Search results for "Hereditary Angioedema Type III"

showing 10 items of 14 documents

Treatment for hereditary angioedema with normal C1-INH and specific mutations in the F12 gene (HAE-FXII).

2016

Hereditary angioedema with normal C1 esterase inhibitor and mutations in the F12 gene (HAE-FXII) is associated with skin swellings, abdominal pain attacks, and the risk of asphyxiation due to upper airway obstruction. It occurs nearly exclusively in women. We report our experience treating HAE-FXII with discontinuation of potential trigger factors and drug therapies. The study included 72 patients with HAE-FXII. Potential triggers included estrogen-containing oral contraceptives (eOC), hormonal replacement therapy, or angiotensin-converting enzyme inhibitors. Drug treatment comprised plasma-derived C1 inhibitor (pdC1-INH) for acute swelling attacks and progestins, tranexamic acid, and danaz…

0301 basic medicineAdultMalemedicine.medical_specialtyExacerbationAdolescentImmunologyAngiotensin-Converting Enzyme InhibitorsGastroenterologyChemopreventionC1-inhibitorHereditary Angioedema Type III03 medical and health sciencesYoung Adult0302 clinical medicineRisk FactorsInternal medicinemedicineImmunology and AllergyHumansHereditary Angioedema Type IIIChildAgedDanazolbiologybusiness.industryEstrogensMiddle Agedmedicine.diseaseSurgeryDiscontinuation030104 developmental biologyTreatment Outcome030228 respiratory systemQuinaprilHereditary angioedemaFactor XIIMutationbiology.proteinDisease ProgressionFemalebusinessComplement C1 Inhibitor ProteinTranexamic acidBiomarkersmedicine.drugAllergy
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Analysis of cold activation of the contact system in hereditary angioedema with normal C1 inhibitor.

2021

Hereditary angioedema (HAE) attacks are caused by excessive activation of the contact system. Understanding how the contact system is activated in HAE, especially in patients with normal C1 inhibitor (HAEnCI), is essential to effectively treat this disease. Contact system activation involves the cleavage of several proteins including Factor XII (FXII), high molecular weight kininogen (HK), prekallikrein, sgp120 (ITIH4) and C1 inhibitor (C1-INH) before the subsequent generation of bradykinin that mediates HAE. In this study, we evaluated the fragmentation and enzymatic activity of contact system proteins in HAEnCI plasma samples before and after contact system activation induced by incubatio…

0301 basic medicineAdultMalemedicine.medical_specialtyHigh-molecular-weight kininogenImmunologyProteinase Inhibitory Proteins SecretoryBradykininBradykininC1-inhibitorHereditary Angioedema Type III03 medical and health scienceschemistry.chemical_compoundYoung Adult0302 clinical medicineInternal medicinemedicineHumansFragmentation (cell biology)Molecular BiologyBlood CoagulationFactor XIIbiologyKininogensPrekallikreinPrekallikreinEstrogensPlasminogenKallikreinMiddle Agedmedicine.diseaseCold Temperature030104 developmental biologyEndocrinologychemistryHereditary angioedemaFactor XIIbiology.proteinFemaleKallikreinsComplement C1 Inhibitor Protein030215 immunologyMolecular immunology
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Recurrent episodes of skin angioedema and severe attacks of abdominal pain induced by oral contraceptives or hormone replacement therapy

2003

Abstract Purpose Recurrent angioedema, characterized by skin swelling, colicky attacks of abdominal pain, and life-threatening laryngeal edema, can be either hereditary or acquired. According to anecdotal reports, it may be associated with use of oral contraceptives and hormone replacement therapy. We investigated potential interactions between these medications and various types of recurrent angioedema in a large cohort of women. Methods Women with recurrent angioedema (n = 516) underwent a thorough medical evaluation. They were then classified by type of angioedema, using standard criteria. Results Of the 516 women, 228 (44%) had used oral contraceptives or hormone replacement therapy, in…

AdultAbdominal painmedicine.medical_specialtyHormone Replacement TherapyPopulationRisk AssessmentSeverity of Illness IndexCohort StudiesAge DistributionRecurrenceimmune system diseasesHumansMedicineHereditary Angioedema Type IIIcardiovascular diseasesAngioedemaRisk factorskin and connective tissue diseaseseducationAgedRetrospective Studieseducation.field_of_studyAngioedemabusiness.industryfood and beveragesRetrospective cohort studyGeneral MedicineMiddle AgedPrognosisDermatologyAbdominal PainSurgeryTransgender hormone therapyFemalemedicine.symptombusinessComplicationContraceptives OralThe American Journal of Medicine
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A novel mutation in the coagulation factor 12 gene in subjects with hereditary angioedema and normal C1-inhibitor.

