Case of IgG4-Related Disease Presenting With Dissecting Aneurysms in the Bilateral Internal Iliac Arteries After the Resolution of Periarteritis

一例IgG4相关疾病患者,在动脉周围炎消退后出现双侧髂内动脉夹层动脉瘤。

阅读:1

Abstract

In this report, we present the case of an 83-year-old man diagnosed with IgG4-related disease (IgG4-RD) who developed dissecting aneurysms in the internal iliac arteries post-resolution of bilateral periarteritis. The patient initially presented with weight loss, anemia, and lymphadenopathy for over 13 years without a definitive diagnosis. Laboratory tests revealed elevated serum IgG4 levels and decreased complement levels, leading to a diagnosis of IgG4-RD. This was confirmed by a biopsy of the left axillary lymph node, which showed dense infiltration of IgG4-positive plasma cells. Contrast-enhanced CT revealed extensive periarterial soft tissue masses around the thoracic aorta, thoracic vertebrae, mediastinum, and internal iliac arteries, which were significantly reduced after the initiation of corticosteroid therapy with high dose prednisolone. Despite the initial improvement in clinical and radiological findings, the patient subsequently developed dissecting aneurysms in both internal iliac arteries. The right internal iliac artery aneurysm exhibited rapid enlargement, necessitating endovascular treatment with stent grafts to prevent rupture. This case highlights the complexity of vascular involvement in IgG4-RD, underscoring the need for careful monitoring even after apparent disease improvement. Although arterial wall thickening improves, the infiltration of IgG4-positive plasma cells persists indicating that the risks of aneurysm and arterial dissection remain. This is the sparsely reported case of bilateral dissecting aneurysms of the internal iliac arteries associated with IgG4-RD, providing new insights into the vascular manifestations and management of IgG4-RD.

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。