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1/144. A case report of heparin resistance due to acquired antithrombin iii deficiency.

    A case of heparin resistance and its management during cardiopulmonary bypass is reported. A patient with a history of post-infarct angina and arrhythmias was treated with intravenous heparin infusion for five days prior to myocardial revascularisation surgery. He required 13,500 IU/kg of heparin to increase his activated clotting time to a therapeutic level for safe institution of cardiopulmonary bypass. This phenomenon of heparin resistance was postulated to be due to consumption of circulating antithrombin III as a result of prior heparinisation. Treatment with fresh frozen plasma restored heparin effectiveness.
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2/144. A case of ovarian hyperstimulation syndrome in which antithrombin iii deficiency occurred because of its loss into ascites.

    OBJECTIVE: To present a case of ovarian hyperstimulation syndrome in which antithrombin III activity in plasma was decreased and in ascites was increased. DESIGN: Case report. SETTING: Hospital-based clinic for reproductive medicine. PATIENT(S): A 27-year-old woman who was transferred to our hospital because of ovarian hyperstimulation syndrome. INTERVENTION(S): Induced abortion. MAIN OUTCOME MEASURE(S): Antithrombin III activity in plasma and ascites. RESULT(S): Antithrombin III activity in ascites was slightly lower than that in plasma. CONCLUSION(S): The loss of antithrombin III into ascites probably caused its deficiency in this case.
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3/144. Primary antiphospholipid syndrome: a cause of catastrophic shunt thrombosis in the newborn.

    This is a unique report of systemic-to-pulmonary artery shunt thromboses secondary to primary antiphospholipid syndrome and antithrombin iii deficiency in a neonate with cyanotic congenital heart disease. This infant with tricuspid atresia experienced thromboses of two modified Blalock-Taussig shunts en route to a bidirectional cavo-pulmonary shunt and potential future Fontan operation. Chronic warfarin anticoagulation has prevented additional thrombo-embolic events.
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4/144. Familial overexpression of beta antithrombin caused by an Asn135Thr substitution.

    We have investigated the basis of antithrombin deficiency in an asymptomatic individual (and family) with borderline levels (approximately 70% antigen and activity) of antithrombin. Direct sequencing of amplified dna showed a mutation in codon 135, AAC to ACC, predicting a heterozygous Asn135Thr substitution. This substitution alters the predicted consensus sequence for glycosylation, Asn-X-Ser, adjacent to the heparin interaction site of antithrombin. The antithrombin isolated from plasma of the proband by heparin-sepharose chromatography contained amounts of beta antithrombin (the very high affinity fraction) greatly increased (approximately 20% to 30% of total) above the trace levels found in normals. Expression of the residue 135 variant in both a cell-free system and COS-7 cells confirmed altered glycosylation arising as a consequence of the mutation. Wild-type and variant protein were translated and exported from COS-7 cells with apparently equal efficiency, in contrast to the reduced level of variant observed in plasma of the affected individual. This case represents a novel cause of antithrombin deficiency, removal of glycosylation concensus sequence, and highlights the potentially important role of beta antithrombin in regulating coagulation.
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5/144. plasma antithrombin iii deficiency in ischaemic stroke in the young.

    A deficiency of plasma antithrombin III has been identified as a potential risk factor for thrombosis. In a pilot study of 56 patients aged less than 40 years who presented with ischaemic stroke of unknown etiology, we detected only one case of plasma antithrombin iii deficiency. Antithrombin III activity was estimated by a chromogenic assay. Hence, antithrombin iii deficiency, though rare, should be considered while evaluating young patients with stroke of unknown etiology.
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6/144. Pulmonary arterial thrombosis in a neonate with homozygous deficiency of antithrombin III: successful outcome following pulmonary thrombectomy and infusions of antithrombin III concentrate.

    We report a newborn male who presented with severe central cyanosis on the third day of life. Partial thrombotic obstruction of the pulmonary trunk secondary to Antithrombin III (homozygous defect of heparin binding site) deficiency was subsequently diagnosed. Surgical thrombectomy, and infusions of Antithrombin III concentrate, led to a successful outcome. We postulate that intrauterine thrombosis occurred to give this unusual presentation.
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7/144. Rapid genetic diagnosis in neonatal pulmonary artery thrombosis caused by homozygous antithrombin Budapest 3.

