Search results for "onset"

showing 10 items of 496 documents

Role of Colchicine Treatment in Tumor Necrosis Factor Receptor Associated Periodic Syndrome (TRAPS): Real-Life Data from the AIDA Network

2020

Objective. To analyze the potential role of colchicine monotherapy in patients with tumor necrosis factor receptor associated periodic syndrome (TRAPS) in terms of control of clinical and laboratory manifestations. Methods. Patients with TRAPS treated with colchicine monotherapy were retrospectively enrolled; demographic, clinical and therapeutic data were collected and statistically analysed after having clustered patients according to different times at disease onset, penetrance of mutations, dosage of colchicine, and different disease manifestations. Results. 24 patients (14 males; 15 with pediatric disease onset) treated with colchicine monotherapy were enrolled. Colchicine resulted in …

Male0301 basic medicineEye DiseasesTRAPSColchicineAIDA NetworkGene mutationGastroenterologyReceptors Tumor Necrosis Factorchemistry.chemical_compoundSettore MED/38 - Pediatria Generale E Specialistica0302 clinical medicineReceptorsPathologyRB1-214ColchicineAge of OnsetYoung adultChildAmyloidosisAmyloidosisSyndromeMiddle AgedColchicine tumor necrosis factor TRAPSInflamacióPenetrancePhenotypeChild PreschoolFemaleJoint DiseasesResearch ArticleAdultRiskmedicine.medical_specialtyAdolescentFeverArticle SubjectImmunologyAdolescent; Adult; Age of Onset; Amyloidosis; Child; Child Preschool; Colchicine; Exanthema; Eye Diseases; Female; Fever; Humans; Joint Diseases; Male; Middle Aged; Mutation; Myalgia; Phenotype; Receptors Tumor Necrosis Factor; Retrospective Studies; Risk; Syndrome; Young AdultLower riskYoung Adult03 medical and health sciencesInternal medicinemedicineHumansPreschoolRetrospective StudiesInflammation030203 arthritis & rheumatologybusiness.industryTRAPSRetrospective cohort studyMyalgiaCell BiologyExanthemamedicine.disease030104 developmental biologychemistryMutationAge of onsetColchicineTumor Necrosis FactorbusinessMediators of Inflammation
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Early-infantile onset epilepsy and developmental delay caused by bi-allelic GAD1 variants

2020

Mice lacking GAD1 show neonatal mortality, but the human phenotype associated with GAD1 disruption is poorly characterized. Neuray et al. describe six patients with biallelic GAD1 mutations, presenting with early-infantile onset epilepsy, neurodevelopmental delay, muscle weakness and non-CNS manifestations.

Male0301 basic medicineGlutamate decarboxylaseMalalties cerebralsNeurotransmissorsNeurodevelopmental delayEpilepsy0302 clinical medicineMESH: ChildAge of OnsetChildcleft palateGAD1AcademicSubjects/SCI01870Glutamate DecarboxylaseGlutamate receptorMuscle weakness//purl.org/becyt/ford/3.1 [https]NeurotransmittersMESH: InfantHypotoniamuscle weakneCleft palateMESH: EpilepsyChild PreschoolMuscle Hypotonia[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]//purl.org/becyt/ford/3 [https]FemaleBrain diseasesAbnormalitiesmedicine.symptomMultiplemedicine.drugcleft palate; epilepsy; GAD1; muscle weakness; neurodevelopmental delayMESH: Glutamate Decarboxylasemedicine.medical_specialtyMESH: Abnormalities MultipleMESH: MutationMESH: Age of OnsetBiologyInhibitory postsynaptic potentialGAD1 cleft palate epilepsy muscle weakness neurodevelopmental delay.gamma-Aminobutyric acidGAD1neurodevelopmental delay03 medical and health sciencesExcitatory synapseInternal medicinemedicineHumansAbnormalities MultiplePreschoolAllelesMESH: Neurodevelopmental Disordersmuscle weaknessMESH: HumansEpilepsyMESH: Muscle HypotoniaMESH: AllelesMESH: Child PreschoolInfantmedicine.diseaseMESH: MaleEpilèpsiaEditor's Choice030104 developmental biologyEndocrinologyNeurodevelopmental DisordersMutationepilepsyAcademicSubjects/MED00310Neurology (clinical)Cleft palate; Epilepsy; GAD1; Muscle weakness; Neurodevelopmental delay; Abnormalities Multiple; Age of Onset; Alleles; Child; Child Preschool; Epilepsy; Female; Glutamate Decarboxylase; Humans; Infant; Male; Muscle Hypotonia; Mutation; Neurodevelopmental DisordersMESH: Female[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology030217 neurology & neurosurgeryReports
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Pyridoxine dependent epilepsies: new therapeutical point of view

