Search results for "Trihexosylceramides"

showing 10 items of 11 documents

Genetics and Gene Therapy of Anderson-Fabry Disease.

2018

Fabry's disease is a genetic disorder of X-linked inheritance caused by mutations in the alpha galactosidase A gene resulting in deficiency of this lysosomal enzyme. The progressive accumulation of glycosphingolipids, caused by the inadequate enzymatic activity, is responsible of organ dysfunction and thus of clinical manifestations. In the presence of a high clinical suspicion, a careful physical examination and specific laboratory tests are required, finally diagnosis of Fabry's disease is confirmed by the demonstration of absence or reduced alpha-galactosidase A enzyme activity in hemizygous men and gene typing in heterozygous females; in fact the performance of enzymatic activity assay …

0301 basic medicineGenetic enhancementChaperone therapyDisease030204 cardiovascular system & hematologyBioinformaticsMice0302 clinical medicineAlpha galactosidase ADrug DiscoveryGenetics (clinical)KidneybiologyTrihexosylceramidesGenetic disorderEnzyme replacement therapyDependovirusRecombinant ProteinsAlpha galactosidase A; Chaperone therapy; Enzyme replacement therapy; Fabry disease; Gene therapy; Viral vectors; Molecular Medicine; Molecular Biology; Genetics; Drug Discovery3003 Pharmaceutical Science; Genetics (clinical)Isoenzymesmedicine.anatomical_structureMolecular Medicinemedicine.symptomGenetic Vectors03 medical and health sciencesGene therapyViral vectorRare DiseasesGeneticGeneticsmedicineAnimalsHumansEnzyme Replacement TherapyMolecular BiologyAlpha-galactosidasebusiness.industryDrug Discovery3003 Pharmaceutical ScienceOrgan dysfunctionGenetic Therapymedicine.diseaseFabry diseaseDisease Models Animal030104 developmental biologyalpha-GalactosidaseMutationbiology.proteinFabry DiseasebusinessBiomarkersCurrent gene therapy
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Standardising clinical outcomes measures for adult clinical trials in Fabry disease: A global Delphi consensus.

2021

International audience; Background: Recent years have witnessed a considerable increase in clinical trials of new investigational agents for Fabry disease (FD). Several trials investigating different agents are currently in progress; however, lack of standardisation results in challenges to interpretation and comparison. To facilitate the standardisation of investigational programs, we have developed a common framework for future clinical trials in FD.Methods and findings: A broad consensus regarding clinical outcomes and ways to measure them was obtained via the Delphi methodology. 35 FD clinical experts from 4 continents, representing 3389 FD patients, participated in 3 rounds of Delphi p…

0301 basic medicineMaleDelphi TechniqueEndocrinology Diabetes and Metabolism[SDV]Life Sciences [q-bio]Delphi methodDisease030105 genetics & heredityKidneyBiochemistry0302 clinical medicineEndocrinologyClinical outcomesClinical Trials as TopicGlobosidesTrihexosylceramidesMiddle Aged3. Good healthClinical trialIsoenzymesTreatment OutcomeInclusion and exclusion criteriaSecondary Outcome MeasureFemaleAdultmedicine.medical_specialtyConsensusLysosomal storage disorders03 medical and health sciencesQuality of life (healthcare)Inherited metabolic disordersGeneticsmedicineHumansEnzyme Replacement TherapyIntensive care medicineMolecular BiologyFabry diseaseSphingolipidsbusiness.industryClinical study designmedicine.diseaseFabry diseaseClinical trialDelphi consensusalpha-GalactosidaseQuality of LifeFabry DiseaseGlycolipidsbusiness030217 neurology & neurosurgeryMolecular genetics and metabolism
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Low-dose agalsidase beta treatment in male pediatric patients with Fabry disease: A 5-year randomized controlled trial.

