資料來源:

Volume 361:1887-1894

Multiple molecular mechanisms can lead to acquired von Willebrand's disease: shearing of high-molecular-weight von Willebrand factor multimers by mechanical stress or proteolysis catalyzed by ADAMTS 13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) in cardiac valvulopathies, degradation of von Willebrand factor multimers by plasmin in disseminated intravascular coagulation, and reduction of von Willebrand factor synthesis in hypothyroidism. In lymphoproliferative disorders, plasma-cell dyscrasias, and autoimmune diseases, circulating anti–von Willebrand factor antibodies can cause qualitative or quantitative deficiencies, and tumor cells can adsorb von Willebrand factor (e.g., by expressing glycoprotein Ib), depleting its circulating levels.

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