2017

Abstract Pyridoxine dependent epilepsies (PDEs) are rare autosomal recessive disorders with onset in neonatal period. Seizures are typically not responsive to conventional antiepileptic drugs, but they cease after parental pyridoxine administration. Atypical forms are characterized partly response to pyridoxine and a late onset of symptoms (up to the age of three years). Prevalence is variable and it has rarely been described. The genes involved in PDEs are the gene encoding for the Alpha-aminoadipic-semialdehyde dehydrogenase (ALDH7A1) and PROSC gene, which encodes a pyridoxal-5-phosphate binding protein. Mutations in the gene encoding for the pyridoxal-5′-phosphate oxidase enzyme (PNPO) a…

Male0301 basic medicineNew therapeutical approachTreatment outcomePNPOBioinformaticsSeverity of Illness IndexEpilepsy0302 clinical medicineLetter to the EditorAnticonvulsant drugsDrugs-resistant seizuresBrain Diseases MetabolicIncidencelcsh:RJ1-570PyridoxineElectroencephalographyPyridoxine dependent epilepsiesPrognosisPyridoxaminephosphate OxidaseTreatment OutcomeChild PreschoolHypoxia-Ischemia BrainConventional anticonvulsant drugAnticonvulsantsFemalemedicine.drugmedicine.medical_specialtyLate onsetRisk Assessment03 medical and health sciencesDrugs-resistant seizureSeizuresInternal medicinePyridoxine administrationmedicineHumansGenetic Predisposition to DiseaseGeneEpilepsyPyridoxaminephosphate Oxidasebusiness.industryInfantlcsh:PediatricsPyridoxinemedicine.disease030104 developmental biologyEndocrinologyConventional anticonvulsant drugsbusiness030217 neurology & neurosurgeryItalian Journal of Pediatrics
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A Recurrent De Novo PACS2 Heterozygous Missense Variant Causes Neonatal-Onset Developmental Epileptic Encephalopathy, Facial Dysmorphism, and Cerebel…

2018

International audience; Developmental and epileptic encephalopathies (DEEs) represent a large clinical and genetic heterogeneous group of neurodevelopmental diseases. The identification of pathogenic genetic variants in DEEs remains crucial for deciphering this complex group and for accurately caring for affected individuals (clinical diagnosis, genetic counseling, impacting medical, precision therapy, clinical trials, etc.). Whole-exome sequencing and intensive data sharing identified a recurrent de novo PACS2 heterozygous missense variant in 14 unrelated individuals. Their phenotype was characterized by epilepsy, global developmental delay with or without autism, common cerebellar dysgene…

