Search results for "enzyme replacement therapy"

showing 10 items of 125 documents

Cholelithiasis in Patients with Gaucher Disease type 1: Risk Factors and the Role of ABCG5/ABCG8 Gene Variants

2016

Background & Aim: Patients with Gaucher disease type 1 (GD1) show an altered lipid profile and a certain degree of insulin resistance, which might contribute to cholelithiasis (CL) and could possibly be associated with ABCG5/ABCG8 gene variants. We aimed to investigate the prevalence of CL in Caucasian adult patients with GD1 and the possible risk factors, including gene variants of the ABCG5/ABCG8 genes.
 Methods: 61 Caucasian patients with GD1 (38 female/23male), aged 18-62 years and 61 healthy subjects matched for age, gender and BMI, without CL, for comparison of lipid profiles. Data before start of enzyme replacement therapy (ERT) were recorded: clinical, haematological, sever…

AdultMale0301 basic medicineHeterozygotemedicine.medical_specialtyAdolescentLipoproteinsmedicine.medical_treatmentSplenectomyABCG8030105 genetics & heredityGastroenterologyWhite PeopleYoung Adult03 medical and health sciencesInsulin resistanceGene FrequencyCholelithiasisRisk FactorsInternal medicineGenotypePrevalencemedicineHumansEnzyme Replacement TherapyGenetic Predisposition to DiseaseATP Binding Cassette Transporter Subfamily G Member 5Genetic Association StudiesGaucher Diseasemedicine.diagnostic_testRomaniabusiness.industryATP Binding Cassette Transporter Subfamily G Member 8HomozygoteGastroenterologyCase-control studyGenetic VariationEnzyme replacement therapyMiddle Agedmedicine.diseaseCross-Sectional StudiesPhenotypeCase-Control StudiesGlucosylceramidaseFemaleLipid profilebusinessDyslipidemiaJournal of Gastrointestinal and Liver Diseases
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Analysis of Renal and Cardiac Outcomes in Male Participants in the Fabry Outcome Survey Starting Agalsidase Alfa Enzyme Replacement Therapy Before an…

2020

Rossella Parini,1,2 Guillem Pintos-Morell,3 Julia B Hennermann,4 Ting-Rong Hsu,5 Nesrin Karabul,6 Vasiliki Kalampoki,7 Andrey Gurevich,7 Uma Ramaswami8 On behalf of the FOS Study Group1Rare Metabolic Diseases Unit, MBBM Foundation, San Gerardo Hospital, Reference Centre for Hereditary Metabolic Disorders (MetabERN), Monza, Italy; 2TIGET Institute, IRCCS San Raffaele Hospital, Milan, Italy; 3Division of Rare Diseases, Reference Centre for Hereditary Metabolic Disorders (MetabERN), University Hospital Vall d’Hebron, Autonomous University of Barcelona, Barcelona, Spain; 4Villa Metabolica, Department of Pediatric and Adolescent Medicine, University Medical Center, Mainz, Germany; 5Dep…

AdultMale0301 basic medicinemedicine.medical_specialtyestimated glomerular filtration rateAdolescentPharmaceutical ScienceRenal functionLeft ventricular hypertrophyFabry Outcome SurveyYoung Adult03 medical and health sciences0302 clinical medicineInternal medicineDrug DiscoverymedicineHumansEnzyme Replacement TherapyEstimated glomerular filtration rateChildAgalsidase alfaOriginal ResearchRetrospective StudiesPharmacologyagalsidase alfaFabry diseaseProteinuriaDrug Design Development and Therapybusiness.industryLeft ventricular hypertrophyEnzyme replacement therapyMiddle Agedmedicine.diseaseFabry diseaseRecombinant Proteinsleft ventricular hypertrophyIsoenzymesTreatment Outcome030104 developmental biologyMale patientalpha-Galactosidase030220 oncology & carcinogenesisEnzyme replacement therapyCohortmedicine.symptombusinessAgalsidase alfa
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Long-term follow-up of endurance and safety outcomes during enzyme replacement therapy for mucopolysaccharidosis VI: Final results of three clinical …

2008

Abstract The objective of this study was to evaluate the long-term clinical benefits and safety of recombinant human arylsulfatase B (rhASB) treatment of mucopolysaccharidosis type VI (MPS VI: Maroteaux-Lamy syndrome), a lysosomal storage disease. Fifty-six patients derived from 3 clinical studies were followed in open-label extension studies for a total period of 97–260 Weeks. All patients received weekly infusions of rhASB at 1mg/kg. Efficacy was evaluated by (1) distance walked in a 12-minute walk test (12MWT) or 6-minute walk test (6MWT), (2) stairs climbed in the 3-minute stair climb (3MSC), and (3) reduction in urinary glycosaminoglycans (GAG). Safety was evaluated by compliance, adve…

