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IMMUNOLOGICALLYMEDIATEDDRUGREACTIONS
Typeof
Reaction
Representative
Examples
Mechanism
Anaphylactic
(type1)
Anaphylaxis
Urticaria
Angioedema
IgE-mediateddegranulationofmastcellswith
resultantmediatorrelease
Cytotoxic(type2) Autoimmune
hemolyticanemia
Interstitialnephritis
IgGorIgMantibodiesagainstcellantigensand
complementactivation
Immunecomplex
(type3)
Serumsickness
Vasculitis
Immunecomplexdepositionandsubsequent
complementactivation
Cellmediated
(type4)
Contactdermatitis
Photosensitivity
dermatitis
ActivatedTcellsagainstcellsurface–bound
antigens
RiskFactors
Factorsthatincreaseapatient’sriskofanADRincludesizeandstructureofdrug,routeofexposure
(cutaneousmostimmunogenic),dose,duration,frequency,gender(women>men),geneticfactors(HLA
type,historyofatopy),priordrugreaction,coexistingmedicalillnesses,andconcurrentmedicaltherapy.
DIAGNOSIS
ClinicalPresentation
A history is essential for making the diagnosis of an allergic drug reaction. Questions should be
directedatestablishingthefollowinginformation:signandsymptoms,timingofthereaction,purpose
of the drug, other medications the patient is receiving, prior exposure to drug or related drug, and
historyofotherallergicdrugreactions.
Urticaria, angioedema, wheezing, and anaphylaxis are all characteristics of IgE-mediated (type 1)
reactions.
Symptomsdonottypicallyoccuronthefirstexposuretothemedicationunlessthepatienthasbeen
exposedtoa structurallyrelated medication. Onreexposure, however, symptoms tendto manifest
acutely(often<1hour).
IgE-mediatedreactionstendtoworsenwithrepeatedexposuretotheoffendingmedication.
Non–IgE-mediatedreactions(anaphylactoid)canbeclinicallyindistinguishablefrom IgE-mediated
reactionsbecausethefinalcommonpathwayfortheirreactionismastcelldegranulation.
Maculopapularexanthemasarethemostcommoncutaneousmanifestationofdrugallergy.
ThesereactionsaremediatedbyTcellsandtypicallydelayedinonset,firstoccurringbetween2and
14daysofexposuretoculpritmedications.Itcanoccursoonerwithsubsequentexposures.Lesions
typicallybeginonthetrunk,especiallyindependentareas,andspreadtotheextremities.
Rarely, these rashes canprogress toa more seriousdrug reactioninvolving blistering ofthe skin
and/orend-organinvolvement.
DRESS(DrugReactionwithEosinophiliaandSystemicSymptoms)isaseriouslife-threateningADR,
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often presenting as rash and fever with systemic involvement, and can manifest as hepatitis,
eosinophilia,pneumonitis,lymphadenopathy,andnephritis.
Symptoms tend to present 2–6 weeks after introduction of medication and resolve few weeks to
monthsafterstoppingtheoffendingagent.CertainviralinfectionssuchasEpstein–Barrvirus,human
herpesvirus (HHV)-6, HHV-7, and cytomegalovirus are associated with increased risk of
complications.
Firstdescribedwithantiepileptic (carbamazepine)agentsbuthasalsobeenreportedtooccurwith
allopurinol,NSAIDs,someantibiotics,andβ-blockers.
Erythema multiforme (EM), SJS, and TEN are all serious drug reactions primarily involving the
skin.
EMischaracterizedmosttypicallybytargetlesions.SJSandTENmanifestwithvaryingdegreesof
sloughingoftheskinandmucousmembranes(<10%inSJSand>30%inTEN).Riskfactorsbeing
HIV,hematologicalmalignancy,systemiclupuserythematosus,andbonemarrowtransplant.
Readministrationorfutureskintestingwiththeoffendingdrugisabsolutelycontraindicated.
