Levin H A, McMillan R, Tavassoli M, Longmire R L, Yelenosky R, Sacks P V
Am J Med. 1975 Aug;59(2):274-80. doi: 10.1016/0002-9343(75)90363-0.
Severe thrombocytopenia developed in a patient with rheumatoid arthritis during gold therapy. Increased numbers of marrow megakaryocytes, shortened 51Cr-labeled platelet survival and platelet phagocytosis by splenic macrophages indicated that thrombocytopenia was due to excessive platelet destruction. Aurothiomalate disodium antigenicity was demonstrated by increased lymphocyte blastogenesis, and accentuation of blood and splenic leukocyte migration in the presence of the gold salt. In vitro splenic immunoglobulin G (IgG) production was markedly increased, and a significant portion of the culture-produced IgG attached specifically to homologous platelets and platelet membranes. Serum antiplatelet antibodies could not be demonstrated, nor could it be shown that gold enhanced the binding of splenic-synthesized IgG to platelets. The data indicate an immunologic mechanism for gold-associated thrombocytopenia and permit speculation as to possible ways in which unidentified antigens may be involved in the pathogenesis in idiopathic thrombocytopenic purpura.
一名类风湿关节炎患者在金制剂治疗期间出现严重血小板减少。骨髓巨核细胞数量增加、51Cr标记的血小板生存期缩短以及脾巨噬细胞对血小板的吞噬作用表明，血小板减少是由于血小板过度破坏所致。通过淋巴细胞增殖增加以及在金盐存在下血液和脾白细胞迁移加剧，证明了硫代苹果酸金钠的抗原性。体外脾免疫球蛋白G（IgG）产生明显增加，并且培养产生的IgG中有很大一部分特异性附着于同源血小板和血小板膜。未检测到血清抗血小板抗体，也未证明金增强了脾合成的IgG与血小板的结合。这些数据表明了与金相关的血小板减少的免疫机制，并允许推测未确定的抗原可能参与特发性血小板减少性紫癜发病机制的可能方式。
