Search results for "type II"

showing 10 items of 607 documents

Mortality and cause of death in mucopolysaccharidosis type II-a historical review based on data from the Hunter Outcome Survey (HOS).

2009

Mucopolysaccharidosis type II (MPS II or Hunter syndrome) is a progressive, multisystemic disease caused by a deficiency of iduronate-2-sulfatase. Patients with the severe form of the disease have cognitive impairment and typically die in the second decade of life. Patients with the less severe form do not experience significant cognitive involvement and may survive until the fifth or sixth decade of life. We studied the relationship of both severity of MPS II and the time period in which patients died with age at death in 129 patients for whom data were entered retrospectively into HOS (Hunter Outcome Survey), the only large-scale, multinational observational study of patients with MPS II.…

AdultMalemedicine.medical_specialtyPediatricsAdolescentIdursulfaseIduronate SulfataseCohort StudiesYoung AdultCause of DeathEpidemiologyGeneticsmedicineHumansMucopolysaccharidosis type IIYoung adultChildGenetics (clinical)Cause of deathMucopolysaccharidosis IIRetrospective StudiesMPS type IIbusiness.industryData CollectionAge FactorsInfantHunter syndromeEnzyme replacement therapymedicine.diseaseSurgeryTreatment OutcomeChild PreschoolFemaleSettore MED/35 - MALATTIE CUTANEE E VENEREEbusinessmedicine.drugCohort studyJournal of inherited metabolic disease
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Influence of risk factors on nitric oxide metabolites at the initial stage of juvenile acute myocardial infarction.

2009

Few data are accessible about the nitric oxide (NO) stable end-products (nitrite/NO2 − and nitrate/NO3 − :N O x) in acute coronary syndromes. An increase in inducible NO synthase (iNOS) was found during experimental myocardial infarction [13] and this increase persisted for 2 weeks. In experimental models of acute myocardial infarction (AMI) other authors [2] observed a NOx increase, a correlation between NOx level and iNOS activity and an inhibitory action carried out by S-methylisothiourea, that is an iNOS inhibitor [5]. The NOx level was also measured in a small group of patients with myocardial infarction in whom the peak of NOx elevation occurred 2 and 3 days after the onset of symptom…

AdultMalemedicine.medical_specialtyPhysiologyMyocardial InfarctionNitric Oxide Synthase Type IIEssential hypertensionNitric OxideNitric oxideCoronary artery diseasechemistry.chemical_compoundYoung AdultGriess testRisk FactorsPhysiology (medical)Internal medicinemedicineJuvenile myocardial infarction cardiovascular risk factors nitrite nitrateHumansMyocardial infarctionNitriteNOxbusiness.industryHematologyVenous bloodMiddle Agedmedicine.diseaseSurgerychemistryCase-Control StudiesCardiologyFemaleCardiology and Cardiovascular MedicinebusinessClinical hemorheology and microcirculation
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Long-Term Efficacy and Safety of the Microsomal Triglyceride Transfer Protein Inhibitor Lomitapide in Patients With Homozygous Familial Hypercholeste…

2017

Homozygous familial hypercholesterolemia is a genetic disorder characterized by low-density lipoprotein (LDL)-receptor dysfunction, markedly elevated levels of LDL-cholesterol (LDL-C) and premature atherosclerosis. Patients are often poorly responsive to conventional lipid-lowering therapies that upregulate LDL-receptor expression.1 Lomitapide inhibits microsomal triglyceride transfer protein, which lipidates nascent apolipoprotein (apo)B-containing lipoproteins. In a pivotal 78-week open-label trial, lomitapide, titrated to the maximal tolerable dose, decreased LDL-C by 50% at the end of the efficacy phase (week 26) in patients with homozygous familial hypercholesterolemia.2 The principal …