2011

In hereditary angioedema with normal C1-inhibitor two different missense mutations of codon p.Thr328* in the coagulation factor 12 gene have been reported in some families. In this study a novel factor 12 gene mutation, the deletion of 72 base pairs (bp) (c.971_1018+24del72*), was identified in a family of Turkish origin, in two sisters with recurrent skin swellings and abdominal pain attacks and in their symptom-free father. This deletion caused a loss of 48 bp of exon 9 (coding amino acids 324* to 340*) in addition to 24 bp of intron 9, including the authentic donor splice site of exon 9. The large deletion of 72 bp was located in the same F12 gene region as the missense mutations p.Thr32…

AdultMaleFactor XII DeficiencyTurkeyImmunologyDNA Mutational AnalysisMutation MissenseGene mutationmedicine.disease_causeC1-inhibitorExonImmunology and AllergyMedicineMissense mutationHumansHereditary Angioedema Type IIISequence DeletionGeneticsMutationAngioedemabiologybusiness.industryAngioedemas HereditaryExonsmedicine.diseaseMolecular biologyIntronsPedigreeHereditary angioedemaFactor XIIMutationbiology.proteinFemalemedicine.symptombusinessComplement C1 Inhibitor ProteinClinical immunology (Orlando, Fla.)
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Hereditary angioedema with normal C1-inhibitor activity in women.

2000

Summary Background Hereditary angioedema (HAE) is a well defined autosomal dominant disease (Mendelian Inheritance in Man #106100) that results from an inherited deficiency of C1 (the activated first component of complement) inhibitor function. We report an unusual variant of HAE with normal biochemical C1-inhibitor function, occurring only in women. Methods We screened 574 patients with recurrent angioedema of the skin for presence of HAE. 283 patients were selected, in whom angioedema was associated with abdominal pain attacks or recurrent life-threatening episodes of upper-airway obstruction, or both, rather than with urticaria. We measured C1-inhibitor concentration and functional activ…

AdultMaleX ChromosomeAdolescentGenetic LinkageComplement C1 Inactivator ProteinsC1-inhibitorEcallantideSex FactorsRecurrenceTerminology as TopicmedicineHumansHereditary Angioedema Type IIISex RatioFamily historyAngioedemaChildDominance (genetics)Genes DominantAngioedemabiologybusiness.industryAutosomal dominant traitComplement C4General MedicineMiddle Agedmedicine.diseaseAbdominal PainPedigreeAirway ObstructionImmunologyHereditary angioedemaMutationbiology.proteinFemalemedicine.symptombusinessmedicine.drugLancet (London, England)
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Hereditary angioedema with normal C1 inhibitor: clinical symptoms and course.

2007

Abstract Purpose A new type of hereditary angioedema was described recently. It was characterized by recurrent bouts of angioedema in various organs and normal C1 inhibitor and was observed mainly in women. Our aim was to conduct a detailed study of the clinical features of this condition. Methods A total of 138 patients with hereditary angioedema and normal C1 inhibitor who belonged to 43 unrelated families were examined through the use of standardized questionnaires. Results A majority of patients with hereditary angioedema and normal C1 inhibitor had skin swellings (92.8%), tongue swellings (53.6%), and abdominal pain attacks (50%). Laryngeal edema (25.4%) and uvular edema (21.7%) also w…

AdultMalemedicine.medical_specialtyAbdominal painPathologyComplement C1 Inactivator ProteinsLaryngeal EdemaC1-inhibitorTongueimmune system diseasesEdemamedicineHumansHereditary Angioedema Type IIIcardiovascular diseasesAngioedemaskin and connective tissue diseasesSerpinsAgedRetrospective StudiesSkinSex CharacteristicsErythema marginatumAngioedemabiologybusiness.industryfood and beveragesGeneral MedicineMiddle Agedmedicine.diseaseDermatologyPedigreeUvulaHereditary angioedemabiology.proteinFemalemedicine.symptombusinessComplement C1 Inhibitor ProteinThe American journal of medicine
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Kallikrein–kinin system and fibrinolysis in hereditary angioedema due to factor XII gene mutation Thr309Lys

2009

In a subgroup of hereditary angioedema (HAE) patients with normal C1-esterase inhibitor levels, HAE is caused by a Thr309Lys mutation in the coagulation factor XII (F12) gene. The aim of this study was to examine elements of the kallikrein-kinin system ('contact system') and the downstream-linked coagulation, complement and fibrinolytic systems in the plasma of six patients with HAE caused by the Thr309Lys mutation and healthy probands. Blood samples were taken from participants during the symptom-free interval between attacks. Samples were analyzed for activity and concentrations of components of the kallikrein-kinin system and linked enzyme systems. The mean FXII clotting activity was 90%…

AdultMalemedicine.medical_specialtyAdolescentMutation MissenseKininsCoagulation Factor XIIFactor XIIaGene mutationYoung AdultInternal medicinemedicineHumansPoint MutationHereditary Angioedema Type IIIComplement Pathway ClassicalAgedAged 80 and overFactor XIIAngioedemaChemistryFibrinolysisDextran SulfateAngioedemas HereditaryPrekallikreinPrekallikreinBlood ProteinsHematologyGeneral MedicineMiddle AgedSilicon Dioxidemedicine.diseaseEnzyme ActivationEndocrinologyAmino Acid SubstitutionChromogenic CompoundsCoagulationTissue Plasminogen ActivatorHereditary angioedemaImmunologyFemaleKallikreinsmedicine.symptomcirculatory and respiratory physiologyBlood Coagulation & Fibrinolysis
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Hereditary angioedema with normal C1-INH withversuswithout specificF12gene mutations

