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Allergic Drug Reactions
Epidemiology*
• It is believed that approximately 2-6% of all hospitalizations are due
to adverse drug reactions.
• 15-30% of hospitalized patients experience adverse drug reaction.
• Drug-attributed deaths occur in 0.01% of surgical inpatients and in
0.14% to 0.17% of medical inpatients.
• Risk of allergic reaction is about 1-3% in the general public.
* Most adverse drug reactions are not reported
Where to report ?
http://www.fda.gov/medwatch
Incidence of Drug Reactions
• Most adverse drug reactions are idiosyncratic
and occur as a result of many factors (genetic,
slow acetylators, co-morbid conditions,
concomitant medication, etc.),
but …
• 6 - 10% of adverse drug reactions are allergic,
and ...
• 10% of drug-related anaphylaxis results in
death
Classification of Drug Reactions
• Type A - common & predictable
– 80-90% of adverse drug reactions
– Often dose dependent
– Produced by known pharmacologic drug actions
• Drug overdose or toxicity - an exaggerated, but
characteristic pharmacologic effect produced at
supratherapeutic doses
• Side effects - excessive expressions of known
pharmacologic effects that occur at recommended doses
• Drug interactions - unusual effects due to the combined
pharmacologic activity of two or more drugs.
Classification of Drug Reactions
• Type B - uncommon & unpredictable
• Drug intolerance - undesirable pharmacologic effect at a
subtherapeutic dosage.
• Idiosyncratic reactions - uncharacteristic reaction
unrelated to the pharmacologic action of the drug.
– Difficult to distinguish from allergic reactions.
• Allergic reactions are immunologically (IgE) mediated
reactions that share the following characteristics:
– occurs in small numbers of patients
– requires prior exposure to the same or chemically related drug
– develops rapidly after re-exposure
• Pseudoallergic reactions - indistinguishable from the
above allergic reactions, but are not IgE-mediated.
*
Classification of Drug Reactions
• Other Reactions • Superinfection: Antibiotics against one organism alters
endogenous flora. Example: pseudomembranous colitis
• Disease-associated: Reactions to drugs which occur
only when the drug is administered in the setting of a
specific disease. Examples: Jarisch-Herxheimer
reaction (PCN/syphilis), ampicillin rash w/ EBV/CMV
• Coincidental: Drug blamed when in fact the primary
disease process is responsible. Example: Viral exanthem
• Psychogenic: Anxiety, hyperventilation, vasovagal rxns
associated w/ drug administration. Example: injections
*
Approach to The Patient With a
Previous Adverse Drug Reaction
Type of Adverse Reaction
Type B
Type A
Intolerance or
Idiosyncratic
Immunologic or
Pseudoallergic
Avoid Drug
Structurally Unrelated
Drug Available – Use It.
Structurally Unrelated
Drug Not Available
Test For Drug Allergy
Available
Test results
Negative
Modify Dose or Choose
Other Drugs Not Associated
With Same Untoward Events
Test results
Positive
Cautiously Administer Drug
if Use is Essential
Previously Blistering, Serum
Sickness, or Drug Fever
Test For Drug Allergy
Not Available
Desensitize if Use is Essential
Typical Features of Allergic Drug
Reactions
• No problems with previous treatment
• If no previous exposure, reactions generally occur
several days into therapy
• The reaction occurs only in a small number of
patients with doses far below the therapeutic range
• Some if not most reactions are due to the metabolites
of the parent drug (e.g. PCN and major and minor
determinants, sulfa and hydroxylamines)
• Specific antibodies or T-cells can be identified with
some drugs
Types of Allergic Drug Reactions
• Multisystem
– Anaphylaxis
• Antimicrobials, proteins
– Anaphylactoid
• RCM, NSAIDs, opiates, tubocurarine, dextrans
– Serum sickness
• Proteins, abx (cefaclor), allopurinol, thiazides, PTU
