2020
Exome Sequencing Reveals Common and Rare Variants in F5 Associated With ACE Inhibitor and Angiotensin Receptor Blocker–Induced Angioedema
Maroteau C, Siddiqui M, Veluchamy A, Carr F, White M, Cassidy AJ, Baranova EV, Rasmussen ER, Eriksson N, Bloch KM, Brown NJ, Bygum A, Hallberg P, Karawajczyk M, Magnusson PKE, Yue Q, Syvänen A, von Buchwald C, Alfirevic A, der Zee A, Wadelius M, Palmer CNA, PREDICTION‐ADR. Exome Sequencing Reveals Common and Rare Variants in F5 Associated With ACE Inhibitor and Angiotensin Receptor Blocker–Induced Angioedema. Clinical Pharmacology & Therapeutics 2020, 108: 1195-1202. PMID: 32496628, PMCID: PMC10306231, DOI: 10.1002/cpt.1927.Peer-Reviewed Original ResearchMeSH KeywordsAgedAngioedemaAngiotensin Receptor AntagonistsAngiotensin-Converting Enzyme InhibitorsCase-Control StudiesDNA Mutational AnalysisEuropeExomeExome SequencingFactor VFemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMaleMiddle AgedMutation RateMutation, MissenseRisk AssessmentRisk FactorsUnited StatesConceptsAngiotensin receptor blockersACEi-AEReceptor blockersLife-threatening adverse reactionsMissense variantsRare variantsCommon variantsRare missense variantsGene risk scoreACE inhibitorsAdverse reactionsDeleterious missense variantsHigh riskRisk scoreAngioedemaEnzyme inhibitorsNeck regionExome sequencingAsian populationsDifferent centersBlood clottingBlockersF5 geneRiskInhibitors
2017
Angiotensin-converting Enzyme Inhibitor and Other Drug-associated Angioedema
Stone C, Brown NJ. Angiotensin-converting Enzyme Inhibitor and Other Drug-associated Angioedema. Immunology And Allergy Clinics Of North America 2017, 37: 483-495. PMID: 28687104, DOI: 10.1016/j.iac.2017.04.006.Peer-Reviewed Original ResearchConceptsDrug-induced angioedemaEnzyme inhibitorsAngiotensin-converting enzyme inhibitorNon-β-lactam antibioticsNonsteroidal antiinflammatory agentsNonallergic angioedemaSubstance PTherapeutic decisionsAngioedemaAntiinflammatory agentsLactam antibioticsOther DrugΒ-lactam antibioticsDrugsPatientsLeukotrienesBradykininGenetic variantsAntibioticsInhibitorsAngiotensinProstaglandinsAgentsHistamineMainstay
2013
An LC–MS assay for the screening of cardiovascular medications in human samples
Dias E, Hachey B, McNaughton C, Nian H, Yu C, Straka B, Brown NJ, Caprioli RM. An LC–MS assay for the screening of cardiovascular medications in human samples. Journal Of Chromatography B 2013, 937: 44-53. PMID: 24013190, PMCID: PMC3800555, DOI: 10.1016/j.jchromb.2013.08.010.Peer-Reviewed Original ResearchConceptsAngiotensin II receptor blockersDrug metabolitesCardiovascular drugsDrug classesHospitalized patientsSingle LC-MS/MS methodLC-MS assayLC-MS/MS methodII receptor blockersCalcium channel blockersCardiovascular drug classesClinical samplesDrug detectionSpiked samplesMS methodCardiovascular medicationsReceptor blockersBeta blockersMedication administrationChannel blockersEnzyme inhibitorsClinical settingBlockersDrugsSimultaneous analysis
2012
Angiotensin-converting enzyme inhibition or mineralocorticoid receptor blockade do not affect prevalence of atrial fibrillation in patients undergoing cardiac surgery*
Pretorius M, Murray KT, Yu C, Byrne JG, Billings FT, Petracek MR, Greelish JP, Hoff SJ, Ball SK, Mishra V, Body SC, Brown NJ. Angiotensin-converting enzyme inhibition or mineralocorticoid receptor blockade do not affect prevalence of atrial fibrillation in patients undergoing cardiac surgery*. Critical Care Medicine 2012, 40: 2805-2812. PMID: 22824930, PMCID: PMC3588582, DOI: 10.1097/ccm.0b013e31825b8be2.Peer-Reviewed Original ResearchConceptsAcute renal failureAngiotensin-converting enzyme inhibitorMineralocorticoid receptor blockadePostoperative atrial fibrillationMineralocorticoid receptor antagonistsAtrial fibrillationPlacebo groupSpironolactone groupRenal failureCardiac surgeryReceptor blockadeReceptor antagonistEnzyme inhibitorsDouble-blind placebo-controlled studyAngiotensin-converting enzyme inhibitionPrevalence of hypotensionElective cardiac surgeryPlacebo-controlled studyRenin-angiotensin systemNormal sinus rhythmEnzyme inhibitionRamipril groupSpironolactone useHospital stayPrimary endpoint
2011
This is not Dr. Conn's aldosterone anymore.
