Search results for "proteine"

showing 10 items of 179 documents

Treating homozygous familial hypercholesterolemia in a real-world setting: Experiences with lomitapide

2015

Homozygous familial hypercholesterolaemia (HoFH) is a rare genetic disease characterised by markedly elevated plasma levels of low-density lipoprotein-cholesterol (LDL-C). Lomitapide is a microsomal triglyceride transfer protein (MTP) inhibitor approved as an adjunct to other lipid-lowering therapies (LLTs), with or without lipoprotein apheresis (LA), for the treatment of adult HoFH. Diet with <20% calories from fat is required. Due to a varying genetic and phenotypic profile of patients with HoFH, individual patients may respond to therapy differently; therefore examining individual cases in a 'real-world' setting provides valuable information on the effective day-to-day manag…

AdultMalemedicine.medical_specialtyCalorieSettore MED/09 - Medicina InternaEndocrinology Diabetes and MetabolismCase studyFamilial hypercholesterolemiaHomozygous familial hypercholesterolemiaFamilial hypercholesterolemiaDiseaseCompound heterozygosityHyperlipoproteinemia Type IIchemistry.chemical_compoundInternal medicineCase study; Familial hypercholesterolemia; Homozygous familial hypercholesterolemia; Lomitapide; Treatment; Cardiology and Cardiovascular Medicine; Endocrinology Diabetes and Metabolism; Internal Medicine; Nutrition and DieteticsInternal MedicinemedicineHumansAdverse effectNutrition and Dieteticsbusiness.industryAnticholesteremic AgentsHomozygoteCholesterol LDLMiddle Agedmedicine.diseaseLomitapideLomitapideTreatmentClinical trialEndocrinologychemistryBenzimidazolesFemaleSteatosisCardiology and Cardiovascular Medicinebusiness
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Enhanced reduction in oxidative stress and altered glutathione and thioredoxin system response to unsaturated fatty acid load in familial hypercholes…

2014

Abstract Objectives Familial hypercholesterolemia (FH) is characterized by increased oxidative stress (OS) levels. In the postprandial state, lipids and lipoproteins modulate OS status through their impact on pro-oxidant and antioxidant mechanisms. The objective of this study was to evaluate in patients with FH the response to an unsaturated oral fat load test (OFLT) by analyzing the mRNA levels of genes involved in the glutathione and thioredoxin antioxidant systems. Design and Methods We analyzed 14 FH patients and 20 normolipidemic and normoglycemic controls. In both groups, mRNA values of antioxidant enzyme genes (glutathione and thioredoxin systems) were determined at baseline and at 2…

AdultMalemedicine.medical_specialtyGPX1Antioxidantmedicine.medical_treatmentGlutamate-Cysteine LigaseClinical Biochemistrymedicine.disease_causeGPX4Gene Expression Regulation EnzymologicGlutathione SynthaseHyperlipoproteinemia Type IIchemistry.chemical_compoundThioredoxinsDietary Fats UnsaturatedInternal medicinemedicineHumansUnsaturated fatty acidGlutathione PeroxidaseChemistryReverse Transcriptase Polymerase Chain ReactionGeneral MedicineGlutathioneFastingMiddle AgedPhospholipid Hydroperoxide Glutathione PeroxidaseGlutathioneOxidative StressPostprandialEndocrinologyGlutathione ReductaseFemaleThioredoxinOxidation-ReductionOxidative stressClinical biochemistry
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Familial HDL deficiency due to ABCA1 gene mutations with or without other genetic lipoprotein disorders

2004

Mutations in ABCA1 have been shown to be the cause of Tangier disease (TD) and some forms of familial hypoalphalipoproteinemia (HA), two genetic disorders characterized by low plasma HDL levels. Here we report six subjects with low HDL, carrying seven ABCA1 mutations, six of which are previously unreported. Two mutations (R557X and H160FsX173) were predicted to generate short truncated proteins; two mutations (E284K and Y482C) were located in the first extracellular loop and two (R1901S and Q2196H) in the C-terminal cytoplasmic domain of ABCA1. Two subjects found to be compound heterozygotes for ABCA1 mutations did not have overt clinical manifestations of TD. Three subjects, all with prema…

