Sulfamethoxazole-induced thrombocytopenia masquerading as posttransfusion purpura: a case report.
Sulfamethoxazole-induced thrombocytopenia masquerading as posttransfusion purpura: a case report.
复制标题
磺胺甲恶唑诱导的血小板减少症伪装成输血后紫癜：病例报告。
DOI：
10.1111/trf.13197
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发表时间：
2015
期刊：
影响因子：
2.9
通讯作者：
Sweeney,JosephD
中科院分区：
文献类型：
--
作者：
Nixon,ChristianP;Cheves,TraceyA;Sweeney,JosephD
背景药物诱导的免疫性血小板减少症（DITP）是一种罕见的临床疾病，其特征是在药物依赖性抗体存在的情况下加速血小板（PLT）清除。将 DITP 与其他免疫介导的疾病（例如输血后紫癜 (PTP) 和自身免疫性血小板减少症）区分开来可能是一项临床挑战。 病例报告 68 岁男性，无既往输血史，因呼吸困难、鼻衄和严重血小板减少症 (<10 × 109/L) 于出院 12 天后被送往急诊科 (ED) 入院接受冠状动脉搭桥术。对血小板减少程度的评估以及围手术期和术后接受多次输血与 PLT 计数急剧下降之间的时间关联表明，PTP 是严重血小板减少的可能原因。开始使用 1 g/kg 静脉注射免疫球蛋白 (IVIG) 治疗，随后 48 小时内 PLT 计数快速增加。随后在提交时收集的样本中鉴定出缺乏血清学特异性的 PLT 抗体。两周后，他再次因鼻出血和严重血小板减少症 (<10 × 109/L) 到急诊室就诊。现在的临床病史显示，该患者在因腿部“出现蜂窝组织”而首次住院后，以及因手术部位红斑和水肿而最终就诊之前，曾由其初级保健医生使用甲氧苄氨嘧啶-磺胺甲恶唑进行治疗。再次施用 IVIG，PLT 计数迅速恢复至基线。随后在原始患者样本中鉴定出磺胺甲恶唑依赖性 PLT 抗体。 结论 本病例报告记录了一个最初被误诊为 PTP 的 IVIG 反应性 DITP 病例，强调了这些免疫介导现象的临床重叠。
BACKGROUNDDrug‐induced immune thrombocytopenia (DITP) is a rare clinical disorder characterized by accelerated platelet (PLT) clearance in the presence of drug‐dependent antibodies. Distinguishing DITP from other immune‐mediated disorders such as posttransfusion purpura (PTP) and autoimmune thrombocytopenia can represent a clinical challenge.CASE REPORTA 68‐year‐old male with no prior transfusion history presented to the emergency department (ED) with dyspnea, epistaxis, and severe thrombocytopenia (<10 × 109/L) 12 days after discharge from a hospital admission for a coronary artery bypass graft. Evaluation of the degree of thrombocytopenia and the temporal association between the peri‐ and postoperative receipt of multiple transfusions and the acute decrease in PLT count indicated PTP as a possible cause of the severe thrombocytopenia. Treatment with 1 g/kg intravenous immunoglobulin (IVIG) was initiated and followed by a rapid 48‐hour increase in the PLT count. PLT antibodies lacking serologic specificity were subsequently identified in a sample collected upon presentation. Two weeks later he again presented to the ED with epistaxis and severe thrombocytopenia (<10 × 109/L). Clinical history now revealed that the patient had been treated with trimethoprim‐sulfamethoxazole by his primary care physician after his first hospitalization for a “cellulitic‐appearing” leg and again before his final presentation for surgical site erythema and edema. IVIG was administered again with a rapid return of PLT count to baseline. Sulfamethoxazole‐dependent PLT antibodies were subsequently identified in the original patient sample.CONCLUSIONThis case report documents a case of IVIG‐responsive DITP initially misdiagnosed as PTP, highlighting the clinical overlap of these immunologic‐mediated phenomena.