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Results for “Antithrombin III Deficiency”

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PubMed1999

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.

Adult↗
PubMed1991

[Pulmonary thromboembolectomy of subacute massive pulmonary thromboembolism in a patient with familial antithrombin III deficiency].

Reported is a case of successful pulmonary thromboembolectomy and inferior caval vein interruption in a patient with subacute massive pulmonary thromboembolism (PTE). He had been complicated by the right atrial and deep vein thrombosis due to type I familial antithrombin III (ATIII) deficiency. Pulmonary embolectomy and caval interruption was performed 20 days after the initial attack and followed by anti-coagulation therapy. Thrombi weighed 50 gm were removed mainly from the left pulmonary artery. The right atrial thrombus which had got smaller by the preoperative fibrinolytic therapy could not be found with right atriotomy. Respiratory function at rest and slightly elevated pulmonary arterial pressure was normalized post-operatively. Although the PTE in this patient was considered to be subacute by the histological findings of the fibrin thrombus removed, tapering of pulmonary arteries in PAG and obstructive intimal hypertrophy of the small vessels in the lungs suggests the chronic nature of the PTE (post-thrombotic obstruction of pulmonary arteries) caused by the hyper-coagulable state. In patients with familial ATIII deficiency, 50% of normal ATIII activity can be expected because they are heterozygotes, so the cardio-pulmonary bypass should be run with special caution to the heparin dosage. Caval vein interruption and warfarin therapy are recommended for prophylaxis of recurrent PTE.

Antithrombin III Deficiency↗