Brown NJ. This is not Dr. Conn's aldosterone anymore. Transactions Of The American Clinical And Climatological Association 2011, 122: 229-43. PMID: 21686229, PMCID: PMC3116341.Peer-Reviewed Original ResearchMeSH KeywordsAldosteroneAngiotensin IIAngiotensin II Type 1 Receptor BlockersAngiotensin-Converting Enzyme InhibitorsAnimalsBlood PressureCytochrome P-450 CYP11B2Disease Models, AnimalEnzyme InhibitorsFibrosisGene Expression RegulationHumansHyperaldosteronismInflammation MediatorsKidneyLigandsMiceMineralocorticoid Receptor AntagonistsMyocardiumRatsReceptors, MineralocorticoidSignal TransductionTime FactorsConceptsMR-independent pathwayPrevalence of hyperaldosteronismAngiotensin receptor blockersMineralocorticoid receptor antagonismSecretion of aldosteroneAldosterone-secreting adenomasPro-fibrotic effectsReceptor blockersResistant hypertensionSevere hypertensionAldosterone concentrationRenal injuryEndogenous aldosteroneACE inhibitorsCardiovascular remodelingAngiotensin IIReceptor antagonismHeart diseaseProfibrotic effectsAldosteroneBaseline valuesEnzyme inhibitorsPatientsPotassium homeostasisHypertension
2010
Bradykinin forming capacity of oversulfated chondroitin sulfate contaminated heparin in vitro
Adam A, Montpas N, Keire D, Désormeaux A, Brown NJ, Marceau F, Westenberger B. Bradykinin forming capacity of oversulfated chondroitin sulfate contaminated heparin in vitro. Biomaterials 2010, 31: 5741-5748. PMID: 20427081, PMCID: PMC2896062, DOI: 10.1016/j.biomaterials.2010.03.074.Peer-Reviewed Original ResearchConceptsContact system activationAnaphylactoid reactionsOversulfated chondroitin sulfateSystem activationSevere anaphylactoid reactionPlasma contact systemHuman plasmaInflammatory peptidesChondroitin sulfateEnzyme inhibitorsBK releaseDrug AdministrationBradykininHeparinSignificant correlationDefinitive evidenceDextran sulfatePlasma dilutionActivationConclusionPatientsPathophysiologyKininsAdministrationPlasma
2007
Dipeptidyl Peptidase IV in Angiotensin-Converting Enzyme Inhibitor–Associated Angioedema
Byrd JB, Touzin K, Sile S, Gainer JV, Yu C, Nadeau J, Adam A, Brown NJ. Dipeptidyl Peptidase IV in Angiotensin-Converting Enzyme Inhibitor–Associated Angioedema. Hypertension 2007, 51: 141-147. PMID: 18025295, PMCID: PMC2749928, DOI: 10.1161/hypertensionaha.107.096552.Peer-Reviewed Original ResearchConceptsEnzyme (ACE) inhibitor-associated angioedemaDipeptidyl peptidase IV activityHistory of angiotensinPeptidase IV activityControl subjectsSubstance PDipeptidyl peptidase IVEnzyme inhibitorsLife-threatening adverse effectsAngiotensin converting enzyme (ACE) inhibitorsEnzyme inhibitionAbsence of angiotensinPrevalence of smokingSera of patientsCase-control studyPeptidase IVSubstrates of angiotensinTissue edemaAssociated angioedemaAminopeptidase P activityVascular permeabilityAngioedemaAngiotensinAminopeptidase N activityAmino-terminal degradation
2006
