Search results for "plasma kallikrein"

showing 3 items of 3 documents

Effect of Lanadelumab Compared With Placebo on Prevention of Hereditary Angioedema Attacks: A Randomized Clinical Trial.

2018

Current treatments for long-term prophylaxis in hereditary angioedema have limitations.To assess the efficacy of lanadelumab, a fully human monoclonal antibody that selectively inhibits active plasma kallikrein, in preventing hereditary angioedema attacks.Phase 3, randomized, double-blind, parallel-group, placebo-controlled trial conducted at 41 sites in Canada, Europe, Jordan, and the United States. Patients were randomized between March 3, 2016, and September 9, 2016; last day of follow-up was April 13, 2017. Randomization was 2:1 lanadelumab to placebo; patients assigned to lanadelumab were further randomized 1:1:1 to 1 of the 3 dose regimens. Patients 12 years or older with hereditary a…

AdultMalemedicine.medical_specialtyRandomizationAdolescentInjections SubcutaneousLanadelumabPlaceboAntibodies Monoclonal Humanizedlaw.invention03 medical and health sciencesYoung Adult0302 clinical medicineRandomized controlled trialDouble-Blind MethodlawInternal medicinemedicineHumans030212 general & internal medicineYoung adultAdverse effectChildPlasma KallikreinAgedHereditary Angioedema Types I and IIbusiness.industryAntibodies MonoclonalCorrectionGeneral MedicineMiddle Agedmedicine.diseaseClinical trial030228 respiratory systemHereditary angioedemaQuality of LifeFemalebusinessJAMA
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Plasma Kallikrein Contributes to Coagulation in the Absence of Factor XI by Activating Factor IX

2019

Objectives: FXIa (factor XIa) induces clot formation, and human congenital FXI deficiency protects against venous thromboembolism and stroke. In contrast, the role of FXI in hemostasis is rather small, especially compared with FIX deficiency. Little is known about the cause of the difference in phenotypes associated with FIX deficiency and FXI deficiency. We speculated that activation of FIX via the intrinsic coagulation is not solely dependent on FXI(a; activated FXI) and aimed at identifying an FXI-independent FIX activation pathway. Approach and Results: We observed that ellagic acid and long-chain polyphosphates activated the coagulation system in FXI-deficient plasma, as could be demo…

Malemedicine.medical_specialtyplasma kallikreinPREKALLIKREIN030204 cardiovascular system & hematologyPATHWAYMice03 medical and health sciencesTissue factor0302 clinical medicineThrombinInternal medicinemedicineAnimalsHEMOSTASIScoagulationBLOOD-COAGULATIONBlood CoagulationFactor XIFactor IXfactor IXPURIFICATIONbusiness.industryMOLECULAR-WEIGHT KININOGENThrombinPrekallikreinKallikreinfactor XIfactor XI deficiencyMice Inbred C57BLDEFICIENCYDisease Models AnimalTHROMBOSISEndocrinologyCoagulationTISSUE FACTOR030220 oncology & carcinogenesisHemostasisFemaleREDUCED INCIDENCECardiology and Cardiovascular Medicinebusinessmedicine.drug
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Predictive Value for Increased Factor XIa and Plasma Kallikrein Activity in Acute Venous Thromboembolism

2021

Abstract Venous thromboembolism (VTE) is associated with increased coagulation activity, which in part can be attributed to the contact pathway of coagulation. Evidence from pre-clinical and epidemiological studies suggests that deficiency in factors of contact activation (e.g. coagulation factors (F) XI and FXII) protects against VTE. However, limited information exists regarding the activation of the contact system in the setting of acute VTE. In the current study, patients with confirmed VTE events (n=321) from the VTEval study and controls (n=300) from the population-based PREVENT-it pilot study were included. Plasma samples were collected from patients after confirmed VTE events or con…

medicine.medical_specialtybusiness.industryImmunologyFactor XIaCell BiologyHematologyBiochemistryPredictive valuePlasma kallikrein activityInternal medicinemedicineCardiologycardiovascular diseasesbusinessVenous thromboembolismBlood
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