Von Drygalski Annette, Curtis Brian R, Bougie Daniel W, McFarland Janice G, Ahl Scott, Limbu Indra, Baker Kelty R, Aster Richard H
Department of Medicine, Medical College of Wisconsin, Milwaukee, USA.
N Engl J Med. 2007 Mar 1;356(9):904-10. doi: 10.1056/NEJMoa065066.
Vancomycin has only rarely been implicated as a cause of thrombocytopenia, and there is only limited evidence that this complication is caused by immune mechanisms. We conducted a study to determine whether thrombocytopenia is caused by vancomycin-dependent antibodies in patients being treated with vancomycin.
We identified and characterized vancomycin-dependent, platelet-reactive antibodies in patients who had been referred for testing during a 5-year period because of a clinical suspicion of vancomycin-induced thrombocytopenia. We obtained clinical information about the patients from their referring physicians.
Drug-dependent, platelet-reactive antibodies of the IgG class, the IgM class, or both were identified in 34 patients, and clinical follow-up information was obtained from 29 of these patients. The mean nadir platelet count in these patients was 13,600 per cubic millimeter, and severe bleeding occurred in 10 patients (34%). Platelet levels returned to baseline in all 26 surviving patients after vancomycin was stopped. In 15 patients, the drug was continued for 1 to 14 days while other possible causes of thrombocytopenia were investigated. Vancomycin-dependent antibodies were not found in 25 patients who had been given vancomycin and in whom thrombocytopenia did not develop.
Severe bleeding can occur in patients with vancomycin-induced immune thrombocytopenia. The detection of vancomycin-dependent antiplatelet antibodies in patients receiving the antibiotic in whom thrombocytopenia develops, and the absence of antibodies in patients given the drug in whom platelet counts remain stable, indicate that these antibodies are the cause of the thrombocytopenia.
万古霉素极少被认为是血小板减少症的病因，且仅有有限证据表明这种并发症是由免疫机制引起的。我们开展了一项研究，以确定接受万古霉素治疗的患者中血小板减少症是否由万古霉素依赖性抗体所致。
我们对5年间因临床怀疑万古霉素诱导的血小板减少症而转诊接受检测的患者体内的万古霉素依赖性血小板反应性抗体进行了鉴定和特征分析。我们从转诊医生处获取了这些患者的临床信息。
在34例患者中鉴定出了IgG类、IgM类或两者皆有的药物依赖性血小板反应性抗体，其中29例患者获得了临床随访信息。这些患者的血小板计数最低点平均为每立方毫米13,600，10例患者（34%）发生了严重出血。在停用万古霉素后，所有26例存活患者的血小板水平均恢复至基线。在15例患者中，在调查血小板减少症的其他可能病因时，万古霉素持续使用了1至14天。在25例接受万古霉素治疗且未发生血小板减少症的患者中未发现万古霉素依赖性抗体。
万古霉素诱导的免疫性血小板减少症患者可能发生严重出血。在发生血小板减少症的接受抗生素治疗的患者中检测到万古霉素依赖性抗血小板抗体，而在接受该药物但血小板计数保持稳定的患者中未检测到抗体，这表明这些抗体是血小板减少症的病因。
