Zuffa E, Vianelli N, Martinelli G, Tazzari P, Cavo M, Tura S
Institute of Hematology Seràgnoli, University of Bologna, Italy.
Haematologica. 1996 Nov-Dec;81(6):533-5.
We report on two patients with Ph+ chronic myeloid leukemia (CML) in chronic phase who developed severe thrombocytopenia during treatment with interferon-alpha 2A (IFN-alpha 2A). In both cases, we detected the presence of platelet-associated antibodies (PAIg) by autoimmune flow cytometry. We postulated an immune mediated platelet destruction mechanism; corticosteroid therapy was employed and interferon therapy was withdrawn, resulting in an increase in platelet count and a reduction of PAIg. Our observation reports the detection of PAIg associated with IFN-alpha 2A therapy in CML and suggests that this immunomodulant drug could induce thrombocytopenia through a mechanism other than antiproliferation.
我们报告了2例慢性期Ph+慢性髓性白血病（CML）患者，他们在接受α-2A干扰素（IFN-α 2A）治疗期间出现了严重的血小板减少症。在这两例病例中，我们通过自身免疫流式细胞术检测到了血小板相关抗体（PAIg）的存在。我们推测存在免疫介导的血小板破坏机制；采用了皮质类固醇疗法并停用了干扰素疗法，结果血小板计数增加，PAIg减少。我们的观察报告了在CML中检测到与IFN-α 2A治疗相关的PAIg，并表明这种免疫调节药物可能通过除抗增殖以外的机制诱导血小板减少症。