PreventionandTreatment
Acute drug reactions such as anaphylaxis should be treated promptly and discontinuation of the
suspecteddrugisthemostimportantinitialapproachinmanaginganallergicdrugreaction.
HLAtesting may be indicated insusceptible populations for prevention of a severe ADRfor some
drugssuchasabacavirandcarbamazepine.
Futureuseofthedruginquestionshouldalwaysbeavoidedunlessthereisnotherapeuticalternative
available.
Ifuseofthedrugmustbeconsidered,acarefulhistoryofthereactionishelpfulindefiningthepotential
risk. Patients may lose their sensitivitytoa drug over time, and determining the date of reactionis
useful. Symptoms that occur with the start ofa drugcourse are more likelyto be IgE-mediated than
symptomsthatdevelopseveraldaysafterthecompletionofacourse.
The types of symptoms are also important. Toxic reactions (e.g., nausea secondary to macrolide
antibiotics or codeine) are notimmunologic reactions and do not necessarilypredictproblemswith
othermembersintheirrespectiveclass.
Referral
IfnoalternativedrugisavailableandthepatienthasahistoryofanIgE-mediatedreaction,thepatient
shouldbereferredtoanallergistforfurtherevaluation.
Theallergistmayperformoneofseveralproceduresifindicateddependingonthemedication,typeof
reaction,andavailabilityoftestingreagents.
SkintestingmaybeperformedtoassessforthepresenceofIgEtothemedication.
Althoughskintestingmay beperformedtonearlyanymedication,sensitivityandspecificity ofthe
skintestresultshavebeenbestestablishedwithpenicillin.
Resultsoftestingtodrugsotherthanpenicillinmustbeinterpretedwithintheclinicalcontextofthe
case.
Gradeddose challenge assesses howthepatient tolerates progressivelylargerdoses ofmedication
(e.g.,1/1000,1/10,andfulldosegiven20minutesapart).
Drug desensitization is defined as induction of temporary state of clinical unresponsiveness or
tolerancetoasuspecteddrug.ItisperformedwhenthepatienthasanidentifiedIgE-mediatedreaction
butstillrequiresthemedication.
Thedrugmustbetakendailyataspecifieddosetomaintainthe“desensitizedstate.”
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Ifadoseofthedrugismissedfollowingadesensitizationprocedure,thenthepatientwilloftenneed
toundergoa repeatdesensitizationas the desensitizationstatewill wanebased onhalf-lifeofthe
drug.
Successful desensitization or graded challenge does not preclude the development of a non–IgE-
mediatedordelayedreaction(e.g.,rash).
Anaphylaxis
GENERALPRINCIPLES
Definition
Anaphylaxisisarapidlydeveloping,life-threateningsystemicreactionmediatedbythereleaseofmast
cellandbasophil-derivedmediatorsintothecirculation.Thepeakseverityisseenusuallywithin5–30
minutes.
Classification
Immunologicanaphylaxis:IgEmediated(type1hypersensitivity)orIgGmediated(rare)
Nonimmunologicanaphylaxis.Previouslyknownaspseudoallergicoranaphylactoidreactions
Epidemiology
Incidenceofanaphylaxisisapproximately50–2000episodesper100,000person-years.Fatalityis
estimatedat0.7%–2%percaseofanaphylaxis.IntheUS,thelifetimeprevalenceofanaphylaxisis
reportedtobe1.6%.
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Etiology
Immunologiccauses
Foods,especiallypeanuts,treenuts,shellfish,finnedfish,milk,andeggs
Insectstings(bees,wasps,andfireants)
Medications
Latexrubber
Bloodproducts
Nonimmunologiccauses
Radiocontrastmedia
Medications(i.e.,NSAIDs,opiates,vancomycin,musclerelaxants,rarelyACEinhibitors,andsulfating
agents)
Hemodialysis
Physicalfactors(coldtemperatureorexercise)
Idiopathic
Pathophysiology
IMMUNOLOGIC
Anaphylaxis is due to sensitization to an antigen and formation of specific IgE to that antigen. On
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reexposure, the IgE onmast cells and basophils binds the antigenand cross-links the IgE receptor,
whichcausesactivationofthecellswithsubsequentsystemicreleaseofpreformedmediators,suchas
histamine.
