Sivakumaran M, Hutchinson R M, Pringle H, Graham S, Primrose L, Wood J K, Lauder I
Department of Haematology, Leicester Royal Infirmary, UK.
Bone Marrow Transplant. 1995 Apr;15(4):531-6.
Thrombocytopenia outlasting anaemia and neutropenia is a well recognised sequel of autologous bone marrow transplantation (BMT) but the pathogenesis remains unclear. Autoimmune destruction of platelets has been suggested as a possible mechanism. We studied 5 patients who had undergone autologous BMT and were found to have persistent thrombocytopenia (< 150 x 10(9)/l) 6 months from transplantation with a normal haemoglobin level and granulocyte count. Apart from a mild reduction in the megakaryocyte numbers in one case, no other quantitative or qualitative defects of the megakaryocyte lineage were present to explain the peripheral thrombocytopenia. Two cases had positive anti-platelet autoantibodies. Immunoglobulin heavy chain gene rearrangement studies of peripheral blood and bone marrow mononuclear cells using the polymerase chain reaction showed evidence of clonal rearrangement in one of the two cases with positive anti-platelet autoantibodies. Our results support the previous reports that anti-platelet antibody-mediated destruction of platelets may play a role in the pathogenesis of post-autologous BMT thrombocytopenia. Furthermore, the demonstration of a clonal B cell expansion in one of the cases with anti-platelet antibodies suggests an aetiological link between clonal B cells, autoantibody production and thrombocytopenia.
血小板减少持续时间超过贫血和中性粒细胞减少是自体骨髓移植（BMT）公认的后遗症，但发病机制仍不清楚。血小板的自身免疫性破坏被认为是一种可能的机制。我们研究了5例接受自体BMT的患者，这些患者在移植后6个月时血红蛋白水平和粒细胞计数正常，但血小板持续减少（<150×10⁹/L）。除1例巨核细胞数量轻度减少外，未发现巨核细胞系存在其他定量或定性缺陷来解释外周血小板减少。2例抗血小板自身抗体呈阳性。使用聚合酶链反应对外周血和骨髓单个核细胞进行免疫球蛋白重链基因重排研究，结果显示在2例抗血小板自身抗体阳性的患者中，有1例存在克隆性重排的证据。我们的结果支持先前的报道，即抗血小板抗体介导的血小板破坏可能在自体BMT后血小板减少的发病机制中起作用。此外，在1例抗血小板抗体阳性的患者中发现克隆性B细胞扩增，提示克隆性B细胞、自身抗体产生和血小板减少之间存在病因学联系。