AdultMalemedicine.medical_specialtySettore MED/09 - Medicina InternaApolipoprotein BSocio-culturaleFamilial hypercholesterolemia030204 cardiovascular system & hematologyGastroenterologyMicrosomal triglyceride transfer proteinLDLTimeSudden cardiac deathHyperlipoproteinemia Type II03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhysiology (medical)Internal medicinemedicineHumans030212 general & internal medicineAdverse effectlomitapidebiologybusiness.industryCholesterolAnticholesteremic AgentsCholesterol LDLlomitapide; Adult; Anticholesteremic Agents; Benzimidazoles; Carrier Proteins; Cholesterol LDL; Female; Humans; Hyperlipoproteinemia Type II; Male; Timemedicine.diseaseLomitapideCholesterolEndocrinologychemistrybiology.proteinBenzimidazolesFemalelipids (amino acids peptides and proteins)lomitapide; Cardiology and Cardiovascular Medicine; Physiology (medical)Carrier ProteinsCardiology and Cardiovascular MedicinebusinessLipoproteinCirculation
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Clinical experience of lomitapide therapy in patients with homozygous familial hypercholesterolaemia.

2014

The microsomal triglyceride transfer protein (MTP) inhibitor lomitapide is a licenced adjunct to a low-fat diet and other lipid-lowering medication, with or without low-density lipoprotein apheresis, for the treatment of adults with homozygous familial hypercholesterolaemia (HoFH). In a recently published phase 3 study, patients with HoFH received lomitapide in addition to maximally tolerated lipid-lowering therapy. Treatment with lomitapide resulted in a mean approximate 50% reduction in LDL-C levels after 26 weeks compared with baseline levels (p < 0.0001). This decrease in LDL-C was maintained at Weeks 56 and 78 (44% [p < 0.0001] and 38% [p = 0.0001], respectively). This paper offers cli…

AdultMalemedicine.medical_specialtySettore MED/09 - Medicina InternaPhases of clinical researchMicrosomal triglyceride transfer proteinHyperlipoproteinemia Type IIchemistry.chemical_compoundYoung AdultInternal medicineHo-FH lomitapide MTPInternal MedicinemedicineEffective treatmentHumansIn patientAdverse effectbiologymedicine.diagnostic_testbusiness.industryAnticholesteremic AgentsHomozygoteGeneral MedicineCholesterol LDLMiddle AgedLomitapideEndocrinologyApheresisTreatment Outcomechemistrybiology.proteinBenzimidazolesFemaleCardiology and Cardiovascular MedicinebusinessLiver function testsAtherosclerosis. Supplements
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Thrombin-antithrombin III complexes in type II diabetes mellitus.

1992

Several studies suggest that diabetes is associated with a hypercoagulable state. Therefore determination of thrombin-antithrombin complex (TAT) could represent a sensitive parameter for specific detection of a latent activation of the clotting system. The present study documents increased plasma TAT in a heterogeneous group of non-insulin-dependent diabetic patients. The finding of increased TAT levels both in diabetic patients with vascular complications and in vascular disease patients without diabetes suggests a relationship between existing vascular disease and the hemostatic mechanism that produces augmented thrombin activity. In acute vascular occlusions the presence of diabetes seem…

AdultMalemedicine.medical_specialtySpecific detectionEndocrinology Diabetes and MetabolismAntithrombin IIIType ii diabetesEndocrinologyReference ValuesDiabetes mellitusInternal medicineInternal MedicinemedicineHumansAgedAged 80 and overHeterogeneous groupVascular diseasebusiness.industryThrombin/Antithrombin IIIAge FactorsThrombinMiddle Agedmedicine.diseaseCerebrovascular DisordersCoagulative necrosisEndocrinologyDiabetes Mellitus Type 2Thrombin activityRegression AnalysisFemalebusinessDiabetic AngiopathiesJournal of diabetes and its complications
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The relative roles of intragenic polymorphisms of the vitamin d receptor gene in lumbar spine degeneration and bone density.