AdultMalemedicine.medical_specialtyHeterozygoteSettore MED/09 - Medicina InternaApolipoprotein BAdolescentPremature coronary artery diseaseTangier diseaseCoronary DiseaseBiologyGene mutationmedicine.disease_causeCompound heterozygosityTangier diseaseInternal medicineGenotypeABCA1 genemedicineHumansChildHypoalphalipoproteinemiaSelection BiasAgedApolipoproteins BGeneticsMutationFamilial defective Apo B (FDB)Apolipoprotein A-ICholesterol HDLnutritional and metabolic diseasesMiddle Agedmedicine.diseaseLipoprotein lipaseTangier disease; Familial HDL deficiency; ABCA1 gene; Familial defective Apo B (FDB); Lipoprotein lipase; Premature coronary artery diseaseEndocrinologyChild PreschoolMutationbiology.proteinlipids (amino acids peptides and proteins)Allelic heterogeneityATP-Binding Cassette TransportersFemaleCardiology and Cardiovascular MedicineFamilial HDL deficiencyATP Binding Cassette Transporter 1
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Oxidative stress and antioxidant enzyme values in lymphomonocytes after an oral unsaturated fat load test in familial hypercholesterolemic subjects

2012

Oxidative stress (OS) has been observed in conditions affecting the cardiovascular system. Familial hypercholesterolemia (FH) is associated with an increased risk of premature coronary heart disease. In the postprandial state, circulating lipids and lipoproteins can modulate OS status. Our aim was to study the response of lymphomonocyte OS status and reactive oxygen species by-products after an oral unsaturated fat load test (OFLT) in those with FH and to compare this response with that obtained in normolipidemic, normoglycemic subjects. We studied 12 patients with FH and 20 healthy controls. In both groups, lymphomonocyte, oxidized/reduced glutathione ratio, and malondialdehyde were determ…

AdultMalemedicine.medical_specialtyIsoprostaneAdolescentFamilial hypercholesterolemiamedicine.disease_causeAntioxidantsMonocytesHyperlipoproteinemia Type IIchemistry.chemical_compoundMalondialdehydePhysiology (medical)Internal medicinemedicineHumansLymphocytesAgedchemistry.chemical_classificationGlutathione Disulfidebusiness.industryGlutathione peroxidaseBiochemistry (medical)Unsaturated fatPublic Health Environmental and Occupational HealthArea under the curveGeneral MedicineMiddle AgedPostprandial PeriodMalondialdehydemedicine.diseaseGlutathioneFats UnsaturatedOxidative StressEndocrinologyPostprandialchemistryFemalebusinessOxidative stressTranslational Research
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A Novel Loss of Function Mutation of PCSK9 Gene in White Subjects With Low-Plasma Low-Density Lipoprotein Cholesterol

2007

Objectives— The PCSK9 gene, encoding a pro-protein convertase involved in posttranslational degradation of low-density lipoprotein receptor, has emerged as a key regulator of plasma low-density lipoprotein cholesterol. In African-Americans two nonsense mutations resulting in loss of function of PCSK9 are associated with a 30% to 40% reduction of plasma low-density lipoprotein cholesterol. The aim of this study was to assess whether loss of function mutations of PCSK9 were a cause of familial hypobetalipoproteinemia and a determinant of low-plasma low-density lipoprotein cholesterol in whites. Methods and Results— We sequenced PCSK9 gene in 18 familial hypobetalipoproteinemia subjects and i…

AdultMalemedicine.medical_specialtyNonsense mutationBiologymedicine.disease_causePolymorphism Single NucleotideRisk AssessmentSensitivity and SpecificityStatistics NonparametricWhite Peopleloss of function mutationHypobetalipoproteinemiaschemistry.chemical_compoundPCSK9 GeneGene FrequencyInternal medicinemedicineHumansGenetic Predisposition to DiseaseMutationhypocholesterolemiaCholesterolIncidencePCSK9Serine EndopeptidasesCholesterol LDLmedicine.diseaseHypocholesterolemiaEndocrinologyfamilial hypobetalipoproteinemiachemistryCodon NonsensePCSK9 geneCase-Control Studiesfamilial hypobetalipoproteinemia hypocholesterolemia loss of function mutation PCSK9 genefamilial hypobetalipoproteinemia; hypocholesterolemia; loss of function mutation; PCSK9 gene.FemaleProprotein ConvertasesHypobetalipoproteinemiaProprotein Convertase 9Cardiology and Cardiovascular MedicineLipoprotein
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Fibrinolysis in hypertriglyceridaemic subjects in response to venous occlusion.

