Search results for "pcsk9"

showing 10 items of 74 documents

Homozygous Familial Hypercholesterolemia in Spain Prevalence and Phenotype-Genotype Relationship

2016

Background— Homozygous familial hypercholesterolemia (HoFH) is a rare disease characterized by elevated plasma levels of low-density lipoprotein cholesterol (LDL-C) and extremely high risk of premature atherosclerotic cardiovascular disease. HoFH is caused by mutations in several genes, including LDL receptor ( LDLR ), apolipoprotein B ( APOB ), proprotein convertase subtilisin/kexin type 9 ( PCSK9 ), and LDL protein receptor adaptor 1 ( LDLRAP1 ). No epidemiological studies have assessed HoFH prevalence or the clinical and molecular characteristics of this condition. Here, we aimed to characterize HoFH in Spain. Methods and Results— Data were collected from the Spanish Dyslipidemia Regist…

Male0301 basic medicineOncologyLdl receptor geneApolipoprotein BLipid-lowering therapyFamilial hypercholesterolemia030204 cardiovascular system & hematologyCompound heterozygosity0302 clinical medicineAutosomal-dominant hypercholesterolemiaRisk FactorsEpidemiologyPrevalenceDiseaseRegistriesGenetics (clinical)Molecular EpidemiologybiologyhypercholesterolemiaHomozygoteDouble-blindMiddle AgedPhenotypeCardiovascular DiseasesApolipoprotein B-100allelesFemalelipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicineMutationsAdultGenetic MarkersHeterozygotemedicine.medical_specialtyInhibitorAdolescentPlacebo-controlled trialHyperlipoproteinemia Type IIlipidsYoung Adult03 medical and health sciencesInternal medicineGeneticsmedicineHumansGenetic Predisposition to DiseaseAlleleAdaptor Proteins Signal TransducingRecessive hypercholesterolemiaPCSK9registriesCholesterol LDLApolipoprotein-bmedicine.disease030104 developmental biologyEndocrinologyReceptors LDLSpainMutationLDL receptorbiology.proteinmutationDyslipidemia
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Proprotein Convertase Subtilisin Kexin Type 9 Inhibition for Autosomal Recessive Hypercholesterolemia—Brief Report

2016

Objective— Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors lower low-density lipoprotein (LDL) cholesterol in the vast majority of patients with autosomal dominant familial hypercholesterolemia. Will PCSK9 inhibition with monoclonal antibodies, in particular alirocumab, be of therapeutic value for patients with autosomal recessive hypercholesterolemia (ARH)? Approach and Results— Primary lymphocytes were obtained from 28 genetically characterized ARH patients and 11 controls. ARH lymphocytes treated with mevastatin were incubated with increasing doses of recombinant PCSK9 with or without saturating concentrations of alirocumab. Cell surface LDL receptor expression measured…

Male0301 basic medicineSettore MED/09 - Medicina Interna[SDV]Life Sciences [q-bio]receptorsalirocumabFamilial hypercholesterolemia030204 cardiovascular system & hematologyproprotein convertase subtilisin kexin type 90302 clinical medicinetherapeuticsLymphocytesCells CulturedhypercholesterolemiaAnticholesteremic AgentsPCSK9 InhibitorsAntibodies MonoclonalMiddle Aged3. Good healthPhenotypeAutosomal Recessive HypercholesterolemiaKexinDrug Therapy CombinationFemalelipids (amino acids peptides and proteins)LovastatinProprotein Convertase 9Cardiology and Cardiovascular Medicinemedicine.drugAdultmedicine.medical_specialtySerine Proteinase InhibitorsAdolescentBiologyAntibodies Monoclonal HumanizedLDLYoung Adult03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseLovastatinAdaptor Proteins Signal TransducingAlirocumabPCSK9receptors LDLCholesterol LDLmedicine.diseaseProprotein convertasetherapeutic030104 developmental biologyEndocrinologyCase-Control Studiesalirocumab; hypercholesterolemia; proprotein convertase subtilisin kexin type 9; receptors LDL; therapeutics; Cardiology and Cardiovascular MedicineMutationLDL receptorHydroxymethylglutaryl-CoA Reductase InhibitorsArteriosclerosis, Thrombosis, and Vascular Biology
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Intensive LDL-cholesterol lowering therapy and neurocognitive function

