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X 连锁无丙种球蛋白血症患者中真菌性坏死性筋膜炎的非典型表现。

Atypical Presentation of Severe Fungal Necrotizing Fasciitis in a Patient with X-Linked Agammaglobulinemia.

机构信息

Primary Immunodeficiency Unit, Allergy and Immunology Research Centre, Institute for Medical Research, National Institutes of Health, Ministry of Health, Selangor, Malaysia.

Pediatric Department, Penang General Hospital, Ministry of Health, Penang, Malaysia.

出版信息

J Clin Immunol. 2021 Aug;41(6):1178-1186. doi: 10.1007/s10875-021-01017-3. Epub 2021 Mar 13.

Abstract

X-linked agammaglobulinemia is a rare primary immunodeficiency due to a BTK mutation. The patients are characteristically deficient in peripheral B cells and serum immunoglobulins. While they are susceptible to infections caused by bacteria, enteroviruses, and parasites, fungal infections are uncommon in XLA patients. Here, we report a boy of Malay ethnicity who suffered from recurrent upper respiratory tract infections and severe progressive necrotizing fasciitis caused by Saksenaea erythrospora. Immunological tests showed a B cell deficiency and hypogammaglobulinemia. Whole-exome sequencing identified a dinucleotide deletion (c.1580_1581del) in BTK, confirmed by Sanger sequencing and predicted to be disease causing by in silico functional prediction tools (Varsome and MutationTaster2) but was absent in the gnomAD database. This mutation resulted in a frameshift and premature termination (p.C527fs), which disrupted the protein structure. The mother was heterozygous at the mutation site, confirming her carrier status. Flow cytometric analysis of monocyte BTK expression showed it to be absent in the patient and bimodal in the mother. This study describes a novel BTK mutation in a defined hotspot and an atypical fungal phenotype in XLA. Further studies are required to understand the pathogenesis of fungal infection in XLA.

摘要

X 连锁无丙种球蛋白血症是一种罕见的原发性免疫缺陷病,由 BTK 突变引起。患者外周血 B 细胞和血清免疫球蛋白明显减少。虽然他们易受细菌、肠道病毒和寄生虫感染,但 XLA 患者的真菌感染并不常见。在这里,我们报告了一名马来族男孩,他患有复发性上呼吸道感染和由红酵母引起的严重进行性坏死性筋膜炎。免疫检查显示 B 细胞缺陷和低丙种球蛋白血症。全外显子组测序发现 BTK 中存在二核苷酸缺失(c.1580_1581del),经 Sanger 测序证实,并通过计算机功能预测工具(Varsome 和 MutationTaster2)预测为致病突变,但在 gnomAD 数据库中不存在。该突变导致移码和过早终止(p.C527fs),破坏了蛋白质结构。母亲在突变部位为杂合子,证实了她的携带者状态。单核细胞 BTK 表达的流式细胞分析显示患者缺失,母亲呈双峰。本研究描述了 X 连锁无丙种球蛋白血症中一个明确热点的新型 BTK 突变和一种非典型真菌表型。需要进一步研究以了解 X 连锁无丙种球蛋白血症中真菌感染的发病机制。

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