Fabry disease is a lysosomal storage disease caused by alpha-galactosidase A deficiency. The classic presentation of Fabry disease involves multiple organs, including kidneys, heart, skin, eyes, and nervous system. Osteonecrosis is rarely reported in patients with Fabry disease. In this article, we describe the case of a 37-year-old white man who had Fabry disease and no risk factors for osteonecrosis but who developed osteonecrosis in both femoral heads and in an unusual site, bilateral distal tibiae. Results of mutation analysis showed a nonsense mutation (R227X) in the alpha-galactosidase A gene. This case suggests that Fabry disease may be a risk factor for development of osteonecrosis. The enzyme replacement therapy currently available may be an effective method of preventing this complication.
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Zhonghua Nei Ke Za Zhi
February 2025
Department of Nephrology, Children's Hospital of Nanjing Medical University, Nanjing210008, China.
Zhonghua Nei Ke Za Zhi
February 2025
Department of Cardiology, Peking University First Hospital, Beijing100034, China Institute of Cardiovascular Disease, Peking University First Hospital, Beijing100034, China Echocardiography Core Lab, Institute of Cardiovascular Disease, Peking University First Hospital, Beijing100034, China.
Zhonghua Nei Ke Za Zhi
February 2025
Department of Nephrology, Heze Municipal Hospital, Heze274000,China.
Ann Med
December 2025
Department of Neurology, Peking University First Hospital, China.
Objective: Whereas a few studies have evaluated vestibular involvement in Fabry disease (FD), the relationship between vestibular/oculomotor abnormalities and disease-specific biomarkers remain unclear. Therefore, we seek to evaluate these quantitatively and analyze their relationship with disease phenotype and biomarkers in FD.
Methods: This cohort study enrolled 37 Chinese FD patients registered in our center.
Int J Mol Sci
January 2025
Institute for Biomedical Research and Innovation (IRIB), National Research Council (CNR), 90146 Palermo, Italy.
Anderson-Fabry disease is a hereditary, progressive, multisystemic lysosomal storage disorder caused by a functional deficiency of the enzyme α-galactosidase A (α-GalA). This defect is due to mutations in the gene, located in the long arm of the X chromosome (Xq21-22). Functional deficiency of the α-GalA enzyme leads to reduced degradation and accumulation of its substrates, predominantly globotriaosylceramide (Gb3), which accumulate in the lysosomes of numerous cell types, giving rise to the symptomatology.
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