Search results for "Inborn errors"

showing 10 items of 40 documents

Newborn screening and disease variants predict neurological outcome in isovaleric aciduria.

2021

Isovaleric aciduria (IVA), a metabolic disease with severe (classic IVA) or attenuated phenotype (mild IVA), is included in newborn screening (NBS) programs worldwide. The long-term clinical benefit of screened individuals, however, is still rarely investigated. A national, prospective, observational, multi-center study of individuals with confirmed IVA identified by NBS between 1998 and 2018 was conducted. Long-term clinical outcomes of 94 individuals with IVA were evaluated, representing 73.4% (for classic IVA: 92.3%) of the German NBS cohort. In classic IVA (N = 24), NBS prevented untimely death except in one individual with lethal neonatal sepsis (3.8%) but did not completely prevent si…

MalePediatricsmedicine.medical_specialtyAdolescentNeurocognitive DisordersDisease03 medical and health sciencesYoung AdultCognitionNeonatal ScreeningMaintenance therapyGermanyGeneticsmedicineHumansProspective StudiesMetabolic diseaseChildAmino Acid Metabolism Inborn ErrorsGenetics (clinical)030304 developmental biology0303 health sciencesNewborn screeningNeonatal sepsisIsovaleryl-CoA Dehydrogenasebusiness.industry030305 genetics & heredityInfant NewbornInfantmedicine.diseasePrognosisIsovaleric AcidemiaPhenotypeChild PreschoolCohortFemalesense organsbusinessNeurocognitiveJournal of inherited metabolic diseaseREFERENCES
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Clinical manifestations and management of four children with Pearson syndrome.

2011

Pearson marrow-pancreas syndrome is a fatal disorder mostly diagnosed during infancy and caused by mutations of mitochondrial DNA. We hereby report on four children affected by Pearson syndrome with hematological disorders at onset. The disease was fatal to three of them and the fourth one, who received hematopoietic stem cell transplantation, died of secondary malignancy. In this latter patient transplantation corrected hematological and non-hematological issues like metabolic acidosis, and we therefore argue that it could be considered as a useful option in an early stage of the disease.

MalePediatricsmedicine.medical_specialtyMitochondrial DiseasesAnemiaMitochondrial diseasemedicine.medical_treatmenttrapianto cellule staminali emopoieticheHematopoietic stem cell transplantationDiseaseDNA MitochondrialLipid Metabolism Inborn Errorsmitochondrial disordersFatal OutcomeMuscular DiseasesCause of Deathhematopoietic stem cell transplantation; mitochondrial disorders; Pearson marrow-pancreas syndrome; trapianto cellule staminali emopoietiche; malattie mitocondriali; sindrome di PearsonGeneticsmedicineCongenital Bone Marrow Failure SyndromesHumansChildGenetics (clinical)Pearson marrow-pancreas syndromeCause of deathPearson syndromebusiness.industryAcyl-CoA Dehydrogenase Long-ChainHematopoietic Stem Cell TransplantationInfantMetabolic acidosissindrome di Pearsonmedicine.diseaseAnemia SideroblasticTransplantationChild PreschoolImmunologymalattie mitocondrialiFemalebusinessGene DeletionAmerican journal of medical genetics. Part A
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Exome sequencing in suspected monogenic dyslipidemias.

2015

Background— Exome sequencing is a promising tool for gene mapping in Mendelian disorders. We used this technique in an attempt to identify novel genes underlying monogenic dyslipidemias. Methods and Results— We performed exome sequencing on 213 selected family members from 41 kindreds with suspected Mendelian inheritance of extreme levels of low-density lipoprotein cholesterol (after candidate gene sequencing excluded known genetic causes for high low-density lipoprotein cholesterol families) or high-density lipoprotein cholesterol. We used standard analytic approaches to identify candidate variants and also assigned a polygenic score to each individual to account for their burden of commo…

MaleSettore MED/09 - Medicina InternaMedical BiotechnologyDNA sequencing; exome; exome sequencing; genetics human; lipids; mendelian geneticsBiologyCardiorespiratory Medicine and HaematologyNovel genelipidsmendelian geneticsGene mappingClinical ResearchGenetics2.1 Biological and endogenous factorsHumansgeneticsExomeDNA sequencinghumanAetiologyMendelian disordersExomeGenetics (clinical)Exome sequencingDyslipidemiasGeneticsInborn ErrorsHuman GenomeHigh-Throughput Nucleotide SequencingAtherosclerosisMetabolismCardiovascular System & Hematologylipids (amino acids peptides and proteins)DNA sequencing; exome; genetics; human; lipidsFemalegeneticCardiology and Cardiovascular Medicineexome sequencingexomeMetabolism Inborn ErrorsCirculation. Cardiovascular genetics
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Long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency: a severe fatty acid oxidation disorder

1994

3-Hydroxyacyl-CoA dehydrogenase deficiency is a newly recognised fatty acid oxidation disorder with a usually fatal outcome. We present a further patient who presented with hypoketotic hypoglycaemia, hepatopathy, secondary carnitine deficiency and increased plasma long-chain acylcarnitines. 3-Hydroxydicarboxylic aciduria was present and the diagnosis confirmed in cultured skin fibroblasts. Our patient is compared with those reported in the literature with respect to clinical symptoms, differential diagnosis and possible therapeutic regimens.