Angiotensin-Converting Enzyme Inhibitor-Associated Angioedema
Byrd JB, Adam A, Brown NJ. Angiotensin-Converting Enzyme Inhibitor-Associated Angioedema. Immunology And Allergy Clinics Of North America 2006, 26: 725-737. PMID: 17085287, DOI: 10.1016/j.iac.2006.08.001.Peer-Reviewed Original ResearchConceptsACE inhibitor-associated angioedemaAngiotensin converting enzyme (ACE) inhibitorsEnzyme inhibitor usersNon-ACE pathwaysInhibitor usersAdverse eventsClinical recognitionSubstance PAssociated angioedemaEnzyme inhibitorsAngioedemaDefective degradationNonsmokersAngiotensinSmokersPathogenesisWhite AmericansBradykininIncidenceEndogenous NO Regulates Plasminogen Activator Inhibitor-1 During Angiotensin-Converting Enzyme Inhibition
Brown NJ, Muldowney JA, Vaughan DE. Endogenous NO Regulates Plasminogen Activator Inhibitor-1 During Angiotensin-Converting Enzyme Inhibition. Hypertension 2006, 47: 441-448. PMID: 16432054, DOI: 10.1161/01.hyp.0000202478.79587.1a.Peer-Reviewed Original ResearchMeSH KeywordsAdultAldosteroneAngiotensin-Converting Enzyme InhibitorsArginineDouble-Blind MethodDrug CombinationsEnzyme InhibitorsFemaleFibrinolysisHemodynamicsHumansInfusions, IntravenousMaleMiddle AgedNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthasePlasminogen Activator Inhibitor 1ProdrugsRamiprilReference ValuesRenin-Angiotensin SystemConceptsPlasminogen activator inhibitor-1Plasminogen activator inhibitor-1 antigenActivator inhibitor-1Salt-replete subjectsL-arginineFibrinolytic balanceInhibitor-1Angiotensin-Converting Enzyme InhibitionNO precursor L-argininePlasminogen activator inhibitor antigenTissue-type plasminogen activator antigenEffect of angiotensinPrecursor L-argininePlasminogen activator antigenNO synthase inhibitorEnzyme inhibitionT-PA activityRenin activityD-dimerInhibitor antigenNormal subjectsSynthase inhibitorEnzyme inhibitorsT-PAAntigen
2004
Angiotensin‐converting enzyme inhibition and smoking potentiate the kinin response to cardiopulmonary bypass
Pretorius M, McFarlane JA, Vaughan DE, Brown NJ, Murphey LJ. Angiotensin‐converting enzyme inhibition and smoking potentiate the kinin response to cardiopulmonary bypass. Clinical Pharmacology & Therapeutics 2004, 76: 379-387. PMID: 15470338, DOI: 10.1016/j.clpt.2004.06.004.Peer-Reviewed Original ResearchConceptsACE inhibitor groupMinutes of CPBCardiopulmonary bypassACE inhibitorsInhibitor groupKinin responseBradykinin concentrationsEffects of CPBCoronary artery bypass surgeryTissue-type plasminogen activator antigenPreoperative ACE inhibitorsArtery bypass surgeryPostoperative day 1Concentrations of bradykininEffect of smokingPlasminogen activator antigenKallikrein-kinin systemSignificant inverse correlationArterial pressureBypass surgeryFibrinolytic responseVenous bloodACE activityDay 1Enzyme inhibitors
2000
Inhibition of aminopeptidase P potentiates wheal response to bradykinin in angiotensin-converting enzyme inhibitor-treated humans.