2019

Abstract Background Fabry disease is a rare, X-linked, lifelong progressive lysosomal storage disorder. Severely deficient α-galactosidase A activity in males is associated with the classic phenotype with early-onset, multisystem manifestations evolving to vital organ complications during adulthood. We assessed the ability of 2 low-dose agalsidase beta regimens to lower skin, plasma, and urine globotriaosylceramide (GL-3) levels, and influence clinical manifestations in male pediatric Fabry patients. Methods In this multicenter, open-label, parallel-group, phase 3b study, male patients aged 5–18 years were randomized to receive agalsidase beta at 0.5 mg/kg 2-weekly (n = 16) or 1.0 mg/kg 4-w…

0301 basic medicineMalemedicine.medical_specialtyAbdominal painAdolescentEndocrinology Diabetes and MetabolismGlobotriaosylceramideUrologyRenal function030105 genetics & heredityBiochemistrylaw.invention03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEndocrinologyRandomized controlled triallawBiopsyGeneticsmedicineHumansEnzyme Replacement TherapyChildMolecular BiologySkinKidneymedicine.diagnostic_testDose-Response Relationship Drugbusiness.industryTrihexosylceramidesEnzyme replacement therapymedicine.diseaseFabry diseaseIsoenzymesmedicine.anatomical_structureTreatment OutcomechemistryChild Preschoolalpha-GalactosidaseFabry Diseasemedicine.symptombusiness030217 neurology & neurosurgeryMolecular genetics and metabolism
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Quantification of the Fabry marker lysoGb3 in human plasma by tandem mass spectrometry

2011

Morbus Fabry is a hereditary metabolic disorder with low prevalence and late clinical manifestation. A defect in the α-galactosidase gene leads to lysosomal accumulation of the glycolipid globotriaosylceramide (Gb3). Gb3 may be used for monitoring of enzyme replacement therapy (ERT), but diagnostic sensitivity is limited. Recently, globotriaosylsphingosine (lysoGb3) was introduced as a promising new marker with significantly better sensitivity. For Fabry diagnosis, clinical studies and possible therapy monitoring, we established a fast and reliable LC-MS/MS assay for quantification of lysoGb3 in human plasma. Protein precipitation and glycolipid extraction from EDTA plasma was performed usi…

AdultMaleAnalyteMolecular Sequence DataClinical BiochemistryGlobotriaosylceramideChemical FractionationTandem mass spectrometryBiochemistryHigh-performance liquid chromatographyAnalytical Chemistrychemistry.chemical_compoundTandem Mass SpectrometrymedicineHumansProtein precipitationDerivatizationChromatography High Pressure LiquidSphingolipidsChromatographyElutionTrihexosylceramidesReproducibility of ResultsCell BiologyGeneral Medicinemedicine.diseaseFabry diseaseCarbohydrate SequencechemistryCase-Control StudiesLinear ModelsFabry DiseaseFemaleGlycolipidsBiomarkersJournal of Chromatography B
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Changes in plasma and urine globotriaosylceramide levels do not predict Fabry disease progression over 1 year of agalsidase alfa.

2013

Globotriaosylceramide concentrations were assessed as potential predictors of change from baseline after 12 months by estimated glomerular filtration rate and left-ventricular mass index using pooled data from three randomized, placebo-controlled agalsidase alfa trials and open-label extensions of patients with Fabry disease.Males (aged 18 years or older) with Fabry disease received agalsidase alfa (0.2 mg/kg every other week for 12 months). A backward-elimination approach evaluated potential predictors (baseline estimated glomerular filtration rate and left-ventricular mass index; age at first dose; baseline and change from baseline at 12 months of globotriaosylceramide (urine, plasma); ur…

AdultMalemedicine.medical_specialtyHeart VentriclesUrologyGlobotriaosylceramideRenal functionUrinechemistry.chemical_compoundYoung Adultstomatognathic systemDouble-Blind MethodMedicineHumansRenal Insufficiency Chronicskin and connective tissue diseasesGenetics (clinical)Alpha-galactosidasebiologybusiness.industryTrihexosylceramidesvirus diseasesEnzyme replacement therapyMiddle Agedmedicine.diseaseFabry diseasedigestive system diseasesRecombinant ProteinsIsoenzymesTreatment Outcomechemistryalpha-Galactosidasebiology.proteinDisease ProgressionBiomarker (medicine)Fabry Diseasesense organsbusinessBiomarkersKidney diseaseGlomerular Filtration RateGenetics in medicine : official journal of the American College of Medical Genetics
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Enzyme replacement therapy in heterozygous females with Fabry disease: results of a phase IIIB study.

