Howard C E, Adams L A, Admire J L, Chu M A, Alred G L
McWhorter School of Pharmacy, Samford University, Birmingham, AL 35229, USA.
Ann Pharmacother. 1997 Mar;31(3):315-8. doi: 10.1177/106002809703100308.
To report a case of thrombocytopenia apparently associated with vancomycin use.
A 58-year-old white man was admitted to the hospital with chronic osteomyelitis of the foot due to methicillin-resistant Staphylococcus aureus that later spread hematogenously to the cervical vertebrae. During the first course of therapy with vancomycin, his platelet count decreased from 397 x 10(3)/mm3 to 22 x 10(3)/mm3. After discontinuation of the drug, it increased to 310 x 10(3)/mm3. During the second course of vancomycin, the platelet count decreased to 77 x 10(3)/mm3, and increased to 404 x 10(3)/mm3 after discontinuation of the drug.
Vancomycin has been reported as a rare cause of thrombocytopenia. Thrombocytopenia can occur as an adverse drug reaction by the following three mechanisms: direct toxic effect, drug absorption (hapten) formation, and an "innocent bystander" immune response.
We suspect that the thrombocytopenia in this patient, which involved an increased number of megakaryocytes in the bone marrow, was due to vancomycin.
报告一例明显与使用万古霉素相关的血小板减少症病例。
一名58岁白人男性因耐甲氧西林金黄色葡萄球菌引起的足部慢性骨髓炎入院,该病菌随后经血行播散至颈椎。在首次使用万古霉素治疗过程中,他的血小板计数从397×10³/mm³降至22×10³/mm³。停药后,血小板计数升至310×10³/mm³。在第二次使用万古霉素治疗过程中,血小板计数降至77×10³/mm³,停药后又升至404×10³/mm³。
已有报道万古霉素是血小板减少症的罕见病因。血小板减少症可通过以下三种机制作为药物不良反应发生:直接毒性作用、药物吸收(半抗原)形成以及“无辜旁观者”免疫反应。
我们怀疑该患者的血小板减少症(骨髓中巨核细胞数量增加)是由万古霉素所致。