The release of mediators ultimately causes capillary leakage, cellular edema, and smooth muscle
contractionsresultingintheconstellationofphysicalsymptoms.
NONIMMUNOLOGIC
Non–IgE-mediatedanaphylaxisisalsomediatedbydirectdegranulationofmastcellsandbasophilsinthe
absenceofimmunoglobulins.
RiskFactors
Persistentasthma:increasedriskoffatalanaphylaxisifasthmaisuncontrolled.
Cardiovasculardisease:increasedriskfordeathinolderage.
Elevated baseline tryptase indicates possible mast cell disorder. Individuals with mastocytosis, a
diseasecharacterizedbya proliferationofmastcells,are athigher riskforsevereanaphylaxis from
bothIgE-andnon–IgE-mediatedcauses.
Previoussensitizationandformationofantigen-specificIgEwithhistoryofanaphylaxis.
Concomitantusedrugs:beta-adrenergicblockers,ACEinhibitors,NSAIDs,alcohol,etc.
Cofactorssuchasexercise,fever,acuteinfection,premenstrualstatus,andemotional.
Sensitivitytoseafoodoriodinedoesnotpredisposetoradiocontrastmediareactions.
Prevention
For all types of anaphylaxis, recognition of potential triggers and avoidance are the best
prevention.
Self-injectableepinephrineandpatienteducationforallpatientswithahistoryofanaphylaxis.
Radiocontrastsensitivityreactions:
Premedicationbeforeprocedureincludegivingprednisone50mgPOgiven13,7,and1hourbefore
procedureanddiphenhydramine50mgPOgiven1hourbeforeprocedure.
Premedicationisnot100%effective,andappropriateprecautionsforhandlingareactionshould
betaken.
Red man syndrome from vancomycin: symptoms can usually be prevented by slowing the rate of
infusionandpremedicatingwithdiphenhydramine(50mgPO)30minutesbeforestartoftheinfusionas
thisisanon–IgE-mediateddrugreaction.
DIAGNOSIS
Diagnosisisbasedprimarilyonhistoryandphysicalexaminationandthedocumentationofthepresence
ofaspecificIgEtothesuspectedallergen(ifthetriggerisIgEmediated).Confirmationofanaphylaxis
can,insomecases,beprovidedbythelaboratoryfindingofanelevatedserumtryptaselevel.However,
theabsenceofanelevatedtryptaseleveldoesnotexcludeanaphylaxis,particularlyiffoodisthe
suspectedcause.
ClinicalPresentation
Theclinicalmanifestationsofallergicandnonimmunologicanaphylaxisarethesame.
Manifestationsincludepruritus,flushing,urticaria, angioedema,respiratorydistress(duetolaryngeal
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edema,laryngospasm,orbronchospasm),hypotension,uterinecramping,abdominalcramping,emesis,
anddiarrhea.
Mostseriousreactionsoccurwithinminutesafterexposuretotheantigen,butinsomecircumstances,
the reaction may be delayed for hours. An example is the galactose-α-1,3-galactose allergy that is
thoughttobe triggered bytick bites and isa cause ofdelayedanaphylaxis(3–6 hours) toredmeats
includingbeef,pork,andlamb.
Some patients experience a biphasic reaction characterized by a recurrence of symptoms after
resolutionofinitialanaphylacticepisode.Timerangeisvariedandtypicallyoccurs1–8hours.
A few patientshaveaprotractedcoursethatrequires severalhourstodaysofcontinuoussupportive
treatment.
HISTORY
Athoroughhistoryistakentohelpidentifythepotentialtrigger,suchasnewfoods,medications,orother
commonlyknownallergens.Alsodocumentingthetimeofonsetofsymptoms—thatis,minutestohoursor
daysafterasuspectedexposure—canhelptoclassifythetypeofanaphylaxis.