Malemedicine.medical_specialtyCardiomyopathyLipid Metabolism Inborn ErrorsFatal OutcomeInternal medicineCarnitineMedicineHumansBeta oxidationchemistry.chemical_classificationCultured skinbusiness.industryLiver DiseasesInfant Newborn3-Hydroxyacyl CoA DehydrogenasesMitochondrial MyopathiesClinical Enzyme Testsmedicine.diseaseDehydrogenase deficiencyHypoglycemiaEnzymeEndocrinologychemistrySecondary carnitine deficiencyPediatrics Perinatology and Child HealthDifferential diagnosisbusinessCardiomyopathiesLong-Chain-3-Hydroxyacyl-CoA DehydrogenaseEuropean journal of pediatrics
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ITPA deficiency and ribavirin level are still predictive of anaemia in HCV–HIV-coinfected patients receiving ribavirin combined with a first-generati…

2017

Background We aimed to determine the impact of inosine triphosphatase (ITPA) deficiency on ribavirin (RBV)-induced anaemia in HIV–HCV-coinfected patients receiving a triple therapy including the haematotoxic direct-acting antiviral agent boceprevir (BOC). Methods Patients of the ANRS HC27 BocepreVIH study were genotyped for two ITPA single nucleotide polymorphisms involved in ITPA deficiency. RBV trough concentration (Ctrough) was determined at week (W)4 and W8. Impact of ITPA deficiency on anaemia, RBV Ctrough, response and haematotoxicity (grade 3/4 anaemia, erythropoietin [EPO] use, RBV dose reduction or transfusion between day [D]0 and W8) was evaluated. Impact of RBV Ctrough on anaemia…

Malemedicine.medical_specialtyGenotype[SDV]Life Sciences [q-bio]Human immunodeficiency virus (HIV)HIV Infectionsmedicine.disease_causeAntiviral AgentsGastroenterologychemistry.chemical_compoundPharmacotherapyGene FrequencyRisk FactorsInternal medicineRibavirinmedicineHumansGenetic Predisposition to DiseasePharmacology (medical)PyrophosphatasesAllelesComputingMilieux_MISCELLANEOUSPharmacologyCoinfectionbusiness.industryRibavirinAnemiaHepatitis CHepatitis C ChronicMiddle Agedmedicine.diseaseFirst generation3. Good health[SDV] Life Sciences [q-bio]Infectious DiseaseschemistryMutationCoinfectionDrug Therapy CombinationFemaleITPAbusinessMetabolism Inborn ErrorsINOSINE TRIPHOSPHATASE
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N-Acetylneuraminic acid storage disease

1985

Increased amounts of free sialic acid were found in body fluids, leukocytes, cultured fibroblasts, and liver tissue of a four-year-old boy with mental retardation, ataxia, and clinical and radiologic findings of a mild mucopolysaccharidosis. A diagnosis of Salla disease was made though in contrast to earlier reports, recurrent upper respiratory infections and hepatosplenomegaly were present already in infancy, and skeletal abnormalities of dysostosis multiplex were found in early childhood. Free sialic acid in the urine was identified as N-acetylneuraminic acid by 1H-NMR spectroscopy. Sialidase activities were normal. Increased amounts of bound sialic acid were found in liver and cultured f…

Malemedicine.medical_specialtyMagnetic Resonance SpectroscopyMucopolysaccharidosisHepatosplenomegalyNeuraminidaseBiologySialidaseDiagnosis Differentialchemistry.chemical_compoundInternal medicineNeuraminic acidGeneticsmedicineHumansCells CulturedGenetics (clinical)Respiratory infectionmedicine.diseaseSialic acidRadiographySalla diseaseEndocrinologyLiverchemistryBiochemistryChild PreschoolSialic Acidsbiology.proteinChromatography Thin Layermedicine.symptomLysosomesNeuraminidaseMetabolism Inborn ErrorsHuman Genetics
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Nephrosis in two siblings with infantile sialic acid storage disease

1990

The diagnosis of infantile sialic acid storage disease (ISSD) was established in two siblings on the basis of typical clinical signs and the biochemical findings of hyperexcretion and intracellular storage of free sialic acid. A severe, steroid resistant nephrosis occurred in both siblings. The activities of lysosomal enzymes, including sialidase, were normal. A combined detection method for sialic acids with Limax flavus agglutinin labelling and phosphotungstic acid staining showed severely alterated sialic acid components in epithelial kidney cells and indicate a causal relationship between the nephrosis and the underlying biochemical defect. Further observations of ISSD patients with ren…