Kim KS, Kumar S, Simmons WH, Brown NJ. Inhibition of aminopeptidase P potentiates wheal response to bradykinin in angiotensin-converting enzyme inhibitor-treated humans. Journal Of Pharmacology And Experimental Therapeutics 2000, 292: 295-8. PMID: 10604961.Peer-Reviewed Original ResearchConceptsDegradation of bradykininACE inhibitionWheal responseACE inhibitor quinaprilEffect of quinaprilNon-ACE pathwaysMetabolism of bradykininDose-response curveCardioprotective effectsIntradermal administrationIntradermal injectionOral administrationHealthy subjectsEnzyme inhibitorsSignificant interactionQuinaprilBradykininAminopeptidase PAngiotensinInhibitionAdministrationHuman skinPresent studyApstatinResponse
1999
Serum metabolism of bradykinin and des-Arg9-bradykinin in patients with angiotensin-converting enzyme inhibitor-associated angioedema
Blais C, Rouleau J, Brown N, Lepage Y, Spence D, Munoz C, Friborg J, Geadah D, Gervais N, Adam A. Serum metabolism of bradykinin and des-Arg9-bradykinin in patients with angiotensin-converting enzyme inhibitor-associated angioedema. Immunopharmacology 1999, 43: 293-302. PMID: 10596866, DOI: 10.1016/s0162-3109(99)00133-2.Peer-Reviewed Original ResearchConceptsDes-Arg9AE patientsC subjectsLife-threatening adverse reactionsEnzyme (ACE) inhibitor-associated angioedemaMetabolism of bradykininLocal inflammatory reactionEnzyme defectPreincubation of seraBK metabolismSensitive enzyme immunoassayB1 agonistSerum metabolismAdverse reactionsControl subjectsInflammatory reactionACEIAngioedemaAbnormal metabolismPatientsEnzyme inhibitorsSynthetic bradykininControl seraBradykininEnzyme immunoassayRole of Angiotensin II in Coagulation and Fibrinolysis
Brown N, Vaughan D. Role of Angiotensin II in Coagulation and Fibrinolysis. Heart Failure Reviews 1999, 3: 193-198. DOI: 10.1023/a:1009757416302.Peer-Reviewed Original ResearchAntithrombotic effectAngiotensin type 1 receptor antagonistType 1 receptor antagonistVascular fibrinolytic balanceRenin-angiotensin systemTissue plasminogen activatorHypertensive patientsInhibitor PAI-1Angiotensin IIFibrinolytic balanceReceptor antagonistVasculoprotective propertiesPlatelet functionEnzyme inhibitorsPAI-1Plasminogen activatorMultiple mechanismsFibrinolysisSubstantial evidenceRecent studiesAngiotensinPatientsProstanoidsAntagonist
1998
Angiotensin-Converting Enzyme Inhibitors
Brown N, Vaughan D. Angiotensin-Converting Enzyme Inhibitors. Circulation 1998, 97: 1411-1420. PMID: 9577953, DOI: 10.1161/01.cir.97.14.1411.Peer-Reviewed Original ResearchConceptsACE inhibitorsVentricular dysfunctionMyocardial infarctionAngiotensin AT1 receptor antagonistAngiotensin converting enzyme (ACE) inhibitorsTissue-bound ACESystemic vascular resistanceCongestive heart failureAT1 receptor antagonistTreatment of hypertensionRoute of eliminationVascular resistanceCardiovascular mortalityDiabetic nephropathyEssential hypertensionHeart failureNatriuretic propertiesRenal diseaseVasoactive substancesAngiotensin IIReceptor antagonistHeart rateSide effectsEnzyme inhibitorsHypertrophic properties
1997
Recurrent angiotensin-converting enzyme inhibitor--associated angioedema.
