• Hematology · Jun 2016

    Clinical Trial

    Change in plasma a disintegrin and metalloprotease with thrombospondin type-1 repeats-13 and von Willebrand factor levels in venous thromboembolic patients.

    • Bulent Karakaya, Anil Tombak, Mehmet Sami Serin, and Naci Tiftik.
    • a Internal Medicine Department , Mersin University Faculty of Medicine , Mersin , Turkey.
    • Hematology. 2016 Jun 1; 21 (5): 295-9.

    ObjectivesVenous thromboembolism (VTE) is an important cause of morbidity and mortality. A disintegrin and metalloprotease with thrombospondin type-1 repeats-13 (ADAMTS-13) is a metalloprotease that cleaves plasma von Willebrand factor (VWF) multimers. The presence of large VWF multimers in the plasma due to ADAMTS-13 deficiency is the main factor in the pathogenesis of thrombotic thrombocytopenic purpura. The present study aimed to investigate the relation of plasma levels of ADAMTS-13 and VWF antigen with VTE.MethodsThe present study included 30 patients with VTE and age- and gender-matched 30 healthy subjects. Patients with any condition (diabetes, icterus, hyperlipidemia, physical, or surgical trauma, acute coronary syndrome, pregnancy, renal insufficiency, liver disease, malignancy, collagen tissue disease, chronic or acute inflammation, drug use affecting thrombocyte function) that could affect plasma VWF antigen or ADAMTS-13 levels were excluded. Plasma ADAMTS-13 and VWF antigen levels in the VTE and control groups were quantitatively determined by enzyme-linked immunosorbent assay method.ResultsThe median ADAMTS-13 level was 280 ng/ml (minimum-maximum, 70-1120 ng/ml) in the VTE group and 665 ng/ml (minimum-maximum, 350-2500 ng/ml) in the control group; the difference between the groups was significant (P < 0.0001). The mean VWF antigen level was 1750 ± 616 mU/ml in the patient group, which was significantly higher than that of the control group (950 ± 496 mU/ml) (P < 0.0001).ConclusionSignificantly lower ADAMTS-13 levels and significantly higher VWF antigen levels were concluded to be the result of a pathological process rather than an etiological factor for VTE.

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