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1/166. 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. ( info)

2/166. 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. ( info)

3/166. 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. ( info)

4/166. 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. ( info)

5/166. 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. ( info)

6/166. Pre-operative coagulopathy management of a neonate with complex congenital heart disease: a case study.

    Severe coagulation defects often develop in neonates undergoing cardiac surgery, both as a result of the surgical intervention, and as pre-existing defects in the hemostatic mechanisms. The following case report describes a newborn patient with complex congenital heart disease and respiratory failure whose pre-operative coagulopathy was aggressively managed prior to surgical correction. A 5-day-old, 2.5 kg child presented with interrupted aortic arch, ventricular septal defect, atrial septal defect, and patent ductus arteriosus. On admission, he was in respiratory arrest suffering from profound acidemia. In addition, the child was hypothermic (30.1 degrees C), septic (streptococcus viridans), and coagulopathic (disseminated intravascular coagulation-DIC). The patient was immediately intubated and initial coagulation assessment revealed the following: prothrombin time (PT) 48.9 s (international normalized ratio (INR) 15.7), activated partial thromboplastin time (aPTT) >106 s, platelet count 30,000 mm(3), fibrinogen 15 mg dL(-1) and antithrombin III (AT-III) 10%. Before cardiac surgery could be performed, the patient's DIC was corrected with the administration of cryoprecipitate (15 ml), fresh frozen plasma (300 ml), and platelets (195 ml). In spite of the large transfusion of fresh frozen plasma, the AT-III activity, measured as a percentage, remained depressed at 33. Initial thromboelastographic (TEG) determination revealed an index of 2.02, and following 100 IU administration of an AT-III concentrate, declined to -2.32. Sequential TEG profiles were performed over several days, with the results used to guide both transfusion and medical therapy. The congenital heart defect correction was subsequently performed with satisfactory initial results, but the patient developed a fungal infection and expired on the 16th post-operative day. The present case describes techniques of coagulation management for a newborn with both a severe hemostatic defect and congenital heart disease. ( info)

7/166. 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. ( info)

8/166. 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. ( info)

9/166. 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. ( info)

10/166. 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. ( info)
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