PHYSICALEXAMINATION
Payspecialattentiontovitalsigns:Bloodpressure,respiratoryrate,andoxygensaturation.
Airwayandpulmonary: Assessforanyevidenceoflaryngealedemaor angioedema.Auscultatelung
fieldstolistenforevidenceofwheezing.Continuetoassessforneedtoprotecttheairway.
Performafocusedcardiovascularexamination.
Skin:Urticariaorerythema.
DiagnosticCriteria
SeeTable11-2fordiagnosticcriteriaforanaphylaxis.
TABLE11-2
ANAPHYLAXIS
Anaphylaxisislikelywhenoneofthefollowingthreecriteriaoccurs:
1. Acute skin and/or mucosal symptoms (e.g., hives, pruritus, flushing, lip/tongue/uvula
swelling)andoneofthefollowing:
a. Respiratorysymptoms(e.g.,wheezing,stridor,shortnessofbreath,hypoxia)
b. Hypotension or associated end-organ dysfunction (e.g., hypotonia, syncope,
incontinence)
2. Exposuretoprobableallergenforthepatientandtwoormoreofthefollowing:
a. Skin/mucosaltissueinvolvement
b. Respiratorysymptoms
c. Hypotensionorend-organdysfunction
d. Persistentgastrointestinalsymptoms(e.g.,emesis,abdominalpain)
3. Decreasedbloodpressureafterexposuretoknownallergenforthepatient:
a. Adults: Systolic blood pressure <90 mm Hg or >30% decrease in systolic blood
pressure
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b. Infantsandchildren:Hypotensionforageor>30%decreaseinsystolicbloodpressure
ModifiedfromSampsonHA,Munoz-FurlongA,CampbellRL,etal.Secondsymposiumonthedefinitionandmanagementof
anaphylaxis:Summaryreport—SecondNationalInstituteofAllergyandInfectiousDisease/FoodAllergyandAnaphylaxisNetwork
symposium.JAllergyClinImmunol.2006;117(2):391-397.Copyright©2006AmericanAcademyofAllergy,Asthmaand
Immunology.Withpermission.
DifferentialDiagnosis
AnaphylaxisduetopreformedIgEandre-exposure:Medications,insectsting,andfoodsarethemost
commoncausesofanaphylaxis.
Exercise-inducedanaphylaxis:anaphylaxisoccursexclusivelyinassociationwithphysical exertion
andothercofactors.Triggersincludefood(wheat,celery,nuts,seafood)andNSAIDs.Treatmentwould
betoavoidexerciseimmediatelyaftereatingcausativefoods.
Causesofnon–IgE-mediatedanaphylaxis
Radiocontrast sensitivity reactions are thought to be from direct degranulation of mast cells in
susceptiblepatientsbecauseofosmoticshifts.
Redman’ssyndromefromvancomycinconsistsofpruritusandflushingofthefaceandneck.
Mastocytosis.
Ingestant-relatedreactionscanmimicanaphylaxis.Thisis usuallyduetosulfitesorthepresence
ofahistamine-likesubstanceinspoiledfish(scombroidosis).
Flushing syndromes include flushingdueto red man syndrome, carcinoid, vasointestinal peptide
(andothervasoactiveintestinalpeptide–secretingtumors),postmenopausalsymptoms,rosacea,use
ofniacin,andalcoholuse.
Otherformsofshocksuchashypoglycemic,cardiogenic,septic,andhemorrhagic.
Vasovagal syncope can be distinguishedfrom anaphylaxis bythepresence ofbradycardia; however,
bradycardiacanoccurinanaphylaxisbecauseoftheBezold–Jarischreflex.
Respiratorydiseasessuchasacutelaryngotracheitisandforeignbodyobstructionintrachea.
Miscellaneous syndromes such as hereditary angioedema (HAE; C1 esterase inhibitor [C1 INH]
deficiencysyndrome),pheochromocytoma,neurologic(seizure,stroke),andcapillaryleaksyndrome.
