Wakakuri Hiroaki, Nakamura Shunichi, Utsumi Kouichi, Shimizu Wataru, Yasutake Masahiro
Department of General Medicine and Health Science, Nippon Medical School.
Int Heart J. 2016 Sep 28;57(5):637-9. doi: 10.1536/ihj.15-475. Epub 2016 Sep 5.
Fabry disease, an X-linked lysosomal storage disorder due to α-galactosidase A deficiency, is associated with dysfunction of various cell types and results in a systemic vasculopathy. We describe a 29-year-old woman with Fabry disease presenting with severe cardiac and renal manifestations. Gene analysis demonstrated a novel mutation (K391E) in the GLA gene. Enzyme replacement therapy (ERT) was started with agalsidase-β after confirming the diagnosis of Fabry disease, resulting in normalization of LV systolic function and improvement of renal function. As early therapy is crucial for preventing life-threatening sequelae, clinicians should consider Fabry disease in young patients presenting with cardiac and renal disease without any likely causes.
法布里病是一种由于α-半乳糖苷酶A缺乏引起的X连锁溶酶体贮积症,与多种细胞类型功能障碍相关,并导致系统性血管病变。我们描述了一名29岁患有法布里病的女性,她出现了严重的心脏和肾脏表现。基因分析显示GLA基因存在一种新的突变(K391E)。在确诊法布里病后开始使用阿加糖酶β进行酶替代治疗(ERT),结果左心室收缩功能恢复正常,肾功能得到改善。由于早期治疗对于预防危及生命的后遗症至关重要,临床医生应考虑到在患有心脏和肾脏疾病且无任何可能病因的年轻患者中存在法布里病的可能性。