1例MOGAD患者在接受利妥昔单抗治疗后出现持续严重的免疫球蛋白缺乏:一份关于利妥昔单抗如何揭示原发性免疫缺陷的病例报告

A. Ali , L. Bernasconi , N. Cantoni , A.C. Lecourt , A.K. Pröbstel , A. Conen , O. Findling
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引用次数: 0

摘要

我们提出了一个年轻的女性患者的临床方案,谁提出了进行性感觉运动四肢瘫痪和疲劳。经调查诊断为抗mog相关疾病(MOGAD)。在高剂量静脉注射类固醇治疗后,开始了以6个月为周期的利妥昔单抗免疫抑制治疗。有了这个,神经系统的状况稳定下来,没有任何进一步的复发。但患者开始出现复发性呼吸道感染,甚至在停止使用利妥昔单抗治疗两年之后。调查显示,潜在的严重IgA缺乏症和IgG缺乏症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Persistent severe immunoglobulin deficiency after treatment with rituximab in a patient with MOGAD: A case report on how rituximab may, or may not, unmask primary immunodeficiencies
We present the clinical scenario of a young female patient, who presented with a progressive sensory motor tetraparesis and fatigue. Upon investigation anti-MOG-associated disease (MOGAD) was diagnosed. After high dose intravenous steroid therapy, an immunosuppressive treatment with rituximab, in six-monthly cycles, was initiated. With this, the neurological condition stabilized without any further relapses. But the patient started to suffer from recurrent respiratory tract infections, even after the treatment with rituximab was paused for two years. Investigations revealed an underlying strikingly severe IgA deficiency alongside an IgG Deficiency.
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