Neuropsychiatriccausessuchaspanicattacksorvocalcorddysfunction.
Idiopathic.
DiagnosticTesting
Epicutaneousskintestingandserum-specificIgEtestingwhenavailabletoidentifytriggerallergens.
Serumtryptasepeaksat1houraftersymptomsbeginandmaybepresentforupto4hours.
TREATMENT
Earlyrecognitionofsignsandsymptomsofanaphylaxisisacriticalfirststepintreatment.
Epinephrineisthemedicationofchoicefortreatmentofanaphylaxis.
Maintainrecumbentpositionwhileassessingandstartingtherapy.
Airway management is a priority. Supplemental 100% oxygen therapy should be administered.
Endotrachealintubationmaybenecessary.Iflaryngealedemaisnotrapidlyresponsivetoepinephrine,
cricothyroidotomyortracheotomymayberequired.
VolumeexpansionwithIVfluidsmaybenecessary.
Medications
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Epinephrineshouldbeadministeredimmediately.Therearenoabsolutecontraindicationsfortreatment
withepinephrineinanaphylaxis.
Adult: 0.3–0.5 mg(0.3–0.5 mL ofa 1:1000 solution)IM in the lateral thigh, repeated at 10- to 15minuteintervalsifnecessary.
Child:1:1000dilutionat0.01mg/kgor0.1–0.3mLadministeredIMinthelateralthigh,repeatedat10to15-minuteintervalsifnecessary.
0.5mLof1:1000solutionsublinguallyincasesofmajorairwaycompromiseorhypotension.
3–5mLof1:10,000solutionviacentralline.
3–5mLof1:10,000solutiondilutedwith10mLofnormalsalineviaendotrachealtube.
For protracted symptoms that require multiple doses ofepinephrine,anIV epinephrinedrip may be
useful;theinfusionistitratedtomaintainadequateBP.
Glucagoncouldreverserefractorybronchospasmandhypotensioninpatientswhoaretakingβadrenergicantagonists.Recommendeddosageis1–5mgintravenouslybolusslowlyover5minutes
followedbyaninfusionat5–15µg/mintitratedtoclinicalresponse.Monitorforsideeffectssuchas
nauseaandvomiting.
Inhaledβ-adrenergicagonistsshouldbeusedtotreatresistantbronchospasm.
Glucocorticoidshavenosignificantimmediateeffectandmaynotpreventbiphasicreactions.
Antihistaminesrelieveskinsymptomsbuthavenoimmediateeffectonthereaction.Theymayshortenthe
durationofthereaction.
Adult:Diphenhydramine25–50mgIMorIV,cetirizine10mgoralorIV
Child:Diphenhydramine12.5–25.0mgIMorIV,cetirizine5–10mgoralorIV
Referral
Referralstoanallergistforfurtherevaluationshouldbeofferedtoallpatientswithahistoryof
anaphylaxis.Moreimportantly,patientswithHymenopterasensitivityshouldbeevaluatedtodetermine
eligibilityforvenomimmunotherapy.
Eosinophilia
GENERALPRINCIPLES
Eosinophilsaregranulocytesthatdevelopedfrombonemarrowpluripotentprogenitorcells.
Eosinophil maturationis promotedbyinterleukins (IL-5, IL-3), andgranulocyte-macrophagecolonystimulatingfactor.
Eosinophils arenormallyseeninperipheral tissuesuchasmucosal tissuesinthegastrointestinaland
respiratorytracts.Theyarerecruitedtositesofinflammation.
Eosinophilscanbeinvolvedinavarietyofinfectious,allergic,neoplastic,andidiopathicdiseases.
Definition
Avalue>500eosinophils/μLisdefinedashavingeosinophilia.
The extent of eosinophilia can be categorized as mild (500–1500 cells/μL), moderate (1500–5000
cells/μL),orsevere(>5000cells/μL).
Thedegreeofeosinophiliaisnotareliablepredictorofeosinophil-mediatedorgandamage.