– Drug fever
• Sulfonamides, β-lactams, methyldopa, quinidine
– Drug-induced SLE
• Procainamide, hydralazine
Types of Allergic Drug Reactions
• Cutaneous
– Urticaria/angioedema
• Antimicrobials, proteins, opiates, ACE-I
– Maculopapular exanthemous eruption
• Sulfonamides, β-lactams, barbiturates, anticonvulsants
– Stevens-Johnson/TENS
• Sulfonamides, β-lactams, phenytoin, carbamazepine
– Fixed drug eruptions
• Sulfonamides, β-lactams, barbiturates, tetracycline
– Photoallergic reactions
• Phenothiazines, sulfonamides, griseofulvin
• Phototoxic reactions (not IgE-mediated)
– Tetracycline, sulfanilamide, chlorpromazine, psoralens
– Allergic contact dermatitis
• Local anesthetics, neomycin, parabens, antihistamines
*
Types of Allergic Drug Reactions
• Hematologic
– Eosinophilia
• Allopurinol, digitalis, ASA, Amp., TC antidepressants
– Hemolytic anemias
• Hapten-type (PCN, cisplatin)
• Innocent bystander (sulfonamide, chlorpromazine,
quinine, para-aminosalicylic acid)
• Autoimmune (methyldopa, penicillin, aldomet)
– Thrombocytopenia
• Quinidine, sulfonamides, heparin
– Granulocytopenia
• Sulfasalazine, procainamide, penicillin, phenothiazines
*
Types of Allergic Drug Reactions
• Hepatic
– Cholestasis
• Macrolides, nitrofurantoin, imipramine, phenothiazines
– Hepatocellular dysfunction (inc. transaminases)
• Valproic acid, halothane, isoniazid, sulfonylurea,
methyldopa
– Granulomatous hepatitis
• Quinidine, allopurinol, methyldopa, sulfonamides
Types of Allergic Drug Reactions
• Renal
– Interstitial nephritis
• β-lactams (methicillin), rifampin, NSAIDs, sulfonamide
– Nephrosis (membranous glomerulonephritis)
• Captopril, NSAIDs, anticonvulsants, probenecid
Types of Allergic Drug Reactions
• Respiratory
– Asthma
• β-lactams, sulfites, NSAIDs, β- blockers
– Pulmonary infiltrates with Eosinophilia (PIE)
• Nitrofurantoin, MTX, NSAID, sulfonamides,
tetracycline, isoniazid
– Rhinitis
• Reserpine, hydralazine, α-blockers, iodides, levodopa
Classification of Drug Reactions
Gell and Coombs:
• Type I: Immediate Hypersensitivity (IgE)
• Type II: Cytotoxic Antibody (IgM or IgG)
• Type III: Immune Complex (IgM or IgG)
• Type IV: Delayed-type Hypersensitivity (T-cell)
Unfortunately, the mechanism for drug reactions
are often unknown, so clinical classification is
more useful.
T
Y
P
E
I
Type I Drug Reactions
• Anaphylaxis
– Implies IgE-mediated
– “Anaphylactoid” = another mechanism
• Angioedema
• Urticaria
• Morbilliform = most common
TYPE II
Type II Reactions
• IgG or IgM recognizes drug adherent to cells
– Activate complement
– Cells cleared by splenic macrophages
• Hemolytic anemia
• Autoimmune thrombocytopenia
Hemolytic Anemia
• Evidence of anemia and hemolysis:
– NCNC or high MCV
– Direct Combs +, high LDH & retic, low haptoglobin
• Drug is hapten, RBC antigen is carrier
– Penicillin
• Antibodies to drug cross-react w/ RBC
– Aldomet, L-dopa, mefenamic acid
• Plasma protein & drug cause immune response
– RBC innocent bystander
– Sulfonamides, phenothiazines, quinine
Immune Thrombocytopenia
• Diagnosis: low platelets o/w normal CBC smear
• Drug adsorbs to platelet surface, forms neo-Ag
– Quinidine complexes w/ gp IIb/IIIa and gp Ib/IX
– Heparin complexes with circ PF4
• IgG Fab binds neoantigen
• In HIT attached IgG Fc binds platelet FcγRII
– Triggers activation and consumption
– Low platelets and thrombosis
• Other drugs: sulfa, β-lactam, indinavir, Lipitor, Ticlid, gold,
acetazolamide and Trental
Type III
Type III Reactions
• Soluble immune complexes of drug & IgG/M
– Complexes deposit in vessel walls
– Activate complement
• Serum sickness
– 1-3 weeks
– Fever, urticaria, serpiginous rash, LAD, arthralgias
– Other rashes are morbilliform or target lesions
• Drug fever
• Vasculitis
TYPE IV
Type IV Reactions
• Protype is allergic contact dermatitis
• Patch testing with the medication is
sometimes performed.