    We report a case of spontaneous left pulmonary artery thrombosis in a 3-day-old male neonate. The presentation of heparin resistance and thrombosis raised the possibility of a type II heparin binding site antithrombin deficiency. A continuous infusion of antithrombin concentrate was used successfully, following failure of plasma, to correct the heparin resistance. Rapid genetic analysis allowed sequencing of the antithrombin gene within 5 working days. This showed the infant to be homozygous for the substitution of C to T at nucleotide 2759. This base change causes mutation of the native leucine at codon 99 to a phenylalanine. This antithrombin variant has been previously reported (antithrombin Budapest 3) and results in reduced binding of heparin to antithrombin. Such a molecular diagnostic approach is feasible and warranted in such cases of neonatal thrombosis because of the diagnostic difficulties encountered.
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8/144. Acute arterial thrombosis with antithrombin iii deficiency in nephrotic syndrome: report of a case.

    nephrotic syndrome frequently causes venous thromboembolic complications. Arterial thrombosis has rarely been reported and is mainly observed in children. Only six cases of lower extremity arterial thrombosis in adults have been reported in the literature. The outcome in these cases was unsatisfactory because of the high rates of limb loss and recurrence of thrombosis. We report successful treatment of a 39-year-old man who suffered from right lower extremity arterial thrombosis associated with decreased levels of serum antithrombin III. He was admitted to our hospital with severe pain in his right foot. No pulse was palpable in his right dorsalis pedis or posterior tibial arteries. His right foot was cold and mottled, with a reduced sensation and motor activity. The laboratory data revealed a serum total protein concentration of 3.9g/dl and an albumin concentration of 1.5 g/dl. The coagulation profile showed a fibrinogen level of 879 mg/dl and antithrombin III value of 9.5%. Right lower extremity arteriography showed a complete occlusion of the right deep femoral artery and popliteal artery, and a filling defect in the common femoral artery. An emergency thrombectomy was performed under general anesthesia. The patient was treated successfully, and surgical treatment was followed by anticoagulant therapy with 1,000 units of antithrombin III. A renal biopsy revealed histologic evidence of minimal change of glomerulonephritis. He was discharged 3 months later, and no recurrence of thrombosis has yet been observed.
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9/144. antithrombin iii deficiency in a patient with multifocal osteonecrosis.

    The authors examined a 35-year-old man who had multifocal osteonecrosis on the right and left femoral heads, left humeral head, and right scaphoid. The patient previously had a diagnosis of Type I congenital antithrombin iii deficiency but had no other risk factors for osteonecrosis. This patient was thought to have systemic thromboembolism because of the increased blood coagulability resulting from antithrombin iii deficiency. thrombophilia (increased likelihood of thrombosis) and hypofibrinolysis (reduced ability to lyse thrombi) have been implicated as causative factors for osteonecrosis. This case shows a possible relationship between thrombophilic antithrombin iii deficiency and multifocal osteonecrosis.
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10/144. Familial antithrombin-III deficiency during cardiopulmonary bypass: a case report.

    The serine protease inhibitor antithrombin-III (AT-III) is the principal in vivo inhibitor of blood coagulation, inactivating mainly thrombin, but also other serine proteases. Binding of AT-III to heparin dramatically increases its inhibitory effect. AT-III deficiency during cardiopulmonary bypass (CPB) can lead to insufficient anticoagulation which cannot be treated by higher doses of heparin. A 60-year-old male with familial AT-III deficiency was admitted to our hospital for coronary artery bypass surgery and aortic valve replacement. Four days before the operation, acenocoumarol was stopped and anti-Xa nadroparincalcium (Fraxiparine) was started. AT-III activity at that time was 56%. Two hours before the operation, a single dose of 4500 IU AT-III concentrate was administered. Heparinization was performed with 400 IU/kg of porcine mucosal heparin, increasing the activated coagulation time (ACT) from a baseline of 115 to 549 s. AT-III activity at that time was above 100% and the plasma D-dimer concentration was 230 ng/l. ACTs during CPB remained above 999 s, whereas the AT-III activity dropped to 54% and the D-dimer increased up to 500 ng/l at the end of CPB. CPB was terminated uneventfully. heparin was reversed with 3 mg/kg protamine chloride, decreasing the ACT to 155 s. In the intensive care unit (ICU), the patientreceived prophylactic Fraxiparine and 1500 IU AT-III, increasing the AT-III activity to 84%. Postoperatively, there was continued blood loss, which necessitated the administration of whole blood and eventually re-exploration. The case presented illustrates an uneventful treatment of a patient with a hereditary AT-III deficiency undergoing CPB. In spite of an uneventful treatment with AT-III pre-CPB, administration of prophylactic AT-III concentrate after surgery should be considered with caution, as this might increase the postoperative morbidity.
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