Classification
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Peripheraleosinophiliacanbedividedintoprimary,secondary,oridiopathic.
Primary eosinophilia is seenwith hematologic disorders where there maybe a clonal expansion of
eosinophils (chronic eosinophilic leukemia) or a clonal expansion of cells that stimulate eosinophil
production(chronicmyeloidorlymphocyticdisorders).
Secondaryeosinophiliaisalsocalledreactiveeosinophilia.Itisapolyclonalexpansionofeosinophils
due to overproduction of IL-5. There are numerous causes such as parasites, allergic diseases,
autoimmunedisorders,toxins,medications,andendocrinedisorderssuchasAddisondisease.
Idiopathiceosinophiliaisconsideredwhenprimaryandsecondarycausesareexcluded.
HYPEREOSINOPHILICSYNDROME
Aproliferativedisorderofeosinophilscharacterizedbysustainedeosinophilia>1500cells/μLfor≥1
monthdocumentedontwooccasionswitheosinophil-mediateddamagetoorganssuchastheheart,
gastrointestinaltract,kidneys,brain,andlung.Allothercausesofeosinophiliashouldbeexcludedto
makethediagnosis.
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Hypereosinophilicsyndrome(HES)occurspredominantlyinmenbetweentheagesof20and50years
andpresentswithinsidiousonsetoffatigue,cough,anddyspnea.
Approximately 10%–15% HES patients have myeloproliferative disorders. Myeloproliferative
variantsofHESare characterizedbyconstitutive expressionofFIP1L1/PDGFRAfusionproteinand
elevatedserumvitaminB12levels.
Lymphocytic-variantHES(L-HES)accounts for 17%–26%HESpatients.Unusual IL-5–producing T
cellsarefoundinL-HES.
Cardiac disease is a major cause ofmorbidity and mortalityinpatients withHES.At presentation,
patientstypicallyareinthelatethromboticandfibroticstagesofeosinophil-mediatedcardiacdamage
with signs of a restrictive cardiomyopathy and mitral regurgitation. An echocardiogram may detect
intracardiac thrombi, endomyocardial fibrosis, or thickening of the posterior mitral valve leaflet.
Neurologicmanifestationsrangefromperipheralneuropathytostrokeorencephalopathy.Bonemarrow
examinationrevealsincreasedeosinophilprecursors.
AcuteeosinophilicleukemiaisararemyeloproliferativedisorderthatisdistinguishedfromHESby
severalfactors:anincreasednumberofimmatureeosinophilsinthebloodand/ormarrow,>10%blast
formsinthemarrow,andsymptomsandsignscompatiblewithanacuteleukemia.Treatmentissimilar
tootherleukemias.
Lymphoma.EosinophiliacanpresentinanyT-orB-celllymphoma.Asmanyas5%ofpatientswith
non-Hodgkin lymphoma and up to 15% of patients withHodgkinlymphoma havemodestperipheral
bloodeosinophilia.EosinophiliainHodgkinlymphomahasbeencorrelatedwithIL-5messengerRNA
expressionbyReed–Sternbergcells.
Atheroembolic disease. Cholesterol embolization can lead to eosinophilia, eosinophiluria, renal
dysfunction,livedoreticularis,purpletoes,andincreasederythrocytesedimentationrate(ESR).
Immunodeficiency. Hyper-IgE syndrome, autoimmune lymphoproliferative syndrome, and Omenn
syndromecanpresentwithrecurrentinfections,dermatitis,andeosinophilia.
Epidemiology
Inindustrializednations,peripheralbloodeosinophiliaismostoftenduetoatopicdisease,whereas
helminthicinfectionsarethemostcommoncauseofeosinophiliaintherestoftheworld.
DIAGNOSIS
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Therearetwoapproachesthatareusefulforevaluatingeosinophilia,eitherbyassociatedclinicalcontext
(Table11-3)orbydegreeofeosinophilia(Table11-4).
