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Myocardial Edema, Myocyte Injury, and Disease Severity in Fabry Disease.

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Background Cardiovascular magnetic resonance can demonstrate myocardial processes in Fabry disease (FD), such as low native T1 (sphingolipid storage) and late gadolinium enhancement (LGE, scar). Recently, high T2 (edema) has been observed in the basal inferolateral wall along with troponin

Association of Nonuveitic Retinal Vasculitis and Tractional Retinoschisis With Cystoid Macular Edema With Fabry Disease.

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Fabry disease and chemosis.

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OBJECTIVE To report the case of a patient with Fabry disease (FD) whose ocular presentation with chronic chemosis we feel is related to FD and to describe the conjunctival fluorescein angiographic findings. METHODS A 51-year-old male patient with FD on enzyme replacement therapy presented with

Diffuse thin glomerular basement membrane in association with Fabry disease in a Chinese female patient.

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We report a 41-year-old Chinese female with Fabry disease and diffuse thinning of the glomerular basement membrane (GBM). The patient presented with peripheral edema, mild proteinuria, microscopic hematuria, normal renal function, hypertension and tinnitus. Family screening showed that her daughter

Pathohistological and ultrastructural study of systemic vasculopathy (Fabry disease).

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Pathomorphological analysis of skin biopsy specimens from patients with Fabry disease showed edema and mucoid swelling of vascular walls in the skin, pronounced telangiectasias, endotheliocyte degeneration and death, compensatory proliferation of pericytes, and mast cell hyperplasia. Ultrastructural

Anderson-Fabry disease: a multiorgan disease.

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Fabry disease (FD) is a rare X-linked lysosomal storage disorder caused by a deficiency of the enzyme α-galactosidase A. FD causes glycolipids, such as globotriaosylceramide (Gb3), to accumulate in the vascular endothelium of several organs (Fig. 2), including the skin, kidneys, nervous system, and

Fabry disease: recognition and management of cutaneous manifestations.

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Fabry disease (angiokeratoma corporis diffusum universale) is a rare, X chromosome-linked lysosomal storage disease. The deficient enzyme, alpha-galactosidase A (alpha-gal A), is responsible for the accumulation of neutral glycosphingolipids within vascular endothelial lysosomes of various organs,

Fabry Disease Presenting with Hypertrophic Cardiomyopathy and Tricuspid Regurgitation.

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A 71-year-old female who was diagnosed with nonobstructive hypertrophic cardiomyopathy since 1999 presented with dyspnea and severe edema on both legs. For the management of her symptom, cardiac surgery including tricuspid annuloplasty, Maze operation and right atrial reduction plasty was performed.

Clinical and molecular characterization of an extended family with Fabry disease.

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OBJECTIVE To characterize clinical manifestations, biochemical changes, mutation of alpha-Galactosidase (alpha-Gal A) gene A (GLA), and functional capability of mutant protein. METHODS Seventeen subjects from a family with a newly diagnosed patient with Fabry disease were enrolled in the present

Effectiveness of immunosuppressive therapy for nephrotic syndrome in a patient with late-onset Fabry disease: a case report and literature review.

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Fabry disease (FD) is an X-linked lysosomal storage disorder caused by mutations of the GLA gene, followed by deficiency in α-galactosidase A (α-gal) activity. Nephrotic syndrome, as the renal phenotype of FD, is unusual. Here, we report the rare case of a patient with FD with

Post-transplant de-novo renal phospholipidosis in a kidney transplant recipient: Fabry disease or something else?

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Renal phospholipidosis is a rare cause of proteinuria and kidney dysfunction. We describe a kidney transplant recipient who presented with slowly rising serum creatinine, nephrotic range proteinuria, and lower extremity edema 10 years post transplant. He was diagnosed with renal phospholipidosis on

[Two cases of heterozygous Fabry disease].

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We report two cases of heterozygous Fabry disease with severe organ damage. Case 1 was a 47-year-old woman. In April 1977, at the age of 27 years, she had proteinuria and edema around the 26th week of her second pregnancy and was diagnosed as toxicosis of pregnancy. She had proteinuria after the

Clinic-Pathologic Features and Renal Outcome of Fabry Disease: Data from a Chinese Cohort.

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BACKGROUND Fabry disease (FD) with life-threatening complications occurs as a result of organ damage in kidneys, heart, and brain. Only a few studies, especially from Asia, report their long-term outcome. METHODS In this monocentric study, patients with Fabry nephropathy confirmed by renal biopsy

Immune-Mediated Myocarditis in Fabry Disease Cardiomyopathy.

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Background Glycosphingolipid accumulation in Fabry cells generates a proinflammatory response that may influence disease evolution and responsiveness to enzyme replacement therapy. This study evaluated incidence, mechanism, and impact of myocarditis in Fabry disease cardiomyopathy ( FDCM ). Methods

Quantitative Myocardial Perfusion in Fabry Disease.

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Fabry disease (FD) is an X-linked lysosomal storage disease resulting in tissue accumulation of sphingolipids. Key myocardial processes that lead to adverse outcomes in FD include storage, hypertrophy, inflammation, and fibrosis. These are quantifiable by multiparametric cardiovascular

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