Male0301 basic medicinePathologyPACS-2Vesicular Transport ProteinsPHENOTYPEBioinformaticsDISEASESensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]Epilepsy0302 clinical medicineMissense mutationGlobal developmental delayAge of OnsetChildGenetics (clinical)Epileptic encephalopathyAPOPTOSIS3. Good healthcerebellar dysgenesisMutation Missense/geneticsintellectual disabilityChild PreschoolEpilepsy GeneralizedFemalePACS2CLINICAL EPILEPSYmedicine.medical_specialtyHeterozygoteGeneralized/geneticsPROTEINSGenetic counselingMutation MissenseMissense/geneticsNeonatal onsetBiologyDIAGNOSISVesicular Transport Proteins/geneticsFacial dysmorphism03 medical and health sciencesDysgenesisAll institutes and research themes of the Radboud University Medical CenterCerebellar DiseasesReportMENDELIAN DISORDERSGeneticsmedicineHumansGeneralized epilepsyPreschoolNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Cerebellar Diseases/geneticsbusiness.industryMUTATIONSInfant NewbornCorrectionInfantFaciesNewbornmedicine.disease030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMutationepilepsyAutismbusinessEpilepsy Generalized/genetics030217 neurology & neurosurgery
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H-ferritin and CD68+/H-ferritin+ monocytes/macrophages are increased in the skin of adult-onset Still's disease patients and correlate with the multi…

2016

Summary Adult-onset Still's disease (AOSD) patients may show an evanescent salmon-pink erythema appearing during febrile attacks and reducing without fever. Some patients may experience this eruption for many weeks. During AOSD, exceptionally high serum levels of ferritin may be observed; it is an iron storage protein composed of 24 subunits, heavy (H) subunits and light (L) subunits. The ferritin enriched in L subunits (L-ferritin) and the ferritin enriched in H subunits (H-ferritin) may be observed in different tissues. In this work, we aimed to investigate the skin expression of both H-and L-ferritin and the number of macrophages expressing these molecules from AOSD patients with persist…

Male0301 basic medicinePathologymedicine.medical_specialtyAdult-onset Still's diseaseDermal immune systemErythemaMacrophageBiopsyImmunologyAntigens Differentiation MyelomonocyticGene ExpressionDiseaseAdult-onset Still's diseaseMonocytesH-Ferritin03 medical and health sciences0302 clinical medicineAntigens CDadult-onset Still's disease; dermal immune system; ferritin; hyperferritinaemic syndrome; macrophagemedicineHumansImmunology and AllergyMonocytes macrophagesMacrophageRNA MessengerSkin030203 arthritis & rheumatologyFerritinbiologyCD68MacrophagesOriginal ArticlesFerritinSettore MED/16 - Reumatologia030104 developmental biologyApoferritinsImmunologyLeukocytes Mononuclearbiology.proteinCytokinesFemaleInflammation Mediatorsmedicine.symptomHyperferritinaemic syndromeStill's Disease Adult-OnsetBiomarkersClinical and Experimental Immunology
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Adult-onset Still's disease: an Italian multicentre retrospective observational study of manifestations and treatments in 245 patients

2016

Adult-onset Still’s disease (AOSD) is a systemic inflammatory condition of unknown aetiology characterized by typical episodes of spiking fever, evanescent rash, arthralgia, leukocytosis and hyperferritinemia. Given the lack of data in Italian series, we promote a multicentric data collection to characterize the clinical phenotype of Italian patients with AOSD. Data from 245 subjects diagnosed with AOSD were collected by 15 centres between March and May 2013. The diagnosis was made following Yamaguchi’s criteria. Data regarding clinical manifestations, laboratory features, disease course and treatments were reported and compared with those presented in other published series of different et…

Male0301 basic medicinePediatricsAdult-onset Still's diseaseSettore MED/16 - REUMATOLOGIALeukocytosisClinical presentationArthritisComorbidityDiseaseLaboratory finding0302 clinical medicineAdrenal Cortex HormonesLeukocytosisAdult-onset Still’s diseaseBiologic drugsMedicine (all)General MedicineMiddle AgedRashRetrospective studyTreatment OutcomeItalyAdult-onset Still’s disease; Biologic drugs; Clinical presentation; Laboratory findings; Retrospective study; Rheumatology; Medicine (all)Antirheumatic AgentsFemalemedicine.symptomStill's Disease Adult-OnsetAdultLaboratory findingsmedicine.medical_specialtyAdolescentFeverNOYoung Adult03 medical and health sciencesRheumatologyInternal medicinemedicineHumansAgedRetrospective Studies030203 arthritis & rheumatologybusiness.industryAdult-onset Still’s disease; Biologic drugs; Clinical presentation; Laboratory findings; Retrospective study; RheumatologyRetrospective cohort studymedicine.diseaseNeutrophiliaRheumatologySurgery030104 developmental biologybusinessBiologic drug
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Application of whole-exome sequencing to unravel the molecular basis of undiagnosed syndromic congenital neutropenia with intellectual disability

