Search results for "Hereditary"

showing 10 items of 650 documents

Tamoxifen may cause life-threatening angioedema attacks in patients with hereditary angioedema

2016

0301 basic medicinemedicine.medical_specialtyAngioedemaTrigger factorbusiness.industryMEDLINEDermatologymedicine.diseaseDermatology03 medical and health sciences030104 developmental biology0302 clinical medicineInfectious Diseases030228 respiratory systemSeverity of illnessHereditary angioedemamedicineIn patientmedicine.symptombusinessTamoxifenmedicine.drugJournal of the European Academy of Dermatology and Venereology
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Shortened Activated Partial Thromboplastin Time May Help in Diagnosing Hereditary and Acquired Angioedema

2016

<b><i>Objective:</i></b> To evaluate whether activated partial thromboplastin time (APTT) could be used in the laboratory diagnosis of hereditary or acquired angioedema (HAE or AAE) with and without C1 inhibitor (C1-INH) deficiency. <b><i>Methods:</i></b> In a prospective investigation, APTT and other coagulation parameters were determined in 149 adult patients with various types of angioedema and in 26 healthy participants (HP). <b><i>Results:</i></b> Mean APTT was significantly shortened in HAE-C1-INH type I (p < 0.0001) and type II (p = 0.0017) and in AAE-C1-INH (p < 0.0001) compared to the HP. APTT was shorten…

0301 basic medicinemedicine.medical_specialtyImmunologyAcquired angioedemaGastroenterologyC1-inhibitorDiagnosis Differential03 medical and health sciencesPredictive Value of TestsInternal medicinemedicineHumansImmunology and Allergyheterocyclic compoundsProspective StudiesAngioedemaProspective cohort studyBlood CoagulationBlood coagulation testAngioedemamedicine.diagnostic_testbiologybusiness.industryAngioedemas HereditaryComplement C4General Medicinerespiratory systembacterial infections and mycosesrespiratory tract diseases030104 developmental biologyCoagulationPredictive value of testsAnesthesiaImmunologybiology.proteinPartial Thromboplastin TimeBlood Coagulation Testsmedicine.symptombusinessComplement C1 Inhibitor ProteinBiomarkerscirculatory and respiratory physiologyPartial thromboplastin timeInternational Archives of Allergy and Immunology
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Development of the Angioedema Control Test—A patient‐reported outcome measure that assesses disease control in patients with recurrent angioedema

2019

Background Recurrent angioedema (AE) is an important clinical problem in the context of chronic urticaria (mast cell mediator-induced), ACE-inhibitor intake and hereditary angioedema (both bradykinin-mediated). To help patients obtain control of their recurrent AE is a major treatment goal. However, a tool to assess control of recurrent AE is not yet available. This prompted us to develop such a tool, the Angioedema Control Test (AECT). Methods After a conceptional framework was developed for the AECT, a list of potential AECT items was generated by a combined approach of patient interviews, literature review and expert input. Subsequent item reduction was based on impact analysis, inter-it…

0301 basic medicinemedicine.medical_specialtyImmunologyValidityContext (language use)Bradykinin03 medical and health sciences0302 clinical medicinemedicineContent validityHumansImmunology and AllergyPatient Reported Outcome MeasuresAngioedemaRetrospective StudiesRecallAngioedemabusiness.industryReproducibility of Resultsmedicine.diseaseDisease control030104 developmental biology030228 respiratory systemHereditary angioedemaPhysical therapyPatient-reported outcomemedicine.symptombusinessAllergy
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Measurement of Bradykinin Formation and Degradation in Blood Plasma: Relevance for Acquired Angioedema Associated With Angiotensin Converting Enzyme …