2017

The key lipid-lowering target is to achieve guideline-recommended low-density lipoprotein cholesterol (LDL-C) levels, usually by using statins. The new treatment strategies for lipid-lowering therapy include using proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors as an exciting approach to reduce residual risk of cardiovascular diseases (CVD). However, concerns about possible adverse effects, including neurocognitive disorders, were issued by the Food and Drug Administration (FDA). The current disputable evidence does not allow definite conclusions as to whether statins contribute to, or cause, clinically meaningful cognitive impairment. Some evidence indicates a high rate of…

MaleApolipoprotein Emedicine.medical_specialtyStatinmedicine.drug_classNeurocognitive DisordersProprotein convertase subtilisin/kexin type 9030204 cardiovascular system & hematologyBioinformatics03 medical and health sciencesCognitionSex Factors0302 clinical medicineRisk FactorsInternal medicinemedicineHumansLipid-lowering drugAnimalsDementiaLow-density lipoprotein cholesterolAge FactorPharmacology (medical)Adverse effectHypolipidemic AgentsPharmacologybusiness.industryPCSK9PCSK9 InhibitorsAge FactorsStatinCognitionCholesterol LDLmedicine.diseaseNeurocognitive functionResidual riskEndocrinologyFemalelipids (amino acids peptides and proteins)Hydroxymethylglutaryl-CoA Reductase InhibitorsbusinessNeurocognitive030217 neurology & neurosurgeryPharmacology & Therapeutics
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Molecular diagnosis of hypobetalipoproteinemia: an ENID review.

2007

Abstract Primary hypobetalipoproteinemia (HBL) includes a group of genetic disorders: abetalipoproteinemia (ABL) and chylomicron retention disease (CRD), with a recessive transmission, and familial hypobetalipoproteinemia (FHBL) with a co-dominant transmission. ABL and CRD are rare disorders due to mutations in the MTP and SARA2 genes, respectively. Heterozygous FHBL is much more frequent. FHBL subjects often have fatty liver and, less frequently, intestinal fat malabsorption. FHBL may be linked or not to the APOB gene. Most mutations in APOB gene cause the formation of truncated forms of apoB which may or may be not secreted into the plasma. Truncated apoBs with a size below that of apoB-3…

MaleCandidate geneSettore MED/09 - Medicina InternaApolipoprotein BGenotypeLocus (genetics)BiologyPolymorphism Single NucleotidePCSK9 GenemedicineHumansFamilial hypobetalipoproteinemiaGenetic TestingAPOB geneApolipoproteins BGeneticsPCSK9AbetalipoproteinemiaChylomicron retention diseasemedicine.diseaseEuropean Network for Inherited Dyslipidemia (ENID)AbetalipoproteinemiaPhenotypePCSK9 geneHypobetalipoproteinemia Familial Apolipoprotein BMutationbiology.proteinlipids (amino acids peptides and proteins)FemaleHypobetalipoproteinemiaMTP geneCardiology and Cardiovascular MedicineCarrier Proteinsuropean Network for Inherited Dyslipidemia (ENID)European Network for Inherited Dyslipidemia (ENID) Familial hypobetalipoproteinemia Abetalipoproteinemia Chylomicron retention disease.Chylomicron retention diseaseAtherosclerosis
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Next-generation-sequencing-based identification of familial hypercholesterolemia-related mutations in subjects with increased LDL–C levels in a latvi…