2016

International audience; Neutropenia can be qualified as congenital when of neonatal onset or when associated with extra-hematopoietic manifestations. Overall, 30% of patients with congenital neutropenia (CN) remain without a molecular diagnosis after a multidisciplinary consultation and tedious diagnostic strategy. In the rare situations when neutropenia is identified and associated with intellectual disability (ID), there are few diagnostic hypotheses to test. This retrospective multicenter study reports on a clinically heterogeneous cohort of 10 unrelated patients with CN associated with ID and no molecular diagnosis prior to whole-exome sequencing (WES). WES provided a diagnostic yield o…

Male0301 basic medicinePediatricsmedicine.medical_specialtyNeutropeniaAdolescentNeonatal onsetNeutropenia03 medical and health sciences0302 clinical medicinecongenital neutropenia[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyIntellectual DisabilityIntellectual disabilityGeneticsmedicineCongenital Bone Marrow Failure SyndromesHumansExomeChildCongenital NeutropeniaGenetic Association StudiesGenetics (clinical)Exome sequencingRetrospective Studiesbusiness.industryHigh-Throughput Nucleotide SequencingInfantSyndromemedicine.disease3. Good healthPhenotype030104 developmental biologyCHD2Child Preschool030220 oncology & carcinogenesisCohortEtiologyFemalebusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyBiomarkersAmerican Journal of Medical Genetics Part A
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Expanding the β-III Spectrin-Associated Phenotypes toward Non-Progressive Congenital Ataxias with Neurodegeneration

2021

(1) Background: A non-progressive congenital ataxia (NPCA) phenotype caused by b-III spectrin (SPTBN2) mutations has emerged, mimicking spinocerebellar ataxia, autosomal recessive type 14 (SCAR14). The pattern of inheritance, however, resembles that of autosomal dominant classical spinocerebellar ataxia type 5 (SCA5). (2) Methods: In-depth phenotyping of two boys studied by a customized gene panel. Candidate variants were sought by structural modeling and protein expression. An extensive review of the literature was conducted in order to better characterize the SPTBN2-associated NPCA. (3) Results: Patients exhibited an NPCA with hypotonia, developmental delay, cerebellar syndrome, and cogni…

Male0301 basic medicineProbandPathologyProtein ConformationSequence Homology<i>SPTBN2 </i>geneb-III spectrin030105 genetics & heredityFluid-attenuated inversion recoveryCohort Studieslcsh:ChemistryNon-progressive congenital ataxia0302 clinical medicineβ-III spectrinSpectrin:enfermedades del sistema nervioso::enfermedades neurodegenerativas [ENFERMEDADES]Age of OnsetChildlcsh:QH301-705.5Spectroscopy:Otros calificadores::Otros calificadores::/genética [Otros calificadores]NeurodegenerationneurodegenerationNeurodegenerative Diseasesnon-progressive congenital ataxiaSyndromeGeneral MedicinePhenotypeHypotoniaComputer Science ApplicationsPhenotype:Nervous System Diseases::Neurodegenerative Diseases [DISEASES]Spinocerebellar ataxiamedicine.symptomSPTBN2 genemedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesCerebellar AtaxiaNeuroimagingBiologyCatalysisArticleInorganic Chemistry03 medical and health sciences:Nervous System Diseases::Central Nervous System Diseases::Brain Diseases::Cerebellar Diseases::Cerebellar Ataxia [DISEASES]:Other subheadings::Other subheadings::/genetics [Other subheadings]medicineHumansAmino Acid SequencePhysical and Theoretical ChemistryNeurodegenerationMolecular BiologyGenetic Association StudiesOrganic ChemistrySpectrinmedicine.diseaseHyperintensitySistema nerviós - Degeneració - Aspectes genèticslcsh:Biology (General)lcsh:QD1-999:enfermedades del sistema nervioso::enfermedades del sistema nervioso central::enfermedades cerebrales::enfermedades cerebelosas::ataxia cerebelosa [ENFERMEDADES]Mutation030217 neurology & neurosurgeryInternational Journal of Molecular Sciences
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Fungal Dysbiosis and Intestinal Inflammation in Children With Beta-Cell Autoimmunity