Drug Hypersensitivity Reactions
• Reactions that can not be easily classified
into the Gel and Coombs Classification.
Erythema Multiforme
Target Lesions
• Three zones:
• An erythematous central papule that may
blister
• an edematous middle ring
• an erythematous outer ring
• Predilection for extremities, Symmetrical
Erythema Multiforme Minor
• Cell-mediated
hypersensitivity
reaction
• Associated with
infections and
drugs (10-20%)
• Target lesions
are
characteristic
Erythema Multiforme Minor
•
•
•
•
Drug should be stopped immediately
Anti-histamines may decrease itching
Steroids (1 mg/kg/day) may be necessary
“Early treatment of erythema multiforme
minor may prevent progression to Erythema
multiforme major.
Stevens Johnson Syndrome
• SJS
– mortality <10%
– Mucus membrane & conjunctival involvement
in 85%
– widespread bullae & purpuric macules of the
face, trunk, and genital areas.
– Constitutional symptoms, <10% epidermal
detachment
• SJS/TEN overlap 10-30% epidermal-lysis
Stevens-Johnson Syndrome
• Drugs caused 50% of cases
• More than 100 drugs have been implicated
as causing EM, SJS and TEN
• High relative risk drugs: sulfonamides,
Ampicillin, anticonvulsants, NSAIDS &
allopurinol cause 2/3 of SJS. (TB drugs in
developing countries)
• Readministration causes recurrence.
EMM and SJS
• Stop the drugs
• Steroids are “controversial…if it is started,
it should be started early in the course of the
disease and in very large doses…”
• Late in the course, TEN could supervene, in
which case steroids are contraindicated
Toxic Epidermal Necrolysis
•
•
•
•
•
•
Epidermal detachment of 30% or more
Almost always drug induced (>80%)
Steroids are contraindicated
Patients are managed in burn units
IVIG has been used in some patients
Mortality 30-40%
Fixed Drug Eruptions
• Fixed drug eruptions (FDEs)
characteristically recur in the same site or
sites each time a particular drug is taken;
with each exposure however, the number of
involved sites may increase.
• Mechansim: Unknown
ANGIOEDEMA
Angioedema
• Abnormal Bradykinin metabolism
– ACE inhibitors
– Reports also with ARBs
• ASA/NSAID reactions: dual mechanism
– COX-1/2 inhibition
– IgE-mediated
• Unusual in IgE-mediated w/o urticaria
Diagnosis
• History
– The cardinal diagnostic tool. Key points include:
• suspicion that an unexplained clinical event may be
caused by a drug
• complete and accurate documentation of all drugs,
including nonprescription ones, taken over the previous
month
• temporal relationships between drug administration and
the onset of symptoms or signs
• correlation of the clinical manifestations with known
reactions induced by a particular drug
• previous tolerance of the drug (sensitization)
• prior history of a similar reaction to the same or cross
reacting drug.
Diagnosis
• History
– A few points regarding the temporal relationship:
• virtually impossible to react allergically on the 1st
exposure to a drug
• Reactions rarely occur within the first 7 days of
treatment; rather, within 2-4 weeks
• the classic IgE-mediated drug allergy typically appears
after the first dose of a new course.
• if a drug has been taken continuously for a year or
more, it is unlikely to cause a reaction (tolerance
induction?)
Testing
Finding a reagent is a problem. Most drugs have
a low molecular weight & are not immunogenic.
The antigenic determinants are unknown.
• Skin testing
– Immediate hypersensitivity (IgE, Type I)
• Prick skin testing, intradermal skin testing
• Most accurate in evaluating protein drugs (insulin, vacc)
• Somewhat useful for PCN, drugs of general anesthesia
– Delayed hypersensitivity (T-cell, Type IV)
• Patch testing
• Most useful for allergic contact dermatitis
Testing
– In-vitro testing (RAST, ELISA, etc.)
• Measures circulating drug specific IgE antibodies
• Less specific and less sensitive than skin testing
• Of limited availability & usefulness
– Provocative challenge
• Oral, SQ, or IV
• Has inherent risk!
Decision Path:
Patient with Drug Allergy History
• The ability to detect drug-specific IgE antibodies
helps to assess the risk for allergic reactions.
– However, the IgE must be clinically relevant (e.g., IgE
anti-insulin antibodies are common in diabetics, but allergic
reactions are rare).
• Conversely, the inability to detect drug-specific IgE
antibodies does not R/O the possibility of sensitivity.
