Asztely F, Gilland E, Wattjes M P, Lycke J
Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
J Neurol Sci. 2015;353(1-2):155-7. doi: 10.1016/j.jns.2015.04.010. Epub 2015 Apr 16.
A multiple sclerosis (MS) patient developed progressive multifocal leukoencephalopathy (PML) after 43 months of natalizumab treatment. New clinical and magnetic resonance imaging (MRI) findings were initially misinterpreted as breakthrough MS disease activity and natalizumab treatment was replaced by rituximab treatment. The patient had a single infusion of rituximab 1000 mg before a definite PML diagnosis was confirmed. Despite undetectable levels of B-cells, JC virus DNA became undetectable in the cerebrospinal fluid by quantitative polymerase chain reaction. The patient partially recovered without any clinical or MRI signs of new MS activity. These findings suggest that B-cell depletion in a non-immune compromised individual did not prevent the patient from clearing the JC virus infection.
一名多发性硬化症（MS）患者在接受那他珠单抗治疗43个月后发生了进行性多灶性白质脑病（PML）。新的临床和磁共振成像（MRI）结果最初被误诊为MS疾病活动突破，那他珠单抗治疗被利妥昔单抗治疗所取代。在确诊明确的PML之前，该患者接受了一次1000 mg利妥昔单抗的输注。尽管B细胞水平检测不到，但通过定量聚合酶链反应，脑脊液中的JC病毒DNA变得检测不到。患者部分恢复，没有任何新的MS活动的临床或MRI迹象。这些发现表明，在非免疫受损个体中B细胞耗竭并未阻止患者清除JC病毒感染。