Malemedicine.medical_specialtyNephrosisKidney GlomerulusBiologyCarbohydrate metabolismSialidasechemistry.chemical_compoundInternal medicinemedicineHumansFamilychemistry.chemical_classificationKidneyInfant Newbornmedicine.diseasePhenotypeStainingSialic acidcarbohydrates (lipids)Microscopy Electronmedicine.anatomical_structureEnzymeEndocrinologychemistryBiochemistryPediatrics Perinatology and Child HealthSialic AcidsNephrosisFemaleLysosomesCarbohydrate Metabolism Inborn ErrorsEuropean Journal of Pediatrics
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Hypoadiponectinemia, cardiometabolic comorbidities and left ventricular hypertrophy

2014

This study was designed to evaluate the prevalence of cardiometabolic comorbidities and the changes in left ventricular geometry and function in 135 subjects subgrouped according to low or normal total adiponectin plasma (ADPN) levels. Left ventricular (LV) internal diameter/height, total LV mass (LVM) and LVM index (LVMI), relative wall thickness (RWT), LV ejection fraction by echocardiography and diastolic parameters by pulsed-wave Doppler were calculated. Body mass index (BMI) (p < 0.0001), waist-to-hip ratio (p < 0.03), triglycerides (p < 0,001), prevalence of obesity (p < 0.005), visceral obesity (p < 0.003), left ventricular hypertrophy (LVH) (p < 0.001), metabolic syndrome (p < 0.000…

Malemedicine.medical_specialtySettore MED/09 - Medicina InternaDiastoleBlood PressureComorbidityLeft ventricular hypertrophyBody Mass IndexCoronary artery diseaseMetabolic DiseasesInternal medicineInternal MedicinemedicineHumansObesityAgedAged 80 and overEjection fractionAdiponectinbusiness.industrymedicine.diseaseAdiponectin Cardiometabolic comorbidities Left ventricular hypertrophyBlood pressureCardiovascular DiseasesEmergency MedicineCardiologyFemaleHypertrophy Left VentricularAdiponectinMetabolic syndromebusinessBody mass indexMetabolism Inborn Errors
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Duchenne muscular dystrophy and idiopathic hyperCKemia segregating in a family

1995

A 7-month-old boy with gross motor delay and failure to thrive presented with rhabdomyolysis following an acute asthmatic episode. During hospitalization an electrocardiographic conversion to a Wolff-Parkinson-White type 1 (WPW) pattern took place. Duchenne muscular dystrophy (DMD) was suspected based on elevated creatine kinase (CK) serum levels, muscle biopsy, and family history. The diagnosis was confirmed by molecular analysis, which documented a deletion corresponding to cDNA probe 1-2a in the dystrophin gene, in the propositus and in an affected male cousin of his mother. "Idiopathic" hyperCKemia was found in the propositus, his father, and 5 of his relatives. We suggest that the unus…

Malemusculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesPediatricsmedicine.medical_specialtyDuchenne muscular dystrophyMolecular Sequence DataGene mutationPolymerase Chain ReactionMuscular DystrophiesGenomic ImprintingPrenatal DiagnosisInternal medicinemedicineHumansFamily historyCreatine KinaseGenetics (clinical)X-linked recessive inheritanceDNA PrimersGenes DominantMuscle biopsyBase Sequencebiologymedicine.diagnostic_testGenetic Carrier ScreeningInfantExonsmedicine.diseasePedigreeEndocrinologyMutationFailure to thrivebiology.proteinFemaleCreatine kinasemedicine.symptomDystrophinMetabolism Inborn ErrorsAmerican Journal of Medical Genetics
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Conformational response to ligand binding in phosphomannomutase2: insights into inborn glycosylation disorder.

2014

Background: Mutations in phosphomannomutase2 cause glycosylation disorder, a disease without a cure that will largely benefit from accurate ligand-bound models. Results: We obtained two models of phospomannomutase2 bound to glucose 1,6-bisphosphate and validated them with limited proteolysis. Conclusion: Ligand binding induces a large conformational transition in PMM2. Significance: We produce and validate closed-form models of PMM2 that represent a starting point for rational drug discovery.

Models MolecularPELEGlycosylationProtein Conformation1Molecular Sequence DataGlucose-6-PhosphateGlycosylation Inhibitor6-bisphosphate; PELE; computer modeling; drug discovery; glycosylation; glycosylation inhibitor; ligand-binding protein; phosphomannomutaseLigandsDrug DiscoveryAnimalsHumansAmino Acid Sequence16-BisphosphateProtein UnfoldingTemperatureLigand-binding Proteinphosphomannomutase 2 and mass spectrometryPhosphotransferases (Phosphomutases)PhosphomannomutaseMutationProteolysisMetabolism Inborn ErrorsMolecular BiophysicsPeptide HydrolasesProtein BindingComputer ModelingThe Journal of biological chemistry
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