Pullarkat V A, Rho H, Murata-Collins J L, Liebman H A
The Division of Hematology, Department of Medicine, The University of Southern California School of Medicine, Los Angeles, California, USA.
Am J Hematol. 2000 Mar;63(3):141-4. doi: 10.1002/(sici)1096-8652(200003)63:3<141::aid-ajh6>3.0.co;2-t.
Severe aplastic anemia is a well-recognized complication of ticlopidine therapy that carries a high mortality. Therapy with colony-stimulating factors or corticosteroids has been largely ineffective in this disorder. We report a case of ticlopidine-induced aplastic anemia that was successfully treated with cyclosporine and high-dose dexamethasone. The patient rapidly responded to immunosuppressive therapy and had a normal hemogram after cessation of immunosuppression. On long-term follow-up, the patient developed a progressive macrocytic anemia. Repeat bone marrow evaluation demonstrated myelodysplasia with erythroid hypoplasia. An associated chromosomal abnormality consisting of a t(3;16) (q21; p13.3) translocation was detected. This is the first report of a chromosomal abnormality associated with ticlopidine induced marrow aplastic anemia.
严重再生障碍性贫血是噻氯匹定治疗中一种公认的并发症，死亡率很高。集落刺激因子或皮质类固醇治疗在这种疾病中大多无效。我们报告一例噻氯匹定诱导的再生障碍性贫血患者，该患者经环孢素和大剂量地塞米松成功治疗。患者对免疫抑制治疗反应迅速，免疫抑制停止后血常规恢复正常。长期随访中，患者出现进行性大细胞贫血。重复骨髓评估显示骨髓发育异常伴红系发育不全。检测到一种由t(3;16)(q21;p13.3)易位组成的相关染色体异常。这是与噻氯匹定诱导的骨髓再生障碍性贫血相关的染色体异常的首次报告。