• Desensitization protocols are indicated in established
cases of drug hypersensitivity where there is NO
substitute and treatment is essential (e.g. penicillin for
neurosyphilis)
Decision Path:
Patient with Drug Allergy History
Treat with
alternative
drug
Is an alternative
drug available
and effective?
Yes
No
Is a reliable test
available?
Treat with
the drug
Negative
Do the
test
Positive
Yes
Desensitize
No
Premedication or
provocation test
or both
Reaction
No Reaction
Continue treatment
Drug Allergy is Tough!
• Our tests are rudimentary.
– What tests?
• Problems with the literature
– These are often anecdotal or uncontrolled.
• Many HCW don’t understand the limitations
we have.
– Results in frustration (for everybody)
Management
• General management principles for patients
with a history of allergy to a specific drug:
– Obtain full clinical details of the reaction
– If allergy is suspected, use an alternative, noncross-reacting drug (available in most situations)
– If none appropriate, refer to someone competent in
testing for drug allergy and in desensitization
– If allergy tests are positive, avoid the drug;
however, desensitization may be
appropriate as a last resort.
– Know how to treat anaphylaxis!
Management
– Localized reactions
• Discontinuing drug is usually sufficient. May use antihistamines for pruritus and steroids for severe reactions
– Systemic reactions
• Anaphylaxis -- discontinue drug (if IV) immediately
and treat with standard treatment protocol (i.e.
epinephrine, diphenhydramine, fluids, etc.)
• Serum sickness -- antihistamines, aspirin, and may use
steroids to accelerate recovery via anti-inflammatory
effects and increase clearance of immune complexes.
– Use oral rather than parenteral drugs if possible
Specific Examples
Penicillin
• Penicillin is the most common cause of anaphylaxis
(1-5 cases/10,000 treatment courses)
• Penicillin allergy prevalence = 1-10% (2%)
• 0.01 - 0.05% of those who receive PCN anaphylax
• 400-800 deaths yearly in US from PCN anaphylaxis
• 75% of patients with PCN anaphylaxis had no prior
history of PCN adverse reaction (sensitization)
• NOT more common in atopics
• Occurs most commonly in adults 20 - 49 years old.
Penicillin
• Penicillin has been implicated in immunologic
reactions spanning all Gel & Coombs classes:
–
–
–
–
Type I -- anaphylaxis
Type II -- cytotoxic (hemolytic anemia)
Type III -- immune complex (serum sickness)
Type IV -- delayed hypersensitivity (fixed drug
eruption)
*
Penicillin
• Cross reactivity with other antibiotics
– Penicillin, ampicillin, cephalosporin, carbapenems,
oxacephems, and clavams possess β-lactam ring
fused to another ring.
– All except clavams have ring side chain(s).
– Side chain IgE possible - PCN skin tests negative!
– Monobactams have only the β-lactam ring.
– Non-IgE mediated maculopapular rash occurs in 5
- 10% of ampicillin Rx & up to 90% if have mono.
– This rash resolved even if therapy continues.
Classes of β-Lactam Antibiotics
PCN Cross Reactivity
• HIGH - carbapenems
(Imipenem, Meropenem)
• LESS - cephalosporins
(1st=10%, 2nd=3%, 3rd=1%)
• LEAST - monobactam
(Aztreonam)
Penicillin Skin Testing
• Testing issues:Pre-pen was approved in
September 2009 by FDA.
• Readily available
• Approximately $75 for the testing reagents
Penicillin, Major/Minor Determinants
Pre-pen (Penicillin Skin Test)
• Elective penicillin skin testing using PRE-PEN and PenG allows
>85% of history-positive patients to receive penicillins and related
beta-lactam antibiotics.
• Published studies of pre-surgical and emergency department use
of penicillin skin testing show that routine use in history-positive
patients reduces medical costs and allows the use of more effective
and often less toxic antibiotics.
• Penicillin skin testing can help promote the goal of curtailing
resistant bacteria by allowing most history-positive patients to be
treated with targeted, bacteriocidal beta-lactam antibiotics.
• Appropriate use of penicillin skin testing will dramatically reduce
the need for penicillin desensitization / challenges, which in the
past 5 years has been the only way to assure safe re-treatment of
history-positive patients.