2003

Summary: Fabry disease is an X-linked glycosphingolipid storage disorder caused by a deficiency of α-galactosidase A. Affected patients experience debilitating neuropathic pain and have premature mortality due to renal failure, cardiovascular disease or cerebrovascular complications. The disease may be X-linked dominant, since most females heterozygous for Fabry disease are affected clinically. We evaluated the safety, efficacy and pharmacokinetics of agalsidase alfa (Replagal) administered intravenously to female patients with Fabry disease in an open-label, single-centre study. Fifteen severely affected patients received agalsidase alfa at 0.2 mg/kg every other week for up to 55 weeks. Ag…

Adultmedicine.medical_specialtyHeterozygoteAdolescentArthritisRenal functionKidneyGastroenterologyAntibodiesArthritis RheumatoidElectrocardiographyPharmacokineticsInternal medicineGeneticsmedicineHumansGenetics (clinical)Vascular diseasebusiness.industryTrihexosylceramidesEnzyme replacement therapymedicine.diseaseFabry diseaseRecombinant ProteinsSurgeryClinical trialIsoenzymesEchocardiographyalpha-GalactosidaseNeuropathic painMutationFabry DiseaseFemalebusinessJournal of inherited metabolic disease
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Determination of globotriaosylceramide in plasma and urine by mass spectrometry

2009

Abstract Background: Fabry disease is an X-chromosomally inherited lysosomal storage disorder leading to accumulation of glycosphingolipids, mainly globotriaosylceramide (ceramide-trihexoside, Gb3). Concentrations of Gb3 in plasma and urine have been used to diagnose Fabry disease and to monitor enzyme replacement therapy with recombinant α-galactosidase. Methods: Gb3 was purified from plasma or urine by combined liquid extraction/protein precipitation and solid-phase extraction, and was detected by flow-injection analysis electrospray mass spectrometry (MS) using multi-reaction-monitoring. Calibration was performed via standard addition using C17-Gb3 as internal standard. The most abundant…

MaleCoefficient of variationClinical BiochemistryGlobotriaosylceramideUrinechemistry.chemical_compoundTandem Mass SpectrometryLiquid chromatography–mass spectrometryBlood plasmamedicineHumansProtein precipitationEnzyme Replacement TherapyChromatographyTrihexosylceramidesSolid Phase ExtractionBiochemistry (medical)General MedicineReference Standardsmedicine.diseaseFabry diseaseLysosomal Storage Diseaseschemistryalpha-GalactosidaseStandard additionCalibrationFabry DiseaseFemaleChromatography Liquidcclm
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Enzyme replacement therapy with agalsidase alfa in children with Fabry disease.

2006

Aim: To assess the effects of enzyme replacement therapy (ERT) in children with Fabry disease. Methods: Safety and efficacy of ERT with agalsidase alfa, 0.2 mg/kg infused over 40 minutes every 2 weeks for 23 weeks, were studied in a multicentre open-label trial in nine boys and four girls. Median age at the start of the study was 11.0 years (range 3.5–18 years). Results: Fifty-four adverse events were reported in 11 patients. No serious adverse events related to ERT were reported. Twelve of the 54 adverse events were considered possibly or probably related to ERT. Infusion reactions (8 mild, 3 moderate) occurred in four boys, in seven infusions. One boy developed IgG antibodies, although he…

MalePediatricsmedicine.medical_specialtyAdolescentGlobotriaosylceramideSweatingchemistry.chemical_compoundQuality of lifemedicineHumansBrief Pain InventoryAdverse effectChildPain Measurementbusiness.industryTrihexosylceramidesGeneral MedicineEnzyme replacement therapymedicine.diseaseFabry diseaseRecombinant ProteinsSurgeryClinical trialIsoenzymesTreatment OutcomeEl NiñochemistryChild Preschoolalpha-GalactosidasePediatrics Perinatology and Child HealthFabry DiseaseFemalebusinessActa paediatrica (Oslo, Norway : 1992)
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Pathogenesis and molecular mechanisms of anderson–fabry disease and possible new molecular addressed therapeutic strategies

