Case Report: VEXAS syndrome with extensive pulmonary, cardiac, and skeletal involvement

病例报告:伴有广泛肺、心脏和骨骼受累的VEXAS综合征

阅读:1

Abstract

VEXAS syndrome is a rare and severe systemic inflammatory disorder caused by somatic mutations in the X-linked UBA1 gene, primarily affecting men. Since its initial description in 2020, it has been recognized for its complex clinical phenotype and tendency to be misdiagnosed. We report a case of a 77-year-old Chinese man diagnosed with VEXAS syndrome. The patient presented with recurrent fever, elevated inflammatory markers, anemia (decreased hemoglobin), multifocal interstitial pneumonia, and cardiac arrhythmia. On the day of admission, the patient developed rapidly progressive respiratory distress with a marked worsening of inflammatory markers. While providing supportive symptomatic treatment, we performed next-generation sequencing (NGS), 18F-fluorodeoxyglucose positron emission tomograph-computed tomography (18FDG PET-CT), and whole-exome sequencing. Based on a presumed clinical diagnosis of small-vessel vasculitis, the patient was empirically treated with glucocorticoids combined with intravenous immunoglobulin (IVIG). Once the patient's condition improved, whole-exome sequencing revealed a UBA1 splice-site mutation (c.118-1G>C), consistent with VEXAS syndrome. After reviewing related reports, we subsequently performed a bone marrow aspiration, which showed characteristic cytoplasmic vacuolization in myeloid precursor cells. Retrospective history review revealed that the patient had developed skin lesions one year before the onset of fever. The clinical presentation of VEXAS syndrome is heterogeneous and associated with high mortality. It can be difficult to distinguish VEXAS from other autoimmune diseases, hematologic malignancies, and infectious diseases. In this case, given the patient's rapidly progressive interstitial pneumonia, we used NGS and 18FDG PET-CT to exclude infection and hematologic malignancy, and focused on empirical treatment for presumed small-vessel vasculitis, which quickly halted disease progression. Meanwhile, whole-exome sequencing ultimately identified the underlying cause.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。