Search results for "Familial"

showing 10 items of 365 documents

Effectiveness of cascade filtration plasmapheresis in two patients affected by familial hypercholesterolemia

1995

Hypercholesterolemia has been recognised as a primary risk factor for coronary heart disease. Reduction of plasma levels of total and LDL cholesterol has been shown to decrease coronary atherosclerosis. Plasmapheresis represents an useful non-pharmacological tool to treat severe hypercholesterolemias. We have evaluated the effectiveness of a system of plasmapheresis using a cascade filtration method in two young male subjects (aged 16 and 26 years) with homozygous familial hypercholesterolemia. Both showed severe coronary atherosclerosis as determined by angiography. Procedures were performed at intervals of 7 days in each case. We observed a mean reduction of plasma levels of total cholest…

AdultMalemedicine.medical_specialtyAdolescentApolipoprotein Bmedicine.medical_treatmentFamilial hypercholesterolemiaFibrinogenGastroenterologyHyperlipoproteinemia Type IIchemistry.chemical_compoundInternal medicinemedicineHumansHyperlipoproteinemia Type IIRisk factorCoronary atherosclerosisbiologybusiness.industryCholesterolCholesterol LDLPlasmapheresisHematologyGeneral Medicinemedicine.diseaseEndocrinologychemistrybiology.proteinlipids (amino acids peptides and proteins)PlasmapheresisbusinessFiltrationmedicine.drugJournal of Clinical Apheresis
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Insulin resistance and oxidative stress in familial combined hyperlipidemia.

2007

Oxidative stress is associated with atherosclerosis. Familial combined hyperlipidemia (FCH) is considered as a human model of primary dyslipidemia and atherosclerosis frequently associated with insulin resistance (IR), but there are few data on its possible relation to oxidative stress. The objective of this study was to evaluate oxidative stress status using different markers in subjects with FCH assessing its possible correlation with anthropometric parameters and IR. This was a cross-sectional study. A cohort of 40 FCH patients (20 with IR (HOMAor=3.2) and 20 without IR (HOMA3.2)), and 20 healthy volunteers were included, all of them non-diabetic, normotensive and non-smokers. We measure…

AdultMalemedicine.medical_specialtyAdolescentHyperlipidemia Familial Combinedmedicine.disease_causeAnthropometric parametersInsulin resistanceInternal medicinemedicineHumansAgedGlutathione Disulfidebusiness.industryVascular diseasenutritional and metabolic diseasesDeoxyguanosineMiddle Agedmedicine.diseaseAtherosclerosisGlutathioneLipidsFamilial combined hyperlipidemiaOxidative StressEndocrinology8-Hydroxy-2'-DeoxyguanosineCohortFemaleInsulin ResistanceCardiology and Cardiovascular MedicinebusinessDyslipidemiaOxidative stressAtherosclerosis
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Small-Bowel Diagnosis in Patients with Familial Adenomatous Polyposis: Comparison of Push Enteroscopy, Capsule Endoscopy, Ileoscopy, and Enteroclysis

2009

BACKGROUND: Conventional upper endoscopy (EGD), EGD with side-view endoscope and ileoscopy are established procedures for endoscopic evaluation of patients with familial adenomatous polyposis (FAP). However, we still have little data on the frequency and relevance of adenomas in those parts of the small bowel which are not accessible to EGD and ileoscopy. Adenomas distal to the duodenum are found more often in FAP patients with known duodenal adenomas. The question is, whether these patients can benefit from additional endoscopic and/or radiographic examinations. METHODS: Between July 2001 and August 2006 we performed comparative small bowel studies with push enteroscopy (PE), capsule endos…

AdultMalemedicine.medical_specialtyAdolescentendocrine system diseasesEndoscopeDuodenumBiopsyRadiographyContrast MediaCapsule EndoscopySensitivity and SpecificityGastroenterologyEndoscopy GastrointestinalFamilial adenomatous polyposislaw.inventionYoung AdultCapsule endoscopylawInternal medicineIntestine SmallmedicinePush enteroscopyHumansIn patientIntubation GastrointestinalAgedbusiness.industryGastroenterologyMiddle Agedmedicine.diseasedigestive system diseasesstomatognathic diseasesCell Transformation NeoplasticJejunummedicine.anatomical_structureAdenomatous Polyposis ColiDuodenumFemaleBarium SulfatePouchbusinessZeitschrift für Gastroenterologie
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Small and dense LDL in Familial Combined Hyperlipidemia and N291S polymorphism of the lipoprotein lipase gene