Brown N, Snowden M, Griffin M. Recurrent angiotensin-converting enzyme inhibitor--associated angioedema. JAMA 1997, 278: 232-3. PMID: 9218671, DOI: 10.1001/jama.278.3.232.Peer-Reviewed Original ResearchConceptsACE inhibitor useACE inhibitorsInhibitor useRecurrent angioedemaEnzyme inhibitorsAngiotensin-converting enzyme inhibitorEpisodes of angioedemaRate of angioedemaRetrospective cohort studyDiagnosis of angioedemaRisk of angioedemaTennessee Medicaid programAngioedema recurrencesCohort studySerious morbidityRecurrent episodesMedical recordsAssociated angioedemaMultiple recurrencesMedicaid enrolleesAngioedemaPatientsRecurrenceNumber of causesMedicaid programRecurrent Angiotensin-Converting Enzyme Inhibitor—Associated Angioedema
Brown N, Snowden M, Griffin M. Recurrent Angiotensin-Converting Enzyme Inhibitor—Associated Angioedema. JAMA 1997, 278: 232-233. DOI: 10.1001/jama.1997.03550030072037.Peer-Reviewed Original ResearchConceptsACE inhibitor useAngiotensin converting enzyme (ACE) inhibitorsACE inhibitorsInhibitor useRecurrent angioedemaEnzyme inhibitorsEpisodes of angioedemaRate of angioedemaRetrospective cohort studyDiagnosis of angioedemaRisk of angioedemaTennessee Medicaid programAngioedema recurrencesCohort studySerious morbidityRecurrent episodesMedical recordsAssociated angioedemaMultiple recurrencesMedicaid enrolleesAngioedemaPatientsRecurrenceNumber of causesMedicaid program
1996
Differential effects of angiotensin converting enzyme inhibitors on the vasodepressor and prostacyclin responses to bradykinin.
Brown NJ, Ryder D, Gainer JV, Morrow JD, Nadeau J. Differential effects of angiotensin converting enzyme inhibitors on the vasodepressor and prostacyclin responses to bradykinin. Journal Of Pharmacology And Experimental Therapeutics 1996, 279: 703-12. PMID: 8930174.Peer-Reviewed Original ResearchConceptsACE inhibitorsVasodepressor responseProstacyclin responsesEnzyme inhibitorsHigh-renin hypertensive patientsContribution of prostacyclinPlacebo-treated subjectsMean arterial pressureProstaglandin-independent mechanismEffect of bradykininDegradation of bradykininBradykinin doseProstacyclin metaboliteHypertensive patientsHypotensive responseVasodepressor effectArterial pressureBlood pressureACE inhibitionPGF1 alphaUrinary excretionProstacyclin productionProstaglandin productionBradykininClass effectAngiotensin converting enzyme inhibitor‐associated angioedema: higher risk in blacks than whites
Burkhart G, Brown N, Griffin M, Ray W, Hammerstrom T, Weiss S. Angiotensin converting enzyme inhibitor‐associated angioedema: higher risk in blacks than whites. Pharmacoepidemiology And Drug Safety 1996, 5: 149-154. PMID: 15073831, DOI: 10.1002/(sici)1099-1557(199605)5:3<149::aid-pds222>3.0.co;2-i.Peer-Reviewed Original ResearchCalcium channel blockersIncidence of angioedemaWhite patientsHigh riskGreater incidenceGreater riskEnzyme (ACE) inhibitor-associated angioedemaRate of angioedemaRetrospective cohort studyRisk of angioedemaACEI exposureACEI useACEI usersAngioedema incidenceCCB usersCohort studyAngioedema casesFirst episodeACEIsChannel blockersAngioedemaMedicaid recipientsFull cohortEnzyme inhibitorsChronic exposure