fabry disease/صداع

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A Sporadic Case of Fabry Disease Involving Repeated Fever, Psychiatric Symptoms, Headache, and Ischemic Stroke in an Adult Japanese Woman.

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Fabry disease can cause various neurological manifestations. We describe the case of a Japanese woman with Fabry disease who presented with ischemic stroke, aseptic meningitis, and psychiatric symptoms. The patient had a mutation in intron 4 of her α-galactosidase A gene, which was not detected in

Fabry disease in children: agalsidase-beta enzyme replacement therapy.

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Fabry disease is a rare, multiorgan disease. The most serious complications involve the kidney, brain and heart. This study aims to assess the effect of enzyme replacement therapy (ERT) using agalsidase-beta in children with Fabry disease. We carried out a nationwide, descriptive and observational

An open-label clinical trial of agalsidase alfa enzyme replacement therapy in children with Fabry disease who are naïve to enzyme replacement therapy.

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BACKGROUND Following a drug manufacturing process change, safety/efficacy of agalsidase alfa were evaluated in enzyme replacement therapy (ERT)-naïve children with Fabry disease. METHODS In an open-label, multicenter, Phase II study (HGT-REP-084; Shire), 14 children aged ≥7 years received 0.2 mg/kg

Fabry disease: case report with emphasis on enzyme replacement therapy and possible future therapeutic options.

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A 38-year-old male Caucasian with Fabry disease presented with angiokeratomas and tortuous conjunctival and retinal vessels. Additionally, the patient showed characteristic skin lesions of psoriasis and seborrheic dermatitis. His past medical history revealed anhidrosis, acral paresthesias,

[Early diagnosis of Fabry disease in children].

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Fabry disease, a rare X-linked lysosomal storage disorder, is caused by deficiency of the enzyme α-galactosidase A. The incidence, ranging from one over 40 000 to one over 11 7000 worldwide is probably underestimated due to its unspecific pattern of presentation. The symptoms, including

Galactosidase Alpha p.A143T Variant Fabry Disease May Result in a Phenotype With Multifocal Microvascular Cerebral Involvement at a Young Age.

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UNASSIGNED A 16-year-old male presented with episodic headaches and a brain magnetic resonance imaging (MRI) that showed multifocal punctate to patchy white matter lesions. The diagnosis of Fabry disease (FD) was suggested upon the finding of significantly reduced plasma alpha-galactosidase A

Aseptic meningitis and ischaemic stroke in Fabry disease.

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BACKGROUND Fabry disease (OMIM 301 500) is an X-linked lysosomal storage disease. Neurological symptoms in Fabry disease mainly include stroke, acroparesthesia, cranial nerve palsies and autonomic dysfunction. We report on aseptic meningitis in Fabry patients. METHODS Clinical analysis, brain

A Retrospective Survey Studying the Impact of Fabry Disease on Pregnancy.

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Fabry disease (FD) is a lysosomal storage disorder resulting from a deficiency of lysosomal enzyme α-galactosidase A (α-gal A). Reduced or missing α-gal A enzyme results in the storage of globotriaosylceramide (GL3) and related glycosphingolipids in the cellular lysosomes throughout the body. The

[Psychiatric and neuropsychological signs and symptoms in patients with fabry disease: literature review].

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Fabry Disease (FD) is an X-linked lysosomal storage disorder (prevalence about 1 : 100 000) caused by a genetic defect associated with a lack of alpha-galactosidase A (alpha-GAL) enzyme activity. As a consequence, neutral glycosphingolipides can not be cleaved and metabolized, and accumulate in

Fabry disease in patients with migraine with aura.

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Anderson-Fabry disease (AFD) is an X-linked recessive lysosomal disease caused by alpha-galactosidase A (alpha-gal) deficiency, causing progressive glycosphingolipid storage in various organ systems. Headache is a frequent symptom. Cerebral magnetic resonance imaging (MRI) often shows multiple white

Social preference weights for treatments in Fabry disease in the UK: a discrete choice experiment.

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Fabry disease is a rare inherited lysosomal storage disorder caused by deficiency of α-galactosidase A. Effective enzyme replacement therapies are available that are administered intravenously. However, a new oral treatment is being developed as an alternative option for patients with amenable

Pregnancy Outcome after Exposure to Migalastat for Fabry Disease: A Clinical Report.

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Our patient was a 37-year-old woman with Fabry disease (GLA p.R112H) with a medical history of recurrent headache, nausea, vomiting, vertigo, and tobacco use (20 cigarettes/day). Fabry disease was diagnosed in 2005 when she experienced proteinuria, preeclampsia, and hypertension (201/130 mm

[Clinical stability of Fabry disease in 54 months' enzyme replacement therapy--follow-up of the first Polish study].

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We present outcomes of 54 months' agalsidase beta enzyme replacement therapy of two 48- and 46-year-old brothers with Fabry disease. The diagnosis was confirmed in 1997, and at that moment serious damage of internal organs was observed. During enzyme replacement therapy in both brothers the

Brain MRI findings in children and adolescents with Fabry disease.

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OBJECTIVE To evaluate the presence of white matter and hemorrhagic lesions in brain MRI of children and adolescents with Fabry disease (FD). METHODS Brain MRI studies in 44 consecutive children and teenagers (20 boys, mean age 14.6 years, range 7-21 years) were evaluated using classic sequences as

The early clinical phenotype of Fabry disease: a study on 35 European children and adolescents.

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Fabry disease (FD) is a debilitating progressive multisystem X-linked lysosomal storage disorder. It was generally believed that the disease affects only adult males. Through systematic pedigree analysis, we identified 35 paediatric FD patients (age 1 to 21 years, mean 12.6 years) in 25 families.

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