antithrombin III deficiency

(redirected from Antithrombin deficiency)

antithrombin III deficiency

Congenital antithrombin III deficiency An AD condition characterized by ↑ risk of DVT and PE. See Antithrombin III.

antithrombin III deficiency

An inherited deficiency of certain protein-splitting enzymes (proteases) which normally participate in the blood clotting cascade sequence. Women with this deficiency are at serious risk of developing THROMBOEMBOLISM in pregnancy and HEPARIN treatment is necessary.
References in periodicals archive ?
protein C or S deficiency, factor V Leiden, antithrombin deficiency, conversion to open surgery and an operative time more than 2 hours were excluded from the study.
A hypercoagulable panel was negative for protein C deficiency, protein S deficiency, Factor V Leiden, antithrombin deficiency, factor II mutation, and antiphospholipid antibody panel.
Amongst the 18 tested for an underlying thrombophilia, four (40.0%) had protein C deficiency, five (50.0%) had protein S deficiency, and two (33.3%) had antithrombin deficiency. Antiphospholipid antibodies (anti-cardiolipin, lupus anticoagulant, and anti-beta2-glycoprotein antibodies) were found in four patients (25.0%), and V617F JAK2 mutation was positive in three patients (20.0%).
Inherited antithrombin deficiency Type IIb alters what and results in what?
Acutely ill patients may have an antithrombin deficiency, resulting in an inaccurately low aPTT and undue coagulation (Zehnder, Price, & Jin, 2012).
Different combinations of the following keywords: "hereditary," "antithrombin deficiency," "ATIII," "pregnancy," "antithrombin concentrate," "case report/series," and "clinical study" were used in the search.
Other mutations are protein C and S deficiency, antithrombin deficiency, activated protein C mutation (G20210A).
Objectives: To determine the frequency of Protein C Protein S (PC and PS) antithrombin deficiency (AT III) and Factor V Leiden mutation (FVL) as a cause of thrombophilia in the patients with venous thromboembolism (VTE) and cerebrovascular accident (CVA).
Therefore, testing for a congenital antithrombin deficiency would have to be delayed until the patient had discontinued warfarin.
These protein deficiencies/abnormalities are genetic and include entities such as antithrombin deficiency, protein C deficiency, protein S deficiency, Factor V Leiden mutation, prothrombin 20210, and dysfibrinogenemia, among others.
Endothelial dysfunction, the release of von Willebrand factor (vWF), platelet activation, enhanced thrombin and fibrin generation, antithrombin deficiency, and impaired fibrinolysis close the pathological chain of enhanced thrombocoagulation associated with vasculitis (perivasculitis) in BD.
The inherited thrombophilias include factor V Leiden, prothrombin G20210A, antithrombin deficiency, protein C deficiency, protein S deficiency, and elevated coagulation factor VIII (FVIII), while acquired thrombophilias include the presence of antiphospholipid antibodies.