Published online Jan 21, 2022. doi: 10.12998/wjcc.v10.i3.1067
Peer-review started: June 22, 2021
First decision: July 26, 2021
Revised: August 9, 2021
Accepted: December 23, 2021
Article in press: December 23, 2021
Published online: January 21, 2022
Processing time: 207 Days and 4 Hours
Fabry disease (FD) is a rare X-linked lysosomal storage disease caused by a deficiency of the enzyme α-galactosidase A.
Herein, we analyzed a four-generation Chinese family. The proband is a 57-year-old woman who was diagnosed with left ventricular hypertrophy and atrial fibrillation 7 years ago. Echocardiography showed an end-diastolic diameter of the interventricular septum of 19.9 mm, left ventricular end-diastolic diameter of 63.1 mm, and moderate-to-severe mitral regurgitation. Cardiac magnetic resonance indicated an enlarged left heart and right atrium, decreased left ventricular systolic and diastolic function, a left ventricular ejection fraction of 20%, and thickening of the left ventricular septum. In March 2019, gene and enzyme activity tests confirmed the diagnosis of FD. Her son was diagnosed with FD after gene and enzyme activity assay, and was prescribed agalsidase-β for enzyme replacement therapy in July 2020. Two sisters of the proband were also diagnosed with FD by genetic testing. Both of them had a history of atrial fibrillation.
A novel mutation was identified in a Chinese family with FD, in which the male patient had a low level of enzyme activity, early-onset, and severe organ involvement. Comprehensive analysis of clinical phenotype genetic testing and enzyme activity testing helped in the diagnosis and treatment of this FD family.
Core Tip: Fabry disease (FD) is a rare X-linked lysosomal storage disorder caused by a deficiency of α-galactosidase A. We present herein a case of novel mutation (348delG:p.G116fs) in exon 2 in a Chinese FD family. Time delay in the diagnosis was 6 years. The proband died of respiratory circulatory failure. The son of the proband had a low level of enzyme activity, early-onset, and severe organ involvement. He was prescribed agalsidase-β for enzyme replacement therapy to delay progression of the disease. This case highlights that clinical phenotype, gene detection, and enzyme activity results should be analyzed comprehensively for patients suspected of having FD.