Mohri H, Tanabe J, Ohtsuka M, Yoshida M, Motomura S, Nishida S, Fujimura Y, Okubo T
First Department of Internal Medicine, Yokohama City University School of Medicine, Japan.
Blood Coagul Fibrinolysis. 1995 Sep;6(6):561-6. doi: 10.1097/00001721-199509000-00010.
Acquired von Willebrand disease (vWD) has been described in a few patients with multiple myeloma. The present study characterizes an inhibitor of von Willebrand factor (vWF) isolated from a patient with multiple myeloma (IgG-kappa). Multimeric analysis of vWF from this patient's plasma showed a reduction in multimers of all sizes. The inhibitor (IgG) detected only the vWF subunit from plasma of normal individuals. It reacted with intact vWF subunit and a 39/34kDa dispase-digested fragment of vWF (residues; Leu480/Val481-Gly718), but did not react with platelet membrane glycoproteins (GPs) or adhesive proteins. The binding of vWF to GPIb mediated by ristocetin and by botrocetin was inhibited by the patient's IgG with an IC50s of 0.3 mg/ml and 0.48 mg/ml, respectively. The platelet aggregation induced by ristocetin or botrocetin was also inhibited by the IgG. These results indicate that this inhibitor may recognize the binding region of vWF to GPIb. Therefore, the antibody to vWF appears to represent the likely pathophysiological mechanism responsible for the acquired vWD in this patient.
获得性血管性血友病(vWD)已在少数多发性骨髓瘤患者中被描述。本研究对从一名多发性骨髓瘤(IgG-κ型)患者分离出的血管性血友病因子(vWF)抑制剂进行了表征。对该患者血浆中的vWF进行多聚体分析显示,各种大小的多聚体均减少。该抑制剂(IgG)仅检测到正常个体血浆中的vWF亚基。它与完整的vWF亚基以及vWF的一个39/34kDa分散酶消化片段(残基;Leu480/Val481-Gly718)反应,但不与血小板膜糖蛋白(GPs)或黏附蛋白反应。该患者的IgG抑制了瑞斯托菌素和蛇毒凝血酶介导的vWF与GPIb的结合,IC50分别为0.3mg/ml和0.48mg/ml。瑞斯托菌素或蛇毒凝血酶诱导的血小板聚集也被IgG抑制。这些结果表明,该抑制剂可能识别vWF与GPIb的结合区域。因此,针对vWF的抗体似乎代表了该患者获得性vWD的可能病理生理机制。