1993

We have measured various fibrinolytic and coagulation parameters (t-PA antigen, PAI, fibrinogen, plasminogen and factor VII) before and after 10 min of venous occlusion in 20 hypertryglyceridaemic subjects (twelve males and eight females, age 38 +/- 4 years, body mass index 23 +/- 1.5) and 20 healthy normal subjects, matched for sex (twelve males and eight females), age (37 +/- 3.5 years) and body mass index (22.8 +/- 1.4). At rest, t-PA:Ag, PAI, fibrinogen, plasminogen and factor VII were significantly (P < 0.005) higher in hypertriglyceridaemic subjects than in normal controls. After venous occlusion, the increase in all parameters except t-PA:Ag was more marked in the patient group than …

AdultMalemedicine.medical_specialtyPathologymedicine.medical_treatmentFibrinogenHyperlipoproteinemia Type IVVeinschemistry.chemical_compoundAntigenInternal medicineOcclusionFibrinolysisPlasminogen Activator Inhibitor 1medicineHumansFactor VIIbusiness.industryFibrinolysisHypertriglyceridemiaFibrinogenPlasminogenHematologyGeneral MedicineFactor VIIMiddle Agedmedicine.diseaseConstrictionLipidsEndocrinologyApolipoproteinsCoagulationchemistryTissue Plasminogen ActivatorFemalebusinessBody mass indexmedicine.drugBlood coagulationfibrinolysis : an international journal in haemostasis and thrombosis
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A Novel APOB Mutation Identified by Exome Sequencing Cosegregates With Steatosis, Liver Cancer, and Hypocholesterolemia

2013

Objective— In familial hypobetalipoproteinemia, fatty liver is a characteristic feature, and there are several reports of associated cirrhosis and hepatocarcinoma. We investigated a large kindred in which low-density lipoprotein cholesterol, fatty liver, and hepatocarcinoma displayed an autosomal dominant pattern of inheritance. Approach and Results— The proband was a 25-year-old female with low plasma cholesterol and hepatic steatosis. Low plasma levels of total cholesterol and fatty liver were observed in 10 more family members; 1 member was affected by liver cirrhosis, and 4 more subjects died of either hepatocarcinoma or carcinoma on cirrhosis. To identify the causal mutation in this f…

AdultMalemedicine.medical_specialtySettore MED/09 - Medicina InternaApolipoprotein BNonsense mutationBiologyArticlehypobetaliproteinemia type 1Hypobetalipoproteinemiasexome fatty liver hypobetalipoproteinemia familial 2Young Adultsymbols.namesakeInternal medicinemedicineHumansExomeHEPATOCELLULAR CARCINOMAExomeExome sequencingApolipoproteins Bfatty liverFamily HealthGeneticsSanger sequencingLiver NeoplasmsFatty liverMiddle AgedHEPATOCELLULAR CARCINOMA; exome; fatty liver; hypobetaliproteinemia type 1medicine.diseasePedigreeFatty LiverHypocholesterolemiaCholesterolEndocrinologyCodon Nonsensebiology.proteinsymbolsFemaleCardiology and Cardiovascular MedicineLiver cancerexomeArteriosclerosis, Thrombosis, and Vascular Biology
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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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Efficacy and safety of lomitapide in familial chylomicronaemia syndrome

2022

Familial chylomicronaemia syndrome (FCS) is a rare autosomal recessive disorder, resulting in elevated triglycerides (TGs), abdominal pain and pancreatitis. Treatment options are limited. Lomitapide, a microsomal triglyceride transfer protein inhibitor, is approved for the treatment of homozygous familial hypercholesterolaemia. Whether its therapeutic use may be extended to FCS remains unknown. The aim of this study was to evaluate the efficacy and safety of lomitapide in adult patients with FCS.The open-label, single-arm 'LOCHNES' study of lomitapide in FCS enrolled patients18 years with genetically confirmed FCS, elevated fasting TG ≥ 750 mg/dL and history of pancreatitis. Patients were a…

AdultPancreatitiSettore MED/09 - Medicina InternaTriglycerideBenzimidazoleLomitapideAbdominal PainPancreatitisHyperlipoproteinemia Type I.HumansBenzimidazolesHyperlipoproteinemia Type ICardiology and Cardiovascular MedicineTriglyceridesFamilial chylomicronaemia syndromeHuman
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