Candidates for Testing
•Any patient with a history of a reaction to a penicillin antibiotic that may
have been IgE-mediated
•Any patient who is currently denied access to beta-lactam antibiotics out
of concern for such reactions
Contraindications for Testing
• Patients with clear histories of severe skin
reactions such as Stevens-Johnson
syndrome, or toxic epidermal necrolysis.
• Type II, type III, type IV hypersensitivity –
although not contraindicated – this test is
not designed to answer these questions.
Sulfonamides (“Sulfa”)
• ~ 3% of patients develop allergic rxn to sulfa
• Rash is the most common reaction
– Generalized maculopapular and/or pruritus
– Rarely
• Urticaria
• Erythema multiforme
• Stevens-Johnson/Toxic Epidermal Necrolysis (very rare)
– More associated w/ sulfa than all other drug classes
• Drug Fever
• Hematologic reactions
– Thrombocytopenia
– Neutropenia
Sulfonamides (“Sulfa”)
• p-aminobenzoic acid rings (PABA)
– Sulfonamide antibiotics
–
–
–
–
• sulfadiazine, sulfamethoxazole, sulfacetamide
Thiazide diuretics
Furosemide
Sulfonylureas
Celecoxib
• BUT - cross sensitivity is very rare
– Arylamine group at N4 position critical for x-rxn
• N4-sulfonamindoyl determinant
• NO cross reaction if drug only contains sulfur
– Amoxicillin, captopril, ranitidine, sulindac, sulfites
*
Sulfonamides (“Sulfa”)
• Sulfonamide metabolism:
– Hepatic N-acetylation
– Cytochrome P-450 N-oxidation.
• Genetically slow acetylators
are more prone to accumulate
oxygenated metabolites.
• Allergic rxns occur when reactive metabolites
act as haptens and link to tissue proteins
• Independent of route of exposure
– Oral, ocular, topical, or vaginal
*
Sulfonamides (“Sulfa”)
• Adverse reactions to drugs metabolized by Nacetylation occur 10x more in AIDS patients
– Decreased glutathione reductase (due to meds?)
– 90% have IgE or IgG to N4-sulfonamindoyl group
– 50% have rash
• Rash only not necessarily contraindication
– Only 20-66% will have recurrence
• Treat rash symptomatically throughout therapy
• Desensitize
• No reliable in vivo or in vitro sensitivity tests
• Mechanism of desensitization is unclear
Vancomycin
• “Red man” syndrome = pruritus & erythema
over face, neck and upper torso
• Occasionally associated with hypotension
• Due to non-immunologically mediated release
of histamine
• Management is slower infusion rate (> 1 hour)
• If still symptomatic, pre-medicate with
hydroxyzine
• True IgE mediated allergic reactions to
vancomycin are rare (and its debatable if this is
simply severe red man vs. true IgE disease)
Local Anesthetics
• IgE-mediated reactions are rare
• Idiosyncratic reactions are common, especially
those associated with autonomic over-activity
(vasovagal)
• Chemically can be classified into two groups:
– Esters: procaine, tetracaine, cocaine, benzocaine
– Amides: lidocaine, mepivacaine, bupivacaine
– Amides do not cross with esters or each other
• Some adverse reactions are due to the presence
of methylparaben preservatives.
Radiocontrast Media
• Most common cause of anaphylactoid reaction
• Various factors including osmolar effects and
complement activation cause histamine
release from basophils
• Treatment protocol:
– Use lower osmolar contrast agents
– Pre-treatment:
• Prednisone 50 mg, 13, 7, & 1 hour before
• Benadryl 50 mg PO or IM 1 hour before
• Ephedrine, H2 blocker use controversial
Anaphylactoid Reactions
• Nonspecific mast cell
release
• May occur with first
exposure
• Opioids
• Anesthetics
• Vancomycin
• ASA, NSAIDs
• Radiocontrast media
Individuals with a hx of anaphylactoid reactions are at increased risk of having another with
future exposures. i.e. Pre-treatment protocols for RCM etc….
Cutaneous Reactions to Aspirin
•
•
•
•
May occur at any age
Symptoms may be delayed (up to 24 hours)
May induce acute urticaria/angioedema
Aspirin and NSAIDS may aggravate preexisting chronic urticaria
• Aspirin desensitization does not seem to
improve chronic urticaria secondary to ASA
Which of the following contain
ASA?
Respiratory Reactions to aspirin
• Severe, prolonged, and occasionally fatal
asthma attacks.