2001

Study Design. A retrospective cohort study. Objectives. To compare the magnitudes of the associations of TaqI polymorphisms of the vitamin D receptor gene with bone density and lumbar spine degeneration in the same sample. Summary of Background Data. Vitamin D receptor gene variations are associated with osteoporosis, osteoarthritis, and disc degeneration. Their role in these conditions remains poorly understood. Methods. Bone density of the spine and femur were determined through DEXA, and lumbar disc degeneration was determined from magnetic resonance imaging assessments of signal intensity, disc narrowing, bulging, anular tears, herniations, and osteophytes. Associations between these me…

AdultMalemedicine.medical_specialtyTaqIBone densityGenotypeOsteoporosisPopulationOsteoarthritisCalcitriol receptorCohort StudiesSpinal Osteophytosischemistry.chemical_compoundBone DensityInternal medicineGenotypeOsteoarthritismedicineHumansOrthopedics and Sports MedicineeducationDeoxyribonucleases Type II Site-SpecificIntervertebral DiscAgedRetrospective Studieseducation.field_of_studyLumbar VertebraePolymorphism Geneticbusiness.industryMiddle Agedmedicine.diseaseEndocrinologychemistryTearsOsteoporosisReceptors CalcitriolTwin Studies as TopicFemaleNeurology (clinical)businessIntervertebral Disc DisplacementSpine
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Cardiac arrhythmias in patients with Danon disease.

2016

Aims Different cardiac arrhythmias have been suggested to be associated with Danon disease, e.g. Wolff–Parkinson–White syndrome. However, a systematic electrophysiological investigation of patients with Danon disease is lacking thus far. Methods and results Seven patients with Danon disease (4 males, 35.8 ± 10.8 years; 3 females, 51.3 ± 19.9 years) from 3 different families were studied. In all patients, the presence of Danon disease was confirmed by western blot of biopsy material or genetic testing. The patients were characterized by 12-lead electrocardiogram (ECG), Holter ECG, echocardiography, and serial implantable cardioverter defibrillator (ICD) interrogations (in ICD recipients). Al…

AdultMalemedicine.medical_specialtyTime Factorsmedicine.medical_treatmentElectric CountershockAction Potentials030204 cardiovascular system & hematologyAsymptomaticSudden cardiac death03 medical and health sciencesQRS complex0302 clinical medicineHeart RateRisk FactorsPhysiology (medical)Internal medicineMedicineHumansDanon diseasecardiovascular diseasesPR intervalAgedbusiness.industryCardiac arrhythmiaAtrial fibrillationArrhythmias CardiacMiddle AgedImplantable cardioverter-defibrillatormedicine.diseaseGlycogen Storage Disease Type IIbDefibrillators ImplantablePrimary PreventionDeath Sudden CardiacEchocardiographycardiovascular systemCardiologyAtrioventricular NodeElectrocardiography AmbulatoryFemalemedicine.symptomCardiology and Cardiovascular MedicinebusinessElectrophysiologic Techniques Cardiac030217 neurology & neurosurgeryEuropace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology
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Effects of enzyme replacement therapy on growth in patients with mucopolysaccharidosis type II

2010

Mucopolysaccharidosis type II (MPS II; Hunter syndrome) is an X-linked, recessive, lysosomal storage disorder caused by deficiency of iduronate-2-sulfatase. It has multisystemic involvement, with manifestations in the brain, upper respiratory tract, heart, abdomen, joints and bones. Bone involvement leads to decreased growth velocity and short stature in nearly all patients. A therapeutic option for patients with MPS II is enzyme replacement therapy (ERT) with idursulfase (Elaprase®). We compared annual growth rates before and during ERT in 18 patients from Mainz, Germany, and Manchester, UK. Group 1 included nine patients who started ERT before 10 years of age; group 2 contained nine patie…

AdultMalemedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesAdolescentIdursulfaseIduronate SulfatasePlaceboShort staturePlacebosYoung AdultChild DevelopmentClinical Trials Phase II as TopicmedicineGeneticsHumansGenetics(clinical)Enzyme Replacement TherapyMucopolysaccharidosis type IIYoung adultGrowth ChartsChildGenetics (clinical)Mucopolysaccharidosis IIbusiness.industrynutritional and metabolic diseasesHunter syndromeEnzyme replacement therapymedicine.diseaseBody HeightSurgerymedicine.anatomical_structureClinical Trials Phase III as TopicAbdomenOriginal Articlemedicine.symptombusinessmedicine.drugJournal of Inherited Metabolic Disease
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Nitric oxide production and endothelium-dependent vasorelaxation ameliorated by N1-methylnicotinamide in human blood vessels.

2012

N 1 -methylnicotinamide (MNA + ) has until recently been thought to be a biologically inactive product of nicotinamide metabolism in the pyridine nucleotides pathway. However, the latest observations imply that MNA + may exert antithrombotic and anti-inflammatory effects through direct action on the endothelium. We examined both in vivo and in vitro whether the compound might induce vasorelaxation in human blood vessels through the improvement of nitric oxide (NO) bioavailability and a reduction of oxidative stress mediated by endothelial NO synthase (eNOS) function. MNA + treatment (100 mg/m 2 orally) in healthy normocholesterolemic and hypercholesterolemic subjects increased the l-argini…

AdultNiacinamidemedicine.medical_specialtyEndotheliumBrachial ArteryNitric Oxide Synthase Type IIIHypercholesterolemiachemistry.chemical_elementCalciumIn Vitro Techniquesmedicine.disease_causeNitric OxideNitric oxidechemistry.chemical_compoundN^{1}-methylnicotinamideDouble-Blind MethodEnosnitric oxideInternal medicineInternal MedicinemedicineHumansflow-mediated dilationCalcimycinCells Culturedendothelial nitric oxide synthaseoxidized low-density lipoproteinbiologyDose-Response Relationship DrugChemistrySuperoxidebiology.organism_classificationendothelial cellsAcetylcholineOxygenVasodilationOxidative Stressmedicine.anatomical_structureEndocrinologysuperoxideEndothelium VascularAcetylcholineOxidative stressmedicine.drugLipoproteinHypertension (Dallas, Tex. : 1979)
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Six novel mutations of the LDL receptor gene in FH kindred of Sicilian and Paraguayan descent

2006

Familial hypercholesterolemia (FH) is an autosomal dominant inherited disease caused by mutations in the gene coding for the low density lipoprotein receptor (LDL-R). It is characterized by a high concentration of low density lipoprotein (LDL), which frequently gives rise to premature coronary artery disease. We studied the probands of five FH Sicilian families with 'definite' FH and one proband of Paraguayan descent with homozygous FH who has been treated with an effective living-donor liver transplantation. In order to seek the molecular defect in these six families, we used direct sequencing to define the molecular defects of the LDL-R gene responsible for the disease. We described three…

AdultProbandhypercholesterolemia LDL receptor gene mutation analysis direct sequencing splicing living-donor transplantationSettore MED/09 - Medicina InternaDNA Mutational AnalysisDirect sequencingHypercholesterolemiaFamilial hypercholesterolemiaBiologyGene mutationSplicingmedicine.disease_causeFrameshift mutationHyperlipoproteinemia Type IIExonGeneticsmedicineHumansMissense mutationRNA MessengerChildSicilyCells CulturedLiving-donor transplantationLDL receptor geneGeneticsMutationIntronExonsGeneral MedicineMiddle Agedmedicine.diseaseLipidsMolecular biologyPedigreeDirect sequencing; Hypercholesterolemia; LDL receptor gene; Living-donor transplantation; Mutation analysis; SplicingMutation analysisReceptors LDLParaguayChild PreschoolMutationBiological Assay
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