{"title":"胺碘酮致血小板减少症1例报告","authors":"J. Burlile, Amit Pathak","doi":"10.52504/001c.7797","DOIUrl":null,"url":null,"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","PeriodicalId":340325,"journal":{"name":"Georgetown Medical Review","volume":"81 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2019-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"Amiodarone-Induced Thrombocytopenia: A Case Report\",\"authors\":\"J. Burlile, Amit Pathak\",\"doi\":\"10.52504/001c.7797\",\"DOIUrl\":null,\"url\":null,\"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\",\"PeriodicalId\":340325,\"journal\":{\"name\":\"Georgetown Medical Review\",\"volume\":\"81 1\",\"pages\":\"0\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2019-05-09\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Georgetown Medical Review\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.52504/001c.7797\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Georgetown Medical Review","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.52504/001c.7797","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Amiodarone-Induced Thrombocytopenia: A Case Report
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