2020

Bradykinin (BK)-mediated angioedema (AE) states are rare acquired or hereditary conditions involving localized edema of the subcutaneous and submucosal tissues. Citrated plasma from healthy volunteers or patients with hereditary angioedema (HAE) with normal level of C1-inhibitor (C1-INH) was used to investigate pathways of BK formation and breakdown relevant to AE physiopathology. The half-life of BK (100 nM) added to normal plasma was 34 s, a value that was increased ~12-fold when the angiotensin converting enzyme (ACE) inhibitor enalaprilat (130 nM) was added (enzyme immunoassay measurements). The BK half-life was similarly increased ~5-fold following 2 daily oral doses of enalapril malea…

0301 basic medicinemedicine.medical_specialtykallikreinsPlasminBradykininTissue plasminogen activator03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicinemedicineB2 receptorsOriginal ResearchplasminFactor XIIlcsh:R5-920tissue plasminogen activatorAngioedemabiologyhereditary angioedema with normal C1 inhibitor levelAngiotensin-converting enzymeGeneral MedicineKallikreinmedicine.disease030104 developmental biologyEndocrinology030228 respiratory systemchemistryHereditary angioedemabiology.proteinMedicinemedicine.symptombradykininlcsh:Medicine (General)medicine.drugFrontiers in Medicine
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Deficiency of plasminogen activator inhibitor 2 in plasma of patients with hereditary angioedema with normal C1 inhibitor levels

2016

Background Hereditary angioedema with normal C1 inhibitor levels (HAE-N) is associated with a Factor XII mutation in 30% of subjects; however, the role of this mutation in the pathogenesis of angioedema is unclear. Objective We sought evidence of abnormalities in the pathways of bradykinin formation and bradykinin degradation in the plasma of patients with HAE-N both with and without the mutation. Methods Bradykinin was added to plasma, and its rate of degradation was measured by using ELISA. Plasma autoactivation was assessed by using a chromogenic assay of kallikrein formation. Plasminogen activator inhibitors (PAIs) 1 and 2 were also measured by means of ELISA. Results PAI-1 levels varie…

0301 basic medicinemedicine.medical_specialtymedicine.medical_treatmentImmunologyBradykinin030204 cardiovascular system & hematologyArticleC1-inhibitor03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineFibrinolysismedicineImmunology and AllergyFactor XIIAngioedemabiologybusiness.industryKallikreinmedicine.disease030104 developmental biologyEndocrinologychemistryPlasminogen activator inhibitor-1Hereditary angioedemabiology.proteinmedicine.symptombusinessJournal of Allergy and Clinical Immunology
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Risk-reducing hysterectomy and bilateral salpingo-oophorectomy in female heterozygotes of pathogenic mismatch repair variants: a Prospective Lynch Sy…

2021

Abstract Purpose To determine impact of risk-reducing hysterectomy and bilateral salpingo-oophorectomy (BSO) on gynecological cancer incidence and death in heterozygotes of pathogenic MMR ( path_MMR ) variants. Methods The Prospective Lynch Syndrome Database was used to investigate the effects of gynecological risk-reducing surgery (RRS) at different ages. Results Risk-reducing hysterectomy at 25 years of age prevents endometrial cancer before 50 years in 15%, 18%, 13%, and 0% of path_MLH1 , path_MSH2 , path_MSH6 , and path_PMS2 heterozygotes and death in 2%, 2%, 1%, and 0%, respectively. Risk-reducing BSO at 25 years of age prevents ovarian cancer before 50 years in 6%, 11%, 2%, and 0% and…

0301 basic medicinemedicine.medical_treatmentDNA Mismatch RepairGynecologic surgery0302 clinical medicineMalalties hereditàriesProspective StudiesProspective cohort studyGenetics (clinical)Mismatch Repair Endonuclease PMS2Incidence (epidemiology)Middle Aged16. Peace & justiceLynch syndrome3. Good health030220 oncology & carcinogenesisFemalesyöpätauditMutL Protein Homolog 1Genetic diseasesHeterozygotemedicine.medical_specialtySalpingo-oophorectomyCirurgia ginecològicaHysterectomyArticle03 medical and health sciencesCàncer colorectalCAPP2medicineHumansLynchin oireyhtymäGynecologyperinnölliset tauditHysterectomyHEREDITARY COLORECTAL-CANCERbusiness.industryEndometrial cancerCancermedicine.diseaseColorectal Neoplasms Hereditary NonpolyposisColorectal cancerASPIRIN030104 developmental biologyClinical researchLynch syndrome3121 General medicine internal medicine and other clinical medicinekohdunpoisto3111 BiomedicineOvarian cancerbusiness
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miR-23b and miR-218 silencing increase Muscleblind-like expression and alleviate myotonic dystrophy phenotypes in mammalian models

