Amiodarone-Induced Thrombocytopenia: A Case Report

J. Burlile, Amit Pathak
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引用次数: 1

Abstract

Case Presentation : An 89-year-old woman with a history of atrial fibrillation, coronary artery disease, hypertension, and recent hospitalization for intraparenchymal and intraventricular hemorrhage presented with new-onset critical thrombocytopenia secondary to amiodarone, which had started approximately 1.5 months prior to presentation. Discussion : The patient’s treatment with amiodarone was stopped on the first day of admission, at which time her platelet count was . She received transfusions of 4 units of platelets during her hospital stay, and her platelet count was at discharge. It increased to at follow-up with outpatient hematology 15 days after presentation and was within normal limits 7 months after hospitalization. There are 2 published reports detailing 5 separate cases of amiodarone-induced immune thrombocytopenia, and at least 8 reports of amiodarone-induced bone marrow granulomas resulting in pancytopenia. Because the patient did not have pancytopenia consistent with myelosuppression, her presentation was not reflective of bone marrow granulomas or a direct, nonimmune-mediated insult. However, the return of her platelet count to a normal level was delayed compared with the timeline presented in previous cases of both amiodarone and non-amiodarone immune-mediated thrombocytopenias. This delay in return to normal platelet count was likely secondary to the patient’s older age in the context of amiodarone’s lipophilic nature and very long half-life. Conclusion : Although a rare complication of amiodarone use, thrombocytopenia should be considered by physicians who prescribe this drug. should prompt a complete blood count, discontinuation of the drug, and monitoring for resolution. If the platelet count recovers and amiodarone is found to be responsible, the medication should not be restarted, and amiodarone should be considered a drug allergy. thrombocytopenia when beginning therapy and to surveil patients with complete blood count monitoring. This patient experienced a late-onset thrombocytopenia after beginning amiodarone, followed by a delayed recovery to normal platelet counts. As previous literature has reported, platelet recovery after amiodarone-induced thrombocytopenia is longer than observed with other drugs. Although this timeline of late onset and delayed recovery is more consistent with previous reports of amiodarone-mediated direct nonimmune toxicity or bone marrow granulomas, the patient’s normal white blood cell count and only mild anemia argue against a nonimmune cause of thrombocytopenia. Her antibody test results were negative, but previous studies have shown immune-mediated amiodarone-Amiodarone-Induced
胺碘酮致血小板减少症1例报告
病例介绍:一名89岁女性,有房颤、冠状动脉疾病、高血压病史,近期因肺内和脑室内出血住院,在就诊前约1.5个月出现胺碘酮继发的新发重症血小板减少症。讨论:患者入院第一天停止胺碘酮治疗,此时其血小板计数为。住院期间输注血小板4单位,出院时血小板计数正常。就诊后15天门诊血液学随访时升高,住院后7个月在正常范围内。有2篇已发表的报告详细介绍了5例胺碘酮诱导的免疫性血小板减少症,至少8例胺碘酮诱导的骨髓肉芽肿导致全血细胞减少症。由于患者没有与骨髓抑制一致的全血细胞减少症,她的表现不能反映骨髓肉芽肿或直接的、非免疫介导的损伤。然而,与先前胺碘酮和非胺碘酮免疫介导的血小板减少病例相比,她的血小板计数恢复到正常水平的时间有所延迟。在胺碘酮的亲脂性和很长的半衰期的背景下,这种延迟恢复正常血小板计数可能是继发于患者的年龄。结论:虽然使用胺碘酮是一种罕见的并发症,但医生在开此药时应考虑血小板减少症。应提示全血细胞计数,停药,并监测解决。如果血小板计数恢复并发现是胺碘酮引起的,则不应重新开始用药,应将胺碘酮视为药物过敏。开始治疗时有血小板减少症,并对患者进行全血细胞计数监测。该患者在开始使用胺碘酮后出现迟发性血小板减少症,随后延迟恢复到正常血小板计数。如既往文献报道,胺碘酮诱导的血小板减少后血小板恢复时间比其他药物更长。虽然这种晚发和延迟恢复的时间线与先前关于胺碘酮介导的直接非免疫毒性或骨髓肉芽肿的报道更为一致,但患者正常的白细胞计数和仅有的轻度贫血表明不是血小板减少症的非免疫原因。她的抗体检测结果为阴性,但先前的研究显示免疫介导的胺碘酮诱导
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