Search results for "Complement C1 Inactivator Proteins"

showing 10 items of 31 documents

International consensus and practical guidelines on the gynecologic and obstetric management of female patients with hereditary angioedema caused by …

2012

Background There are a limited number of publications on the management of gynecologic/obstetric events in female patients with hereditary angioedema caused by C1 inhibitor deficiency (HAE-C1-INH). Objective We sought to elaborate guidelines for optimizing the management of gynecologic/obstetric events in female patients with HAE-C1-INH. Methods A roundtable discussion took place at the 6th C1 Inhibitor Deficiency Workshop (May 2009, Budapest, Hungary). A review of related literature in English was performed. Results Contraception : Estrogens should be avoided. Barrier methods, intrauterine devices, and progestins can be used. Pregnancy : Attenuated androgens are contraindicated and should …

Complement C1 Inactivator ProteinsAbortionCardiovascularEcallantidechemistry.chemical_compoundDelivery Obstetric; Complement C1 Inactivator Proteins; Humans; Infant Newborn; Breast Neoplasms; Genetic Counseling; Pregnancy; Lactation; Genital Diseases Female; Infant; Contraception; Hereditary Angioedema Types I and II; Menstruation; Pregnancy Complications Cardiovascular; Chemoprevention; Prenatal Diagnosis; Menopause; FemalePregnancyIcatibantPrenatal DiagnosisImmunology and AllergyfertilityHereditary Angioedema Types I and IItreatmentObstetricsVaginal deliveryMenstruationContraceptioncontraceptionGenital DiseasesHereditary angioedemaFemalepregnancyMenopausedeliverymedicine.symptomComplement C1 Inhibitor ProteinDeliverymedicine.drugmedicine.medical_specialtyPregnancy Complications CardiovascularImmunologyBreast NeoplasmsGenetic CounselingIntrauterine deviceChemopreventionbreast cancermedicineHumansLactationGynecologyPregnancygenetic counselingAngioedemabusiness.industryangioedemaInfant NewbornInfantObstetricDelivery ObstetricNewbornmedicine.diseasehereditary angioedemaPregnancy ComplicationsSettore MED/16 - ReumatologiachemistryC1 inhibitor deficiencybusinessGenital Diseases FemaleJournal of Allergy and Clinical Immunology
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The modulation of immune complex aggregation by classical pathway-mediated reactions.

1985

Abstract Classical pathway (CP)-triggered reactions of complement-modulated immune complex(IC) aggregation (tetanus toxoid/human anti-tetanus toxoid-IgG; ICs of equivalence) were investigated turbidimetrically during the early stages of reaction. Monospecific Fab'- or Fab-fragments (rabbit) directed against certain complement components were used to block the complement function in normal human serum (NHS). Additionally, parts of the reactions were studied using purified complement components. C1q in serum generated by the addition of EDTA as well as purified C1q were found to increase the IC aggregation. In contrast to C1q, macromolecular C1 is able to inhibit IC aggregation, whereas addit…

EffectorChemistryComplement Activating EnzymesComplement C1qImmunologyToxoidHematologyAntigen-Antibody ComplexComplement System ProteinsComplement C1 Inactivator ProteinsImmune complexComplement componentsComplement (complexity)Classical complement pathwayBiochemistrySolubilityComplement C1ImmunologyImmunology and AllergyHumansComplement Pathway ClassicalComplement ActivationFunction (biology)MacromoleculeImmunobiology
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Functional C1-inhibitor diagnostics in hereditary angioedema: Assay evaluation and recommendations

2008

Hereditary angioedema (HAE) is an autosomal dominant disease characterized by recurrent episodes of potentially life-threatening angioedema. The most widespread underlying genetic deficiency is a heterozygous deficiency of the serine protease inhibitor Cl esterase inhibitor (C1-Inh). In addition to low C4 levels, the most important laboratory parameter for correct diagnosis of HAE or angioedema due to acquired C1-Inh deficiency is reduced C1-Inh function (fC1-Inh). No direct recommendations about the assays for fC1-Inh or sample handling conditions are available, although this would prove especially useful when a laboratory first starts to offer assays on fC1-Inh for HAE diagnosis. In the p…

ImmunologyMESH: Complement C1 Inactivator ProteinsEnzyme-Linked Immunosorbent AssayMESH: Blood Specimen CollectionComplement C1 Inactivator Proteins[SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunityC1-inhibitor03 medical and health sciences0302 clinical medicinemedicineHumansImmunology and AllergyMESH: Angioedemaheterocyclic compoundsAngioedema030304 developmental biologySample handlingBlood Specimen Collection0303 health sciencesMESH: HumansAngioedemabiologybusiness.industryTemperatureAutosomal dominant traitMESH: Enzyme-Linked Immunosorbent Assaybiochemical phenomena metabolism and nutritionrespiratory system[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismSerum samplesmedicine.diseasebacterial infections and mycosesMESH: Temperature3. Good healthC1 esteraserespiratory tract diseases030228 respiratory systemImmunologyHereditary angioedemabiology.proteinmedicine.symptombusinessJournal of Immunological Methods
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Clinical studies of sudden upper airway obstruction in patients with hereditary angioedema due to C1 esterase inhibitor deficiency.