2021

Anderson–Fabry disease (AFD) is a rare disease with an incidenceof approximately 1:117,000 male births. Lysosomal accumulation of globotriaosylceramide (Gb3) is the element characterizing Fabry disease due to a hereditary deficiency α-galactosidase A (GLA) enzyme. The accumulation of Gb3 causes lysosomal dysfunction that compromises cell signaling pathways. Deposition of sphingolipids occurs in the autonomic nervous system, dorsal root ganglia, kidney epithelial cells, vascular system cells, and myocardial cells, resulting in organ failure. This manuscript will review the molecular pathogenetic pathways involved in Anderson–Fabry disease and in its organ damage. Some studies reported that i…

ReviewConstriction Pathologicendothelial dysfunctionPathogenesisMicechemistry.chemical_compoundKCa3.1 activitypodocyturiaProtein IsoformsEndothelial dysfunctionBiology (General)SpectroscopyglobotriaosylceramideGlobosidesMicrogliabiologyTOR Serine-Threonine KinasesTrihexosylceramidesmiR-26a-5pGeneral MedicineMitochondriaComputer Science ApplicationsCell biologymiR-152-5pChemistrymedicine.anatomical_structureCerebrovascular CirculationAnderson–Fabry disease Endothelial dysfunction Globotriaosylceramide KCa3.1 activity MiR-1307-5p MiR-152-5p MiR-21-5p MiR-26a-5p Podocyturia Valvular dysfunctionmiR-21-5pSignal TransductionQH301-705.5GlobotriaosylceramideCatalysisInorganic ChemistryAutophagymedicineAnimalsHumansEnzyme Replacement TherapyPhysical and Theoretical ChemistryMolecular BiologyMechanistic target of rapamycinQD1-999PI3K/AKT/mTOR pathwaySphingolipidsAnderson–Fabry diseasebusiness.industryMicrocirculationOrganic ChemistryEndothelial Cellsmedicine.diseaseFabry diseaseSphingolipidMicroRNAschemistrymiR-1307-5palpha-Galactosidasebiology.proteinFabry DiseaseGlycolipidsvalvular dysfunctionLysosomesbusiness
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Fabry Disease With Concomitant Lewy Body Disease

2019

AbstractAlthough Gaucher disease can be accompanied by Lewy pathology (LP) and extrapyramidal symptoms, it is unknown if LP exists in Fabry disease (FD), another progressive multisystem lysosomal storage disorder. We aimed to elucidate the distribution patterns of FD-related inclusions and LP in the brain of a 58-year-old cognitively unimpaired male FD patient suffering from predominant hypokinesia. Immunohistochemistry (CD77, α-synuclein, collagen IV) and neuropathological staging were performed on 100-µm sections. Tissue from the enteric or peripheral nervous system was unavailable. As controls, a second cognitively unimpaired 50-year-old male FD patient without LP or motor symptoms and 3…

complications [Lewy Body Disease]MalePathologyAutopsyDisease0302 clinical medicineHypokinesiapathology [Brain]Lysosomal storage diseasespathology [Neurons]metabolism [alpha-Synuclein]metabolism [Fabry Disease]pathology [Astrocytes]Neuronsα-Synuclein0303 health sciencesParkinsonismTrihexosylceramidesBrainGeneral MedicineMiddle AgedParkinson diseasecomplications [Fabry Disease]Neurologymetabolism [Neurons]alpha-Synucleinmedicine.symptomLewy Body Diseasemedicine.medical_specialtymetabolism [Lewy Body Disease]Context (language use)Substantia nigrametabolism [Trihexosylceramides]Pathology and Forensic Medicineblood supply [Brain]03 medical and health sciencesCellular and Molecular Neuroscienceα-Galactosidase AmedicineHumansddc:610030304 developmental biologypathology [Lewy Bodies]Fabry diseasebusiness.industryPars compactapathology [Lewy Body Disease]Lewy bodies/neuritesOriginal Articlesmetabolism [Lewy Bodies]medicine.diseaseFabry diseasemetabolism [Brain]AstrocytesLewy BodiesNeurology (clinical)CD77pathology [Fabry Disease]business030217 neurology & neurosurgeryJournal of Neuropathology and Experimental Neurology
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