• Asthma attacks typically begin within 30
minutes to 3 hours after ingestion
• These attacks are also associated with
profound nasal congestion, rhinorrhea, and
conjunctivitis
Mechanism for aspirin induced
asthma
• Hypothesized that inhibition of cyclooxygenase
pathway by aspirin /NSAID.
• Results in shunting to second pathway of
arachidonic acid metabolism
• This results in the production of leukotrienes
(especially LTC4, LTD4, and LTE4)
• All potent inhibitors of cyclooxygenase will
provoke respiratory symptoms in aspirin sensitive
asthmatics
Anaphylactoid Reactions to ASA
• Shares similarities with anaphylaxis
– specific for ASA
– Does not cross reactive with other NSAIDS
– requires more than one dose (prior
sensitization)
– typically do not have underlying nasal polyps,
asthma, or urticaria
• Desensitization for anaphylactoid reactions
is controversial/rarely indicated- high risk
of fatal anaphylactoid reactions
Acetaminophen and ASA
sensitivity
• Acetaminophen is generally much better
tolerated in aspirin sensitive patients
• In high doses, may have some
cyclooxygenase inhibition
• In one study with a dosages >1000mg, 34%
had respiratory symptoms with 22%
experiencing bronchospasm
• This reaction is felt to be dosage dependent
Drug
Desensitization
Drug Desensitization
• Desensitization is DANGEROUS!
– Slow motion anaphylaxis?
• Desensitization is TRANSIENT!
– It requires ongoing drug exposure.
• Skin test reactivity and clinical sensitivity may return
within 48 hours if administration is interrupted.
Drug Desensitization
• Goal: convert a drug-allergic patient from a
highly sensitive state to a drug-tolerant state
• Used primarily, but not solely, for IgEmediated hypersensitivity
• Effective in these drug sensitivities:
•
•
•
•
•
Penicillin
Sulfonamides
Cephalosporins
Vancomycin
Aminoglycosides
•
•
•
•
•
•
Insulin
Measles vaccine
Heparin
Antivenoms
Tetanus toxoid
ASA*
Drug Desensitization
• Mechanism of Action
– Antigen-specific, mast cell desensitization.
– Mediator-depletion does not play a role.
• Wheal & flair reaction to penicillin is abolished while
IgE response to other antigens remains intact.
– The underlying mechanism remains unclear.
• A slow rate of IgE receptor aggregation may generate a
suppressor signal
• Univalent drug-hapenated proteins prevent the crosslinking of drug-specific IgE on mast cells
Theories of Drug Desensitization
Inflammatory mediators
Mast cell
Suppression of
activation signals
Mast cell
IgE
Penicillin
• Complications of Penicillin Desensitization
– Mild pruritus or pruritic rashes in ~ 5% during
desensitization and in ~25% during subsequent
full-dose therapy.
– ~ 5% may experience drug-induced serum
sickness, hemolytic anemia, or nephritis late in
the course of full-dose therapy
• Result of IgG induced during desensitization?
– Acute reactions during desensitization may
require suppressive medication / adjustment in
desensitization dosage and/or dose intervals.
*
Penicillin
• Desensitization
Protocols vary depending
on the urgency, required
route, and unit dose of
penicillin (the drug)
β-lactam IV Densensitization Protocol
Dose # Time Dose (Unit) Cumulative Dose
1
2
3
4
5
6
7
8
0800
0830
0900
0930
1000
1030
1100
1130
1
10
100
1,000
10,000
100,000
1,000,000
1,300,000
1
11
111
1,111
11,111
111,111
1,111,111
2,411,111
Desensitization vs. Drug Challenges
• Desensitization:
– PRO: Relatively safely administer the Rx desired.
– CON: You never know if they are really still allergic,
so repeat is common in future. May take long time for
Pharmacist to prepare.
• Drug Challenge:
– PRO: If they pass, they likely can tolerate the Rx now
and related Rx in the future. Generally quick to prepare.
– CON: Risky, since you are looking to cause an allergic
reaction. (absence of a reaction is re-assuring). May end
up desensitizing anyway (if fail challenge).
Summary
Drug allergy can be a significant problem in
medical practice. The diagnosis is made
primarily from the history as there are few
specific, accurate diagnostic tests. If a patient
has a drug allergy, alternative drugs should be
used in the future. However, if the particular
drug is considered essential in subsequent
therapy, various techniques may allow its use.