2015

Background Hereditary angioedema with normal C1-INH may be linked to specific mutations in the coagulation factor 12 (FXII) gene (HAE-FXII) or mutations in genes that are still unknown (HAE-unknown). To assess the differences in transmission and inheritance, clinical features, and laboratory parameters between patients with HAE-FXII and HAE-unknown. Methods Sixty-nine patients with HAE-FXII from 23 unrelated families and 196 patients with HAE-unknown from 65 unrelated families were studied. Results Both HAE-FXII and HAE-unknown are inherited as autosomal-dominant traits with incomplete penetrance. The male to female ratio was 1 : 68 in HAE-FXII and 1 : 6.3 in HAE-unknown. The maternal to pa…

AdultMalemedicine.medical_specialtyDatabases FactualOffspringImmunologyGene mutationSeverity of Illness IndexCohort StudiesYoung Adultchemistry.chemical_compoundAge DistributionInternal medicineHumansImmunology and AllergyMedicineHereditary Angioedema Type IIIAge of OnsetSex DistributionRetrospective Studiesmedicine.diagnostic_testAngioedemabusiness.industryIncidenceAngioedemas HereditaryMiddle AgedPrognosismedicine.diseasePenetranceRecombinant ProteinsPedigreePhenotypeEndocrinologychemistryPlasminogen activator inhibitor-1Factor XIIMutationHereditary angioedemaFemalemedicine.symptombusinessComplement C1 Inhibitor ProteinPartial thromboplastin timeAllergy
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Hereditary angioedema caused by missense mutations in the factor XII gene: clinical features, trigger factors, and therapy.

2009

Background Hereditary angioedema caused by mutations in the factor XII gene is a recently described disease entity that occurs mainly in women. It differs from hereditary angioedema caused by C1 inhibitor deficiency. Objective To assess the clinical symptoms, factors triggering acute attacks, and treatments of this disease. Methods Thirty-five female patients with hereditary angioedema and the factor XII mutations p.Thr309Lys and p.Thr309Arg who came from 13 unrelated families were studied. The observation period was 8.4 years on average (range, 2-26 years). Results Patients had on average 12.7 ± 7.9 angioedema attacks per year. Recurrent facial swellings occurred in all patients; skin swel…

Adultmedicine.medical_specialtyAbdominal painAdolescentmedicine.medical_treatmentImmunologyMutation MissenseSeverity of Illness IndexC1-inhibitorYoung AdultRisk FactorsSurveys and QuestionnairesImmunology and AllergyMedicineHumansHereditary Angioedema Type IIIAge of OnsetChildProgesteroneDanazolPregnancyAngioedemabiologybusiness.industryDanazolAngioedemas HereditaryHormone replacement therapy (menopause)Middle Agedmedicine.diseaseDermatologySurgeryPedigreeTranexamic AcidHereditary angioedemaFactor XIIbiology.proteinFemalemedicine.symptombusinessmedicine.drugThe Journal of allergy and clinical immunology
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Increased Activity of Coagulation Factor XII (Hageman Factor) Causes Hereditary Angioedema Type III

2006

International audience; Hereditary angioedema (HAE) is characterized clinically by recurrent acute skin swelling, abdominal pain, and potentially life-threatening laryngeal edema. Three forms of HAE have been described. The classic forms, HAE types I and II, occur as a consequence of mutations in the C1-inhibitor gene. In contrast to HAE types I and II, HAE type III has been observed exclusively in women, where it appears to be correlated with conditions of high estrogen levels--for example, pregnancy or the use of oral contraceptives. A recent report proposed two missense mutations (c.1032C-->A and c.1032C-->G) in F12, the gene encoding human coagulation factor XII (FXII, or Hageman factor…

MaleTime FactorsKinins030204 cardiovascular system & hematologyMESH: Founder Effect[SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunityLinkage Disequilibrium0302 clinical medicineMissense mutationHereditary Angioedema Type IIIGenetics(clinical)MESH: Models GeneticGenetics (clinical)MESH: Heterozygote0303 health sciencesFactor XII[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyFounder EffectMarkov ChainsPedigree3. Good healthMESH: Linkage DisequilibriumFactor XIIHereditary angioedemaFemalemedicine.symptomMESH: Factor XIIHeterozygotemedicine.medical_specialtyMESH: MutationMESH: PedigreeMESH: Bayes TheoremCoagulation Factor XIIBiology03 medical and health sciencesMESH: Markov ChainsReportInternal medicinemedicineGeneticsHumansMESH: AngioedemaAngioedema030304 developmental biologyMESH: HumansModels GeneticAngioedemaHaplotypeMESH: Time FactorsBayes TheoremHeterozygote advantageMESH: Haplotypesmedicine.diseaseMESH: KininsMESH: MaleEndocrinologyHaplotypesMutationImmunologyMESH: Microsatellite RepeatsMESH: FemaleMicrosatellite RepeatsThe American Journal of Human Genetics
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