AdultMaleArylsulfatase Bmedicine.medical_specialtyAdolescentN-Acetylgalactosamine-4-SulfataseEndocrinology Diabetes and MetabolismMucopolysaccharidosis type VIWalkingMotor ActivityPlaceboBiochemistryEndocrinologyInternal medicineGeneticsmedicineHumansChildAdverse effectMolecular BiologyGlycosaminoglycansMucopolysaccharidosis VIbusiness.industryMucopolysaccharidosis VIEnzyme replacement therapymedicine.diseaseRecombinant ProteinsSurgeryClinical trialMaroteaux–Lamy syndromeTreatment OutcomeChild PreschoolFemalebusinessFollow-Up StudiesMolecular Genetics and Metabolism
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Ocular Changes in Patients With Mucopolysaccharidosis I Receiving Enzyme Replacement Therapy

2007

Objective To describe the progression of ocular changes in patients with mucopolysaccharidosis I receiving enzyme replacement therapy. Methods Three male and five female patients with mucopolysaccharidosis I were followed up for 4 years while undergoing enzyme replacement therapy with α-L-iduronidase (Aldurazyme). Visual acuity, corneal clouding, intraocular pressure, ophthalmoscopy, and optic disc measurements were performed yearly. Results Vision remained stable in 5 patients and deteriorated by at least 2 Snellen lines in 3 patients. Deterioration in 2 of these patients was related to progressive corneal clouding. Visual acuities improved in 1 patient after bilateral penetrating keratopl…

AdultMaleIntraocular pressuremedicine.medical_specialtyVisual acuityAdolescentgenetic structuresMucopolysaccharidosis Imedicine.medical_treatmentOptic DiskVisual AcuityCorneal DiseasesIduronidaseDouble-Blind MethodOptic Nerve DiseasesMucopolysaccharidosis IHumansMedicineChildInfusions IntravenousPapilledemaIntraocular PressureCorneal transplantationbusiness.industryEnzyme replacement therapyRecombinant Proteinseye diseasesSurgeryOphthalmoscopyOphthalmologymedicine.anatomical_structureDisease ProgressionOptic nerveFemalesense organsmedicine.symptombusinessOptic discArchives of Ophthalmology
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The early clinical phenotype of Fabry disease: a study on 35 European children and adolescents.

2003

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. Predominant signs in this cohort were: acroparesthesia, hypohidrosis, and cornea verticillata. Neurological and psychological changes, such as tinnitus, recurrent vertigo, headache, diminished level of activity, fatigue, and depression were often observed. Angiokeratoma and gastrointestinal symptoms were frequent. Some patients also showed cardiac abnormalities. Six children and adolescents (three …

AdultMalePediatricsmedicine.medical_specialtyAdolescentDiseaseRisk AssessmentSeverity of Illness IndexCohort StudiesAge DistributionSeverity of illnessmedicineHumansCornea verticillataGenetic Predisposition to DiseaseSex DistributionChildDepression (differential diagnoses)business.industryIncidenceEnzyme replacement therapymedicine.diseasePrognosisFabry diseaseHealth SurveysAngiokeratomaSurgeryEuropePhenotypeChild PreschoolPediatrics Perinatology and Child HealthFabry DiseaseFemalemedicine.symptombusinessCohort studyEuropean journal of pediatrics
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Hearing impairment as an early sign of alpha-mannosidosis in children with a mild phenotype: Report of seven new cases.

2019

Alpha-mannosidosis (AM) is a very rare (prevalence: 1/500000 births) autosomal recessive lysosomal storage disorder. It is characterized by multi-systemic involvement associated with progressive intellectual disability, hearing loss, skeletal anomalies, and coarse facial features. The spectrum is wide, from very severe and lethal to a milder phenotype that usually progresses slowly. AM is caused by a deficiency of lysosomal alpha-mannosidase. A diagnosis can be established by measuring the activity of lysosomal alpha-mannosidase in leucocytes and screening for abnormal urinary excretion of mannose-rich oligosaccharides. Genetic confirmation is obtained with the identification of MAN2B1 muta…

AdultMalePediatricsmedicine.medical_specialtyAdolescentHearing lossAlpha-mannosidosisUrinary systemYoung Adultalpha-MannosidaseIntellectual DisabilityIntellectual disabilityExome SequencingGeneticsmedicineHumansChildHearing LossGenetics (clinical)Exome sequencingCoarse facial featuresbusiness.industrySiblingsEnzyme replacement therapymedicine.diseaseHypotoniaPhenotypeChild Preschoolalpha-MannosidosisFemalemedicine.symptombusinessLysosomesAmerican journal of medical genetics. Part A
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Pharmacokinetics, pharmacodynamics, and safety of moss-aGalactosidase A in patients with Fabry disease.

