINCI gene mutation (AT III Akita, M352R). This suggests that antithrombin deficiency can cause renal artery obstruction, inducing renal hypertension through vascular thrombosis even in children.
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29/144. Recurrent renal vein thrombosis and renal failure associated with antithrombin-III deficiency.

    This paper describes a healthy 13-year-old girl presenting with acute flank pain and anuria due to renal vein thrombosis. A similar spontaneous and unexplained thrombosis resulted in the loss of the contralateral kidney 1 year earlier. Urgent surgical thrombectomy and anticoagulation resulted in moderate recovery of renal function. Predisposition to venous thrombosis in this child was secondary to a marked familial deficiency of circulating antithrombin-III. An early diagnosis of this condition is essential for the formulation of preventive measures and may lead to specific therapeutic intervention at the onset of acute thrombotic complications.
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30/144. The pregnant antithrombin III deficient patient: management without antithrombin III concentrate.

    Pregnant patients with antithrombin III (AT III) deficiency have an unacceptably high risk of venous thromboembolism (VTE). Antithrombotic therapy is therefore recommended. The reported clinical experience of such prophylaxis is limited. Some authors have recommended the use of AT III concentrate in addition to heparin in the management of these patients. We report successful management with heparin alone during pregnancy and the postpartum period in two patients with AT III deficiency. Both patients had experienced VTE during a prior pregnancy; one also experienced VTE during the reported pregnancy. Both patients were therefore at particularly high risk of further VTE. Based on the good results in these two patients, and a review of previously reported cases, we propose that heparin alone, in a dose to maintain the APTT in a therapeutic range, provides adequate prophylaxis and treatment for VTE during pregnancy and delivery in many AT III deficient subjects.
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