2018

Functional depletion of the alternative splicing factors Muscleblind-like (MBNL 1 and 2) is at the basis of the neuromuscular disease myotonic dystrophy type 1 (DM1). We previously showed the efficacy of miRNA downregulation in Drosophila DM1 model. Here, we screen for miRNAs that regulate MBNL1 and MBNL2 in HeLa cells. We thus identify miR-23b and miR-218, and confirm that they downregulate MBNL proteins in this cell line. Antagonists of miR-23b and miR-218 miRNAs enhance MBNL protein levels and rescue pathogenic missplicing events in DM1 myoblasts. Systemic delivery of these “antagomiRs” similarly boost MBNL expression and improve DM1-like phenotypes, including splicing alterations, histo…

0301 basic medicinemusculoskeletal diseasesMalecongenital hereditary and neonatal diseases and abnormalitiesScienceMyoblasts SkeletalGeneral Physics and AstronomyMice TransgenicBiologyMyotonic dystrophyGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineRNA interferencemicroRNAmedicineMBNL1Gene silencingAnimalsHumansMyotonic DystrophyGene SilencingRNA Messengerlcsh:ScienceMuscle Skeletal3' Untranslated RegionsMultidisciplinaryThree prime untranslated regionAlternative splicingQRNA-Binding ProteinsGeneral Chemistrymedicine.diseaseMyotoniaCell biologyUp-RegulationAlternative SplicingDisease Models AnimalMicroRNAs030104 developmental biologyPhenotypechemistrylcsh:Q030217 neurology & neurosurgeryHeLa CellsNature Communications
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Apert Syndrome With FGFR2 758 C > G Mutation: A Chinese Case Report

2018

Background: Apert syndrome is considered as one of the most common craniosynostosis syndromes with a prevalence of 1 in 65,000 individuals, and has a close relationship with point mutations in FGFR2 gene.Case report: Here, we described a Apert syndrome case, who was referred to genetic consultation in our hospital with the symptom of craniosynostosis and syndactyly of the hands and feet. Craniosynostosis, midfacial retrusion, steep wide forehead, larger head circumference, marked depression of the nasal bridge, short and wide nose and proptosis could be found obviously, apart from these, ears were mildly low compared with normal children and there was no cleft lip and palate. Mutation was i…

0301 basic medicinemusculoskeletal diseasesPediatricsmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesNasal bridgelcsh:QH426-470Case ReportApert syndromeCraniosynostosis03 medical and health sciencesExonsymbols.namesake0302 clinical medicineGeneticsmedicineSyndactylyGenetics (clinical)NoseSanger sequencingbusiness.industryPoint mutationmedicine.diseaseexons sequencingcraniosynostosislcsh:Genetics030104 developmental biologymedicine.anatomical_structureFGFR2genetic mutationsymbolsMolecular Medicinebusiness030217 neurology & neurosurgeryApert syndromeFrontiers in Genetics
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Therapeutic Potential of AntagomiR-23b for Treating Myotonic Dystrophy

2020

Myotonic dystrophy type 1 (DM1) is a chronically debilitating, rare genetic disease that originates from an expansion of a noncoding CTG repeat in the dystrophia myotonica protein kinase (DMPK) gene. The expansion becomes pathogenic when DMPK transcripts contain 50 or more repetitions due to the sequestration of the muscleblind-like (MBNL) family of proteins. Depletion of MBNLs causes alterations in splicing patterns in transcripts that contribute to clinical symptoms such as myotonia and muscle weakness and wasting. We previously found that microRNA (miR)-23b directly regulates MBNL1 in DM1 myoblasts and mice and that antisense technology (“antagomiRs”) blocking this microRNA (miRNA) boost…