TABLE11-3
CAUSESOFEOSINOPHILIA
EosinophiliaAssociatedWithAtopicDisease
Allergicrhinitis Atopicdermatitis
Asthma
EosinophiliaAssociatedWithPulmonaryInfiltrates
Chroniceosinophilicpneumonia Allergicbronchopulmonaryaspergillosis
Acuteeosinophilicpneumonia Coccidioidomycosis
Tropicalpulmonaryeosinophilia Löfflersyndrome(larvaetravelinginlung)
EosinophiliaAssociatedWithParasiticInfection
Helminths(Ascarislumbricoides,Strongyloidesstercoralis,hookworm,Toxocaracanisor
Toxocaracati,Trichinella)
Protozoa(Dientamoebafragilis,Sarcocystis,andIsosporabelli)
EosinophiliaAssociatedWithPrimaryCutaneousDisease
Atopicdermatitis Eosinophilicfolliculitis
Eosinophilicfasciitis Episodicangioedemawithanaphylaxis
Eosinophiliccellulitis
EosinophiliaAssociatedWithMultiorganInvolvement
Drug-inducedeosinophilia Eosinophilicleukemia
Eosinophilicgranulomatosiswithpolyangiitis Systemicmastocytosis
Hypereosinophilicsyndrome Lymphomas
MiscellaneousCauses
Eosinophilicgastroenteritis Transplantrejection
Interstitialnephritis Atheroembolicdisease
Eosinophiliamyalgiasyndrome Adrenalinsufficiency
Retroviralinfections(HIV,humanT-lymphotropicvirustype1)
TABLE11-4
CLASSIFICATIONOFEOSINOPHILIABASEDONTHEPERIPHERALBLOOD
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EOSINOPHILCOUNT
PeripheralBloodEosinophilCount(cells/μL)
500–2000 2000–5000 >5000
Allergicrhinitis Intrinsicasthma Eosinophiliamyalgia
syndrome
Allergicasthma Allergicbronchopulmonary
aspergillosis
Hypereosinophilic
syndrome
Foodallergy Helminthiasis Episodicangioedema
witheosinophilia
Urticaria Drugreactions EGPA
Addisondisease Vascularneoplasms Leukemia
Pulmonaryinfiltrateswith
eosinophiliasyndromes
Eosinophilicgranulomatosiswith
polyangiitis(EGPA)
Solidneoplasms Eosinophilicfasciitis
Nasalpolyposis HIV
ClinicalPresentation
HISTORY
A history is important in narrowing the differential diagnosis of eosinophilia. It is important to
determineifthe patienthas symptoms ofatopic disease (rhinitis, wheezing, rash) or cancer (weight
loss, fatigue,fever,night sweats) andtoevaluatefor otherspecific organ involvementsuch as lung,
heart,ornerves.Prioreosinophilcountcanhelpdeterminethedurationandmagnitudeofeosinophilia.
A completemedication list, including over-the-counter supplements, and a full travel, occupational,
anddietaryhistoryshouldbeobtained.
Anypetcontactshouldbeascertainedforpossibleexposuretotoxocariasis.
PHYSICALEXAMINATION
Physicalexaminationshouldbeguidedbythehistory,withaspecialfocusontheskin,upperandlower
respiratorytracts,andcardiovascularandneurologicsystems.
LABORATORIES
Initial laboratory evaluations generally include complete blood count (CBC) with differential and
eosinophil count, liver function tests, serum chemistries and creatinine, serum vitamin B12 level,
troponin,markersofinflammation(e.g.,ESRand/orC-reactiveprotein[CRP]),andurinalysis.Further
diagnostic studies are based on clinical presentations and initial findings. Mild eosinophilia
associatedwithsymptomsofrhinitisorasthmaisindicativeofunderlyingatopicdisease,whichcan
beconfirmedbyskintesting.
Depending on the travel history, stool examination for ova and parasites should be done on three
separateoccasions.Becauseonlysmallnumbersofhelminthsmaypassinthestoolandbecausetissue-
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