Department of Laboratory Medicine, University of California at San Francisco, San Francisco, California; Department of Internal Medicine, University of California at San Francisco, San Francisco, California; Clinical Laboratory, San Francisco General Hospital, San Francisco, California; Blood Centers of the Pacific, San Francisco, California.
Transfusion. 2013 Nov;53(11):2715-21. doi: 10.1111/trf.12138. Epub 2013 Mar 3.
Antibody-mediated drug-induced thrombocytopenia (DIT) typically requires the presence of the sensitizing drug in the plasma. Therefore, platelet (PLT) counts often start to recover 1 to 2 days after discontinuation of the offending medication. We present a case of ceftriaxone-induced DIT that resulted in severe, prolonged thrombocytopenia.
A 65-year-old woman with liver and renal insufficiency was transferred to our hospital for liver transplant evaluation. Two days after a 5-day course of ceftriaxone, her PLT count declined from a stable baseline of approximately 70 × 10(9) /L to a value of 3 × 10(9) /L, with coincident onset of mucocutaneous purpura. Her PLT count remained in the 1 × 10(9) to 6 × 10(9) /L range until her death 13 days later, despite intravenous immune globulin, steroids, and PLT transfusions. The persistently low PLT count impeded central catheter placement for hemodialysis and possible therapeutic plasmapheresis. A strong ceftriaxone-dependent, PLT-reactive antibody was identified in a sample drawn 7 days after ceftriaxone was last administered, and ceftriaxone remained detectable in her serum for at least 8 days after the last dose.
A ceftriaxone-dependent, PLT-reactive antibody was responsible for the persistent thrombocytopenia in this patient. Although DIT is generally expected to improve within a few days of drug discontinuation, impaired drug clearance can significantly alter the outcome. This case highlights the importance of altered drug metabolism and clearance in critically ill patients, especially those with combined hepatic and renal dysfunction. DIT should be strongly suspected in patients with acute thrombocytopenia, and all treatment options to reduce serum drug levels should be seriously considered.
抗体介导的药物诱导性血小板减少症（DIT）通常需要药物在血浆中存在。因此，停药后 1 至 2 天血小板（PLT）计数通常开始恢复。我们报告了一例头孢曲松引起的 DIT，导致严重的、持续性血小板减少症。
一名 65 岁女性因肝肾功能不全转入我院进行肝移植评估。头孢曲松治疗 5 天后的两天，她的 PLT 计数从稳定的基线水平（约 70×10(9)/L）降至 3×10(9)/L，同时出现黏膜皮肤瘀点。尽管静脉注射免疫球蛋白、类固醇和 PLT 输注，但她的 PLT 计数仍在 1×10(9)至 6×10(9)/L 范围内，直到 13 天后死亡。在最后一次给予头孢曲松后 7 天抽取的样本中发现了一种强烈的、与头孢曲松相关的、与 PLT 反应的抗体，并且在最后一次给药后至少 8 天，头孢曲松仍可在她的血清中检测到。
一种与头孢曲松相关的、与 PLT 反应的抗体导致了该患者的持续性血小板减少症。尽管一般预期在停药后几天内 DIT 会改善，但药物清除受损会显著改变结局。该病例强调了改变药物代谢和清除对重症患者的重要性，特别是那些合并肝肾功能不全的患者。对于急性血小板减少症患者，应强烈怀疑 DIT，并且应认真考虑所有降低血清药物水平的治疗选择。