0301 basic medicinemusculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesMyotonic dystrophyArticleantagomiR03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDrug DiscoverymicroRNAMedicineMBNL1AntagomirProtein kinase AmiRNAmyotonic dystrophybusiness.industrylcsh:RM1-950Muscle weaknessmedicine.diseaseMyotoniaMbnl1030104 developmental biologylcsh:Therapeutics. Pharmacologychemistry030220 oncology & carcinogenesisRNA splicingCancer researchHSALR miceMolecular Medicinemedicine.symptomDM1antisense oligonucleotidesbusinessMolecular Therapy: Nucleic Acids
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International BEAT-PCD Consensus Statement for Infection Prevention and Control for Primary Ciliary Dyskinesia in collaboration with ERN-LUNG PCD Cor…

2021

Introduction In primary ciliary dyskinesia (PCD) impaired mucociliary clearance leads to recurrent airway infections and progressive lung destruction, and concern over chronic airway infection and patient-to-patient transmission is considerable. So far, there has been no defined consensus on how to control infection across centres caring for patients with PCD. Within the BEAT-PCD network, COST Action and ERS CRC together with the ERN-Lung PCD core a first initiative has now been taken towards creating such a consensus statement. Methods A multidisciplinary international PCD expert panel was set up to create a consensus statement for infection prevention and control (IP&C) for PCD, covering …

:Otros calificadores::Otros calificadores::/prevención & control [Otros calificadores]Infeccions respiratòries en els infantsPrimary Ciliary DyskinesiaStatement (logic)Respiratory SystemMULTICENTERRECOMMENDATIONS0302 clinical medicineOriginal Research ArticlesPandemicSTENOTROPHOMONAS-MALTOPHILIAInfection control:Pathological Conditions Signs and Symptoms::Pathologic Processes::Disease Attributes::Chronic Disease [DISEASES]030212 general & internal medicinePrimary ciliary dyskinesiaMalalties transmissibles - Transmissió:Environmental Health::Health::Environmental Illness::Communicable Diseases::Communicable Disease Control [PUBLIC HEALTH]FOUNDATIONbiologyTransmission (medicine)R:Congenital Hereditary and Neonatal Diseases and Abnormalities::Congenital Abnormalities::Abnormalities Multiple::Ciliopathies::Congenital Hereditary and Neonatal Diseases and Abnormalities::Ciliary Motility Disorders [DISEASES]:afecciones patológicas signos y síntomas::procesos patológicos::atributos de la enfermedad::enfermedad crónica [ENFERMEDADES]:salud ambiental::salud::enfermedad ambiental::enfermedades transmisibles::control de enfermedades transmisibles [SALUD PÚBLICA]medicine.anatomical_structureMedicinePatient representativesLife Sciences & BiomedicinePulmonary and Respiratory Medicinemedicine.medical_specialty3610 Medicine & health:enfermedades y anomalías neonatales congénitas y hereditarias::anomalías congénitas::anomalías múltiples::ciliopatías::enfermedades y anomalías neonatales congénitas y hereditarias::trastornos de la motilidad ciliar [ENFERMEDADES]:Other subheadings::Other subheadings::/prevention & control [Other subheadings]03 medical and health sciencesotorhinolaryngologic diseasesmedicineIntensive care medicineScience & TechnologyCYSTIC-FIBROSISLungbusiness.industryPSEUDOMONAS-AERUGINOSAMalalties cròniques - PrevencióCAREEFFICACYmedicine.diseasebiology.organism_classificationrespiratory tract diseases030228 respiratory systemNontuberculous mycobacteria610 Medizin und GesundheitbusinessERJ Open Research
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