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Related to Antithrombin III: antithrombin III test, protein C
ATIIIAntithrombin III (anticoagulant)
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There was no difference in most treatment details; however, gabexate was significantly used in the control group, and antithrombin III was significantly used in the rTM group.
Anti-cardiolipin antibodies (IgM/IgG), antithrombin III, as well as the protein C activity were within normal range.
Normal distribution of quantitative variables (protein C, protein S, antithrombin III, DD, FDPs, CRP, hs-CRP, WBC count, procalcitonin) was evaluated using Kolmogorov-Smirnow Z (K - S) test.
In these conditions hypercoagulable disorders including Protein C and S deficiency, Hyperhomocysteinemia, elevated levels of Factor VIII, Antithrombin III deficiency, polycythemia vera and Systemic Lupus Erythromatosus in addition to malignancy, trauma, and instrumentation are responsible for development of aortic floating thrombus [6-10].
Coagulation test revealed antithrombin III (AT III) defciency [repeated twice at different times, result: 68 (80-120)].
In blood, thrombin is inhibited by such serpins (serine protease inhibitors) as antithrombin III, heparin cofactor II or protein C inhibitor (21, 25, 26), with antithrombin playing the predominant role.
These 11 Asian studies (Table 1) reported 8 anticoagulation strategies including: Antithrombin III (ATIII), low-molecular-weight heparin (LMWH) plus Warfarin plus Aspirin, LMWH plus Warfarin, Urokinase + Aspirin, Warfarin, Alprostadil, Aspirin, LMWH plus Aspirin.
A thorough workup for underlying thrombophilia was unrevealing including protein S and C deficiency, lupus anticoagulant, anticardiolipin antibody, Factor V Leiden mutation, ANA positivity, antithrombin III deficiency, Vitamin B12 level, homocysteine level, hemoglobin electrophoresis, and rapid plasma reagin.
The activated platelets could result in forming platelet factor 4 (PF4), while the formed thrombin could couple with antithrombin III to generate thrombin-antithrombin III (TAT) complexes [31].
In a cohort study containing three cohorts of families with a hereditary deficiencies of protein C, protein S, and antithrombin III, compared with nondeficient family members, subjects with protein S or protein C deficiency but not antithrombin III deficiency had a higher risk for arterial thromboembolism before 55 years of age that was independent of their history of prior venous thromboembolism [4].
Prothrombotic workups including protein C activity, protein S activity, antithrombin III level, APC resistance, lupus anticoagulant, anticardiolipin antibodies, factor VIII inhibitor screening, and factor V Leiden defect were all negative, except for heterozygous mutation for prothrombin G20210A; the d-dimer level was normal 0.14 mcg/mL (0-0.5) and coagulation tests revealed low FVIII levels.