2009

18 pagesm 2 figures. -- PMID: 19335919 [PubMed]

AdultMalemedicine.medical_specialtyApolipoprotein BAdolescentEndocrinology Diabetes and MetabolismPopulationClinical BiochemistryHyperlipidemia Familial CombinedMutation MissenseBlood lipidschemistry.chemical_compoundYoung AdultHigh-density lipoproteinEndocrinologyInternal medicinePrevalenceMedicineShort PaperHumanseducationlcsh:RC620-627AgedBiochemistry medicalLipoprotein lipaseeducation.field_of_studyPolymorphism Geneticmedicine.diagnostic_testbiologyCholesterolbusiness.industryBiochemistry (medical)Cholesterol LDLMiddle AgedAtherosclerosisLipidslcsh:Nutritional diseases. Deficiency diseasesLipoprotein LipaseEndocrinologychemistrySpainLow-density lipoproteinCase-Control Studiesbiology.proteinFemalelipids (amino acids peptides and proteins)businessLipid profile
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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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Lipoprotein phenotype and insulin resistance in familial combined hyperlipidemia.

2001

The study objective was to investigate the relationship of insulin resistance (IR) with the lipoprotein phenotype in familial combined hyperlipidemia (FCH). Thirty-seven FCH men diagnosed by clinical and biochemical criteria and classified as lipoprotein phenotype IIa (n = 9), IIb (n = 17), or IV (n = 11) were compared with a healthy control group of 30 men of similar age, body mass index (BMI), waist to hip ratio (WHR), and systolic and diastolic blood pressure. In all subjects, the plasma lipoprotein profile and baseline and post-oral glucose tolerance test (OGTT) glucose and insulin plasma values were measured. An intravenous glucose tolerance test was performed and IR was studied by the…

AdultMalemedicine.medical_specialtyEndocrinology Diabetes and Metabolismmedicine.medical_treatmentLipoproteinsHyperlipidemia Familial CombinedEndocrinologyWaist–hip ratioInsulin resistanceReference ValuesInternal medicineInsulin SecretionmedicineHumansInsulinPancreatic hormoneHypertriglyceridemiaGlucose tolerance testmedicine.diagnostic_testChemistryInsulinHypertriglyceridemiaArea under the curveGlucose Tolerance TestMiddle Agedmedicine.diseaseEndocrinologyPhenotypeInsulin ResistanceLipoproteinMetabolism: clinical and experimental
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Association of C677T polymorphism in MTHFR gene, high homocysteine and low HDL cholesterol plasma values in heterozygous familial hypercholesterolemi…

2010

Aim: to investigate the association of C677T polymorphism in the methylene tetrahydrofolate reductase (MTHFR) gene, homocysteine plasma values (Hcy), and plasma HDL cholesterol in heterozy-gous familial hypercholesterolemia (hFH).Methods: One hundred and twenty-five hFH subjects were studied. Plasma lipid, lipoprotein, vitamin B12, folic acid and Hcy values were determined. C677T polymorphism in the MTHFR gene was detected by SSCP-PCR. Genetic diagnosis of FH was determined by a three-step protocol using SSCP-PCR, Southern blot, long PCR and automatic sequencing.Results: We found significant differences in plasma HDL-C (CC 1.39±0.34, CT 1.33±0.39 and TT 1.14±0.26 mmol/L, p=0.028) between th…

AdultMalemedicine.medical_specialtyHeterozygoteApolipoprotein BHomocysteineHypercholesterolemiaFamilial hypercholesterolemiaPolymerase Chain Reactionchemistry.chemical_compoundInternal medicineGenotypeInternal MedicinemedicineHumansVitamin B12HomocysteineMethylenetetrahydrofolate Reductase (NADPH2)Polymorphism Single-Stranded ConformationalApolipoproteins BGeneticsPolymorphism GeneticbiologyCholesterolbusiness.industryBiochemistry (medical)Cholesterol HDLMiddle Agedmedicine.diseaseEndocrinologychemistryReceptors LDLMethylenetetrahydrofolate reductaseMutationbiology.proteinFemaleCardiology and Cardiovascular MedicinebusinessLipoproteinJournal of atherosclerosis and thrombosis
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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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