Fritz E, Ludwig H, Scheithauer W, Sinzinger H
Blood. 1986 Aug;68(2):514-20.
Various defects in platelet function have been reported as being associated with multiple myeloma. In 30 myeloma patients and 15 healthy controls, we investigated platelet survival using in vitro labeling of autologous platelets with 111indium-oxine and measuring the in vivo kinetics of the radioisotope. Significantly shortened platelet half-life in patients averaged 73 hours, while platelet half-life in the healthy controls averaged 107 hours. In myeloma patients, serum levels of thromboxane B2, beta-thromboglobulin, and platelet factor 4 were significantly elevated; aggregation indices were within the pathological range; platelet counts and spleen-liver indices, however, were comparable to those of the healthy control group. No statistical correlation was found between platelet half-life and paraprotein concentrations. Our findings suggest an initial--so far unexplained--intravascular process of platelet activation and consumption that finally manifests in shortened platelet half-life. It seems that overt thrombocytopenia develops only when the compensatory capacity of the bone marrow finally becomes exhausted. Further studies should be able to elucidate the pathophysiologic processes involved.
据报道，血小板功能的各种缺陷与多发性骨髓瘤相关。我们对30例骨髓瘤患者和15名健康对照者进行了研究，采用111铟-氧喹啉对自体血小板进行体外标记，并测量放射性同位素在体内的动力学，以此来研究血小板存活情况。患者的血小板半衰期显著缩短，平均为73小时，而健康对照者的血小板半衰期平均为107小时。在骨髓瘤患者中，血栓素B2、β-血小板球蛋白和血小板因子4的血清水平显著升高；聚集指数处于病理范围内；然而，血小板计数和脾肝指数与健康对照组相当。未发现血小板半衰期与副蛋白浓度之间存在统计学相关性。我们的研究结果表明，最初存在一个迄今无法解释的血小板激活和消耗的血管内过程，最终表现为血小板半衰期缩短。似乎只有当骨髓的代偿能力最终耗尽时，才会出现明显的血小板减少。进一步的研究应该能够阐明其中涉及的病理生理过程。