2015

Background Familial hypercholesterolemia (FH) is one of the commonest monogenic disorders, predominantly inherited as an autosomal dominant trait. When untreated, it results in early coronary heart disease. The vast majority of FH remains undiagnosed in Latvia. The identification and early treatment of affected individuals remain a challenge worldwide. Most cases of FH are caused by mutations in one of four genes, APOB, LDLR, PCSK9, or LDLRAP1. The spectrum of disease-causing variants is very diverse and the variation detection panels usually used in its diagnosis cover only a minority of the disease-causing gene variants. However, DNA-based tests may provide an FH diagnosis for FH patients…

MaleNonsynonymous substitutionApolipoprotein BCoronary Artery DiseaseFamilial hypercholesterolemiaDiseaseCohort StudiesPCSK9Genetics(clinical)Family historyGenetics (clinical)Aged 80 and overGeneticseducation.field_of_studybiologySerine EndopeptidasesHigh-Throughput Nucleotide SequencingAutosomal dominant traitMiddle AgedLDLRAP1Apolipoprotein B-100Femalelipids (amino acids peptides and proteins)Proprotein ConvertasesProprotein Convertase 9APOBResearch ArticleAdultPopulationPolymorphism Single NucleotideLDLHyperlipoproteinemia Type IIYoung AdultGeneticsmedicineHumanseducationAdaptor Proteins Signal TransducingAgedDiagnostic toolsPCSK9Cholesterol LDLmedicine.diseaseLatviaGenetics PopulationLDLRReceptors LDLMutationNext-generation sequencingbiology.proteinBMC Medical Genetics
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Cardiovascular Efficacy and Safety of Bococizumab in High-Risk Patients

2017

Item does not contain fulltext BACKGROUND: Bococizumab is a humanized monoclonal antibody that inhibits proprotein convertase subtilisin-kexin type 9 (PCSK9) and reduces levels of low-density lipoprotein (LDL) cholesterol. We sought to evaluate the efficacy of bococizumab in patients at high cardiovascular risk. METHODS: In two parallel, multinational trials with different entry criteria for LDL cholesterol levels, we randomly assigned the 27,438 patients in the combined trials to receive bococizumab (at a dose of 150 mg) subcutaneously every 2 weeks or placebo. The primary end point was nonfatal myocardial infarction, nonfatal stroke, hospitalization for unstable angina requiring urgent re…

MaleSTATIN THERAPYAnticholesteremic Agents/adverse effectsAntibodieVascular damage Radboud Institute for Health Sciences [Radboudumc 16]Injections Subcutaneous/adverse effects030204 cardiovascular system & hematologyBococizumablaw.inventionPCSK90302 clinical medicineRandomized controlled triallawRisk FactorsGENETIC-VARIANTSCardiovascular DiseaseMonoclonalAnticholesteremic Agent030212 general & internal medicineMyocardial infarctionTreatment FailureHumanizedProprotein Convertase 9/antagonists & inhibitorsMedicine(all)Antibodies; Antibodies Monoclonal Humanized; Anticholesteremic Agents; Cardiovascular Diseases; Cholesterol LDL; Double-Blind Method; Female; Follow-Up Studies; Humans; Hypercholesterolemia; Injections Subcutaneous; Lipids; Male; Middle Aged; Proprotein Convertase 9; Risk Factors; Treatment Failure; Medicine (all)Anticholesteremic AgentsMedicine (all)PCSK9 InhibitorsAntibodies; antibodies monoclonal humanized; anticholesteremic agents; cardiovascular diseases; cholesterol LDL; double-blind method; female; follow-up studies; humans; hypercholesterolemia; injections subcutaneous; lipids; male; middle aged; proprotein convertase 9; risk factors; treatment failure; medicine (all)Vascular damage Radboud Institute for Molecular Life Sciences [Radboudumc 16]General MedicineLipidMiddle AgedLipids3. Good healthLDL/bloodMulticenter StudyCholesterolTRIALSCholesterol LDL/bloodCardiovascular DiseasesAntibodies Monoclonal Humanized/adverse effectsanticholesteremic agentsRandomized Controlled Trialsubcutaneouslipids (amino acids peptides and proteins)FemaleProprotein Convertase 9Cardiovascular Diseases/prevention & controlREDUCING LIPIDSHumanmedicine.medical_specialtyanimal structuresInjections SubcutaneousHypercholesterolemiaHypercholesterolemia/drug therapyPlaceboAntibodies Monoclonal HumanizedInjections SubcutaneouAntibodiesLDLInjectionsFollow-Up StudielipidsEVENTS03 medical and health sciencesantibodies monoclonal humanizedDouble-Blind MethodInternal medicinemedicineJournal ArticleHumansComparative StudyMETAANALYSISAlirocumabbusiness.industryUnstable anginaLipids/bloodPCSK9Risk FactorfungiAntibodies/bloodCholesterol LDLta3121medicine.diseaseSurgerycardiovascular diseasesEvolocumabREDUCTIONHumanized/adverse effectsSubcutaneous/adverse effectsbusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyFollow-Up Studies
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The c.43_44insCTG variation in PCSK9 is associated with low plasma LDL-cholesterol in a Caucasian population.