2020

Although gut bacterial dysbiosis is recognized as a regulator of beta-cell autoimmunity, no data is available on fungal dysbiosis in the children at the risk of type 1 diabetes (T1D). We hypothesized that the co-occurrence of fungal and bacterial dysbiosis contributes to the intestinal inflammation and autoimmune destruction of insulin-producing beta-cells in T1D. Fecal and blood samples were collected from 26 children tested positive for at least one diabetes-associated autoantibody (IAA, GADA, IA-2A or ICA) and matched autoantibody-negative children with HLA-conferred susceptibility to T1D (matched for HLA-DQB1 haplotype, age, gender and early childhood nutrition). Bacterial 16S and funga…

Male0301 basic medicinebeta-Defensinstype 1 diabetessuolistomikrobistoAutoimmunityGut floramedicine.disease_causeautoimmuniteettiAutoimmunityFeces0302 clinical medicineautoimmuunisairaudetInsulin-Secreting CellsHLA-DQ beta-ChainsImmunology and AllergyMedicineChildFinlandOriginal ResearchCandida2. Zero hungerRISKMUCOSAtulehdusbiologyGUT MICROBIOTAdysbiosisFungal antigen3. Good healthChild PreschoolgutCATHELICIDIN LL-37Femalemedicine.symptomlcsh:Immunologic diseases. AllergyAdolescentImmunologyInflammationIMMUNITY03 medical and health sciencesmycobiomeSaccharomycesSEROCONVERSIONHumansPERMEABILITYAntibodies FungalTYPE-1AutoantibodiesType 1 diabetesbusiness.industrynuoruustyypin diabetesAutoantibodymedicine.diseasebiology.organism_classificationDiabetes Mellitus Type 1030104 developmental biologyMycoseshiivasienetinflammation3121 General medicine internal medicine and other clinical medicineImmunologyANTIBODIESONSET3111 BiomedicineCalprotectinbusinesslcsh:RC581-607Dysbiosis030215 immunology
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DNA Methylation Analysis to Unravel Altered Genetic Pathways Underlying Early Onset and Late Onset Neonatal Sepsis. A Pilot Study

2021

Background: Neonatal sepsis is a systemic condition widely affecting preterm infants and characterized by pro-inflammatory and anti-inflammatory responses. However, its pathophysiology is not yet fully understood. Epigenetics regulates the immune system, and its alteration leads to the impaired immune response underlying sepsis. DNA methylation may contribute to sepsis-induced immunosuppression which, if persistent, will cause long-term adverse effects in neonates.Objective: To analyze the methylome of preterm infants in order to determine whether there are DNA methylation marks that may shed light on the pathophysiology of neonatal sepsis.Design: Prospective observational cohort study perf…

Male0301 basic medicinelcsh:Immunologic diseases. AllergyNeonatal intensive care unitgenetic structuresImmunologyPilot ProjectsLate onsetAdaptive ImmunityBioinformaticsCohort StudiesDiagnosis DifferentialSepsissepsis03 medical and health sciences0302 clinical medicineHumansImmunology and AllergyMedicineProspective StudiesEpigeneticsOriginal ResearchGenomeDNA methylationimmunosuppressionNeonatal sepsisbusiness.industryInfant Newbornneonatology and pediatric intensive careMethylationmedicine.diseaseImmunity Innate030104 developmental biologyinflammation030220 oncology & carcinogenesisDNA methylationBiomarker (medicine)FemaleNeonatal Sepsisbusinesslcsh:RC581-607Infant PrematureFrontiers in Immunology
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