2019

Moss-aGalactosidase A (moss-aGal) is a moss-derived version of human α-galactosidase developed for enzyme replacement therapy in patients with Fabry disease. It exhibits a homogenous N-glycosylation profile with >90% mannose-terminated glycans. In contrast to mammalian cell produced α-galactosidase, moss-aGal does not rely on mannose-6-phosphate receptor mediated endocytosis but targets the mannose receptor for tissue uptake. We conducted a phase 1 clinical trial with moss-aGal in six patients with confirmed diagnosis of Fabry disease during a 28-day schedule. All patients received a single dose of 0.2 mg/kg moss-aGal by i.v.-infusion. Primary endpoints of the trial were safety and pharmaco…

AdultMalePhases of clinical researchPharmacologyExcretion03 medical and health sciencesPharmacokineticsGermanyGeneticsmedicineHumansEnzyme Replacement TherapyInfusions IntravenousGenetics (clinical)030304 developmental biology0303 health sciencesKidneySphingolipidsbusiness.industry030305 genetics & heredityEnzyme replacement therapyMiddle Agedmedicine.diseaseFabry diseasemedicine.anatomical_structureTreatment OutcomePharmacodynamicsalpha-GalactosidaseFabry DiseaseFemaleGlycolipidsbusinessMannose receptorJournal of inherited metabolic disease
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De novo mutation in a male patient with Fabry disease: a case report

2014

Abstract Background Fabry disease is an X-linked inherited metabolic condition where the deficit of the α-galactosidase A enzyme, encoded by the GLA gene, leads to glycosphingolipid storage, mainly globotriaosylceramide. To date, more than 600 mutations have been identified in human GLA gene that are responsible for FD, including missense and nonsense mutations, small and large deletions. Such mutations are usually inherited, and cases of de novo onset occur rarely. Case presentation In this article we report an interesting case of a 44-year-old male patient suffering from a severe form of Fabry disease, with negative family history. The patient showed signs such as cornea verticillata, ang…

AdultMaleProtein Foldingα-galactosidase ADe novo mutationNonsense mutationD165H mutationGlobotriaosylceramideMutation MissenseCase ReportBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundGermline mutationmedicineMissense mutationHumansPoint MutationThrombophiliaEnzyme Replacement TherapyAmino Acid SequenceChildGLA geneConserved SequenceGerm-Line MutationMedicine(all)GeneticsMutationFabry diseaseSequence Homology Amino AcidBiochemistry Genetics and Molecular Biology(all)Point mutationGeneral MedicineEnzyme replacement therapymedicine.diseaseFabry diseasePedigreeStrokechemistryAmino Acid Substitutionalpha-GalactosidaseKidney Failure ChronicFemaleSymptom AssessmentSequence AlignmentBMC Research Notes
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Thromboembolic events in Fabry disease and the impact of factor V Leiden

2015

Although several reports suggest an increased thromboembolic event rate, especially regarding strokes and TIAs at early age in patients with Fabry disease (FD), the risk for patients with FD to experience these events, the clinical relevance of additional risk factors including the concurrence of factor V Leiden (FVL), and the benefit of enzyme replacement therapy (ERT) regarding these events remain unclear.Three hundred four consecutively recruited patients with FD were evaluated for their lifetime occurrence of thromboembolic events such as stroke, TIA, deep vein thrombosis, and pulmonary embolism. The thromboembolic risk was determined in patients with FD and concurrent FVL, and the impa…

AdultMaleRiskmedicine.medical_specialtyAdolescentEndocrinology Diabetes and MetabolismDeep veinComorbidityBiochemistryYoung AdultEndocrinologyInternal medicineGeneticsmedicineFactor V LeidenHumansEnzyme Replacement TherapyChildMolecular BiologyStrokeAgedAged 80 and overVenous Thrombosisbusiness.industryHazard ratioFactor VEnzyme replacement therapyMiddle Agedmedicine.diseaseFabry diseaseThrombosisComorbidityPulmonary embolismStrokemedicine.anatomical_structureIschemic Attack TransientChild PreschoolFabry DiseaseFemaleNeurology (clinical)Pulmonary EmbolismbusinessNeurology
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A phase II/III clinical study of enzyme replacement therapy with idursulfase in mucopolysaccharidosis II (Hunter syndrome)

2006

Purpose: To evaluate the safety and efficacy of recombinant human iduronate-2-sulfatase (idursulfase) in the treatment of mucopolysaccharidosis II. Methods: Ninety-six mucopolysaccharidosis II patients between 5 and 31 years of age were enrolled in a double-blind, placebo-controlled trial. Patients were randomized to placebo infusions, weekly idursulfase (0.5 mg/kg) infusions or every-other-week infusions of idursulfase (0.5 mg/kg). Efficacy was evaluated using a composite endpoint consisting of distance walked in 6 minutes and the percentage of predicted forced vital capacity based on the sum of the ranks of change from baseline. Results: Patients in the weekly and every-other-week idursul…

AdultMaleVital capacitymedicine.medical_specialtyAdolescentIdursulfaseVital CapacityIduronate SulfatasePlacebolaw.inventionchemistry.chemical_compoundDouble-Blind MethodRandomized controlled trialElosulfase alfalawInternal medicinemedicineHumansMucopolysaccharidosis type IIChildGenetics (clinical)GlycoproteinsMucopolysaccharidosis IIbusiness.industryHunter syndromeDrug ToleranceEnzyme replacement therapymedicine.diseaseRecombinant ProteinsSurgerychemistryChild PreschoolSafetybusinessmedicine.drugGenetics in Medicine
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