2006

Abstract The genetic etiology of familial hypobetalipoproteinemia (FHBL) is unclear in the majority of cases. Mutations in apolipoprotein B (APOB) are the only confirmed causes of FHBL. Recently, loss-of-function mutations of PCSK9 gene have been shown to be associated with the hypocholesterolemia phenotype. Our primary goal was to confirm that mutations in PCSK9 could be another cause of FHBL. Using the sequencing approach, we found that the c.43_44insCTG variation in PCSK9, a common in-frame insertion in both African American and Caucasian populations, is associated with the hypocholesterolemia phenotype in three FHBL families. Then we tested whether this variation could be associated wit…

MaleSettore MED/09 - Medicina InternaApolipoprotein BDNA Mutational Analysismedicine.disease_causePCSK9Hypobetalipoproteinemiaschemistry.chemical_compoundGene Frequencyapolipoprotein BChildGenetics (clinical)Aged 80 and overMutationeducation.field_of_studybiologySerine EndopeptidasesMiddle AgedPedigreefamilial hypobetalipoproteinemiaPhenotypeChild Preschoollipids (amino acids peptides and proteins)FemaleProprotein ConvertasesProprotein Convertase 9Adultmedicine.medical_specialtyAdolescentPopulationMolecular Sequence DataWhite PeopleLDLlipidInternal medicineGeneticsmedicineHumanseducationAllele frequencyAgedhypocholesterolemiaCholesterolPCSK9Cholesterol HDLCholesterol LDLmedicine.diseaseHypocholesterolemiaEndocrinologychemistryMutationbiology.proteinLipoproteinHuman mutation
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PCSK9 rs11591147 R46L loss-of-function variant protects against liver damage in individuals with NAFLD

2020

Background and Aims: The proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a key role in cholesterol homeostasis, and its inhibition represents an effective therapy to lower low-density lipoprotein cholesterol (LDL-C) levels. In this study, we examined the impact of the PCSK9 rs11591147 loss-of-function (LOF) variant on liver damage in a multicenter collection of patients at risk of nonalcoholic steatohepatitis (NASH), in clinical samples and experimental models. Methods: We considered 1874 consecutive individuals at risk of NASH as determined by histology. The SNP rs11591147, encoding for the p.R46L variant of PCSK9, was genotyped by TaqMan assays. We also evaluated 1) PCSK9 mRNA…

Malemedicine.medical_specialtyProprotein Convertase 9.GastroenterologyPCSK903 medical and health sciencesMice0302 clinical medicineFibrosisNon-alcoholic Fatty Liver DiseaseSettore BIO/13 - Biologia ApplicataInternal medicineNonalcoholic fatty liver diseaseMedicineSNPAnimalsHumansFIBROSISLoss functionSettore MED/12 - GastroenterologiaHepatologybusiness.industryAnimalPCSK9ConfoundingNASHCholesterol LDLProprotein convertasemedicine.diseaseLiver030220 oncology & carcinogenesisKexin030211 gastroenterology & hepatologyProprotein Convertase 9businessHuman
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Efficacy and Safety of Alirocumab in Reducing Lipids and Cardiovascular Events