2003

Background Hereditary angioedema due to C1 esterase inhibitor deficiency is clinically characterized by recurrent and self-limiting skin, intestinal, and laryngeal edema. Asphyxiation by laryngeal edema is the main cause of death among patients who die of hereditary angioedema. This study describes the age at which laryngeal edema first occurs, the time between onset and full development, and the effectiveness of therapy and prophylaxis. Methods Information on 123 patients with hereditary angioedema was obtained from medical histories and reports by the general practitioners, emergency physicians, and hospitals involved. Results Sixty-one patients (49.6%) experienced a total of 596 laryngea…

LarynxAdultAbdominal painAdolescentComplement C1 Inactivator ProteinsLaryngeal EdemaEcallantideRisk FactorsEdemaInternal MedicinemedicineHumansAge of OnsetAngioedemaChildAgedbusiness.industryAirway obstructionLaryngeal EdemaMiddle Agedmedicine.diseasemedicine.anatomical_structureAnesthesiaChild PreschoolHereditary angioedemaAge of onsetmedicine.symptombusinessmedicine.drugArchives of internal medicine
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Risk of laryngeal edema and facial swellings after tooth extraction in patients with hereditary angioedema with and without prophylaxis with C1 inhib…

2010

Objective Tooth extractions may trigger clinical symptoms of hereditary angioedema due to C1 inhibitor deficiency (HAE-C1-INH). The aim of this study was to determine how many tooth extractions were followed by symptoms of HAE-C1-INH in patients with and without preoperative short-term prophylaxis with C1 inhibitor concentrate. Study design Tooth extractions and clinical symptoms of HAE-C1-INH were determined from clinical record files of 171 patients with HAE-C1-INH. Results Facial swelling or potentially life-threatening laryngeal edema, or both, occurred in 124/577 tooth extractions (21.5%) without prophylaxis. Similar symptoms occurred in a fewer proportion of patients undergoing extrac…

LarynxAdultMalemedicine.medical_specialtyTime FactorsPremedicationComplement C1 Inactivator ProteinsLaryngeal EdemaChemopreventionC1-inhibitorRisk FactorsEdemamedicineEdemaHumansRisk factorGeneral DentistryRetrospective StudiesbiologyDose-Response Relationship Drugbusiness.industryAngioedemas HereditaryRetrospective cohort studyLaryngeal Edemamedicine.diseaseSurgerymedicine.anatomical_structureTreatment OutcomeOtorhinolaryngologyFaceHereditary angioedemaInjections IntravenousTooth Extractionbiology.proteinSurgeryPremedicationFemaleOral Surgerymedicine.symptombusinessComplement C1 Inhibitor ProteinFollow-Up StudiesOral surgery, oral medicine, oral pathology, oral radiology, and endodontics
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Novel complement C1 inhibitor BSF468248 does not improve brain damage after cortical vein occlusion

2003

BSF468248 is a novel potent complement C1 inhibitor. To determine whether BSF468248 is effective against focal cerebral ischemia, we evaluated the change of cerebral blood flow (CBF) and infarction volume using a photochemically-induced cortical vein occlusion model in rats in blind studies. In 22 Wistar rats, two adjacent cortical veins were occluded by photochemical thrombosis and fiberoptic illumination under controlled anesthesia and ventilation. Just after the occlusion, BSF468248 or physiological saline was administrated. In the low-dose study, a treatment group (n = 7) was administered BSF468248 1 mg/kg bolus and 1 mg/kg continuously for 30 min. The same volume of saline was given to…

MaleCerebral veinsPhotochemistrymedicine.medical_treatmentComplement C1 Inactivator ProteinsRats Sprague-DawleyBolus (medicine)OcclusionmedicineAnimalsRats WistarInfusions IntravenousSalineCerebral Cortexbusiness.industryCerebral InfarctionBlood flowCortical Veinmedicine.diseaseCerebral VeinsThrombosisRatsDisease Models AnimalTreatment OutcomeCerebral blood flowRegional Blood FlowBrain InjuriesCerebrovascular CirculationAnesthesiaIntracranial ThrombosisbusinessOligopeptidesMethods and Findings in Experimental and Clinical Pharmacology
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Novel Small Molecule Inhibitor of C1s Exerts Cardioprotective Effects in Ischemia-Reperfusion Injury in Rabbits

2001

Abstract Myocardial ischemia-reperfusion injury can be related to complement activation with generation of chemotactic agents, adhesion molecule expression, release of cytokines and oxygen-derived free radicals, and subsequent neutrophil accumulation. In the present study the cardioprotective effects of a novel highly selective small molecule C1s inhibitor (C1s-INH-248, Knoll) were examined in a rabbit model of myocardial ischemia (I) and reperfusion (R; i.e., 60 min I + 180 min R). In in vitro tests (enzyme activity and SRBC lysis) C1s-INH-248 demonstrated profound inhibitory potency. In vivo C1s-INH-248 (1 mg/kg body weight) administered 5 min before reperfusion significantly attenuated m…

MaleNecrosisEndotheliumNeutrophilsG proteinImmunologyMyocardial IschemiaIschemiaMyocardial Reperfusion InjuryComplement C1 Inactivator ProteinsPharmacologyHemolysisLeukocyte CountClassical complement pathwaySuperoxidesIn vivomedicineAnimalsImmunology and AllergyComplement Activationbusiness.industryHemodynamicsmedicine.diseaseComplement systemmedicine.anatomical_structureAnesthesiaEndothelium VascularRabbitsmedicine.symptombusinessReperfusion injuryThe Journal of Immunology
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C1-esterase inhibitor reduces infarct volume after cortical vein occlusion.

1999

In order to clarify the role of complement as a mediator of cerebral infarct growth, we inhibited the classical complement activation pathway in a photochemical cortical vein occlusion model. Immediately after occlusion, rats were infused with either 0.9% saline (vehicle), or C1-esterase inhibitor (C1-INH) over 30 min. Regional cerebral blood flow (rCBF) decreased after occlusion, and was about 50% of baseline after 2 h. No difference was noted between experimental groups. Mean arterial blood pressure (MABP) and arterial blood gases were likewise unaffected by the treatment. However, administration of C1-INH had significantly reduced infarct volume by 72%, as evaluated after 5 days survival…

MalePhotochemistryHemodynamicsComplement C1 Inactivator ProteinsVeinsOcclusionmedicineAnimalsCerebral perfusion pressureRats WistarMolecular BiologyCerebral infarctionbusiness.industryGeneral NeuroscienceCerebral Infarctionmedicine.diseaseCortical VeinRatsBlood pressureCerebral blood flowAnesthesiaCerebrovascular CirculationArterial bloodNeurology (clinical)businessDevelopmental BiologyBrain research
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Proteome analysis of myocardial tissue following ischemia and reperfusion--effects of complement inhibition.

2006

Myocardial ischemia-reperfusion injury can be related to complement activation with generation of chemotactic mediators, release of cytokines, leukocyte accumulation, and subsequent severe tissue injury. In this regard, activation of transcription factors (i.e., NFkappaB) and de novo protein synthesis or inflammatory protein degradation seems to play an important role. In the present study, we analyzed the cardiac protein expression following myocardial ischemia (60 min) and reperfusion (180 min) in a rabbit model utilizing two-dimensional electrophoresis and nanoHPLC/ESI-MS/MS for biochemical protein identification. To achieve cardioprotective effects, we used a novel highly selective smal…

MaleProteomeG proteinNeutrophilsMolecular Sequence DataBiophysicsIschemiaMyocardial IschemiaMyocardial Reperfusion InjuryProtein degradationComplement C1 Inactivator ProteinsBiochemistryAnalytical ChemistrySuperoxide dismutaseClassical complement pathwayElectrocardiographyNecrosismedicineProtein biosynthesisAnimalsAmino Acid SequenceMolecular BiologyCreatine KinasebiologySuperoxide DismutaseMyocardiumalpha-Crystallin B ChainComplement System Proteinsmedicine.diseaseMolecular biologyComplement systembiology.proteinCreatine kinaseRabbitsMicrotubule-Associated ProteinsBiomarkersBiochimica et biophysica acta
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Beneficial effects of C1 esterase inhibitor in ST-elevation myocardial infarction in patients who underwentsurgical reperfusion: a randomized double-…

2007

Background: The inflammatory cascade has been hypothesized to be an important mechanism of post-ischaemic myocardial reperfusion injury and several studies demonstrated that C1 esterase inhibitor (C1 -INH) is effective in post-ischaemia myocardial protection. Therefore, we aimed to investigate prospectively in a randomised double-blind study the cardioprotective effects of C1-INH in ST segment elevation myocardial infarction (STEMI) in patients who underwent emergent reperfusion with coronary artery bypass grafting (CABG). Methods: In this study, we enrolled 80 patients affected with STEMI who underwent emergent CABG. Patients were assigned in two groups (C1-INH group: receive 1000 Ul of C1…

MalePulmonary and Respiratory MedicineCardiac function curvemedicine.medical_specialtyMean arterial pressureCardiotonic AgentsMyocardial InfarctionCardiac indexMyocardial ReperfusionComplement C1 Inactivator ProteinsCoronary artery bypass surgeryReperfusion therapyDouble-Blind MethodInternal medicinemedicineHumansProspective StudiesMyocardial infarctionCoronary Artery BypassInfusions IntravenousSTEMI patients CABG C1 esterase inhibitor Reperfusion injury Complement cascade Myocardial function recoverybusiness.industryST elevationTroponin IComplement C4aGeneral MedicineMiddle Agedmedicine.diseaseMyocardial ContractionComplement Inactivating AgentsTreatment OutcomeComplement C3aCardiologyFemaleSurgeryCardiology and Cardiovascular MedicinebusinessReperfusion injury
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