2015

BACKGROUND: Alirocumab, a monoclonal antibody that inhibits proprotein convertase subtilisin-kexin type 9 (PCSK9), has been shown to reduce low-density lipoprotein (LDL) cholesterol levels in patients who are receiving statin therapy. Larger and longer-term studies are needed to establish safety and efficacy.METHODS: We conducted a randomized trial involving 2341 patients at high risk for cardiovascular events who had LDL cholesterol levels of 70 mg per deciliter (1.8 mmol per liter) or more and were receiving treatment with statins at the maximum tolerated dose (the highest dose associated with an acceptable side-effect profile), with or without other lipid-lowering therapy. Patients were …

Malemedicine.medical_specialtySettore MED/09 - Medicina InternaIntention to Treat AnalysiHypercholesterolemiaUrologyalirocumabBococizumabPharmacologyPlaceboAged; Antibodies Monoclonal; Anticholesteremic Agents; Cardiovascular Diseases; Cholesterol LDL; Double-Blind Method; Drug Therapy Combination; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypercholesterolemia; Intention to Treat Analysis; Male; Middle Aged; Medicine (all)law.inventionchemistry.chemical_compoundcardiovascular eventsDouble-Blind MethodRandomized controlled triallawCardiovascular DiseaseAnticholesteremic AgentMedicineproprotein convertase subtilisin–kexin type 9 (PCSK9)High Cardiovascular Risk PatientsAgedAlirocumabalirocumab; cholesterol; cardiovascular eventsCholesterolbusiness.industryMedicine (all)PCSK9Antibodies MonoclonalcholesterolCholesterol LDLGeneral MedicineMiddle AgedLomitapideEvolocumabchemistrylow-density lipoprotein (LDL) cholesterol[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologieDrug Therapy CombinationFemalelipids (amino acids peptides and proteins)Hydroxymethylglutaryl-CoA Reductase Inhibitorbusiness[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyHumanNew England journal of medicine
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Role of PCSK9 in the course of ejection fraction change after ST-segment elevation myocardial infarction: a pilot study

2020

Altres ajuts: Conselleria d'Educació, Investigació, Cultura i Esport GV/2018/116 Proprotein convertase subtilisin/kexin type 9 (PCSK9) has emerged as a therapeutic target for reducing plasma low-density lipoprotein cholesterol. Beyond lipid control, recent findings suggest a deleterious effect of this protein in the pathogenesis of postmyocardial infarction left ventricle remodelling and heart failure-related complications. The aim of this study was to assess the relationship between circulating PCSK9 and 6 month cardiac magnetic resonance imaging-derived left ventricular ejection fraction (LVEF) after a first ST-segment elevation myocardial infarction (STEMI). We prospectively evaluated 40…

Malemedicine.medical_specialtylcsh:Diseases of the circulatory (Cardiovascular) systemLeft ventricular ejection fractionCardiac magnetic resonancemedicine.medical_treatmentMyocardial InfarctionInfarctionAngiotensin-Converting Enzyme InhibitorsPilot Projects030204 cardiovascular system & hematologyVentricular Function LeftPCSK9Angiotensin Receptor Antagonists03 medical and health sciences0302 clinical medicineCardiac magnetic resonance imagingOriginal Research ArticlesInternal medicinemedicineST‐segment elevation myocardial infarctionHumansST segmentOriginal Research Article030212 general & internal medicineMyocardial infarctioncardiovascular diseasesAgedKillip classEjection fractionmedicine.diagnostic_testbusiness.industryPercutaneous coronary interventionStroke VolumeMiddle Agedmedicine.diseaseST-segment elevation myocardial infarctionlcsh:RC666-701Heart failureCardiologyST Elevation Myocardial InfarctionProprotein Convertase 9Cardiology and Cardiovascular Medicinebusiness
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