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morphology resembles plaque psoriasis although
erythrodermic, guttate, scalp, and palmoplantar
reactions have been described (Fowler et al.
2019). Skin histology revealed an overlap of pso-
riasis and spongiosis features. Most cases
resolved with either topical steroids or discontinuation of dupilumab.
Eczematous dermatitis has also been reported
as a paradoxical reaction with Dupilumab,
although these tend to be localised/regional
affecting the periocular region, the face and neck
(de Wijs et al. 2020). The majority of patients
suffering from eczematous dermatitis were
being treated for pre-existing atopic dermatitis,
although Zhu et al. argued that the onset of facial
dermatitis was new and only came on after starting dupilumab (Zhu etal. 2019). Some are of the
opinion that this facial dermatitis may be a manifestation of undiagnosed allergic contact dermatitis although larger studies with biopsy and patch
test may be required to further dene this subset
of patients (de Wijs etal. 2020; Jaros etal. 2020).
Facial erythema (without dermatitis) affects
5–10% of patients, some of them diagnosed as
rosacea (Jaros et al. 2020). Alopecia has been
reported in 3.8% of the Dutch cohort (Ariëns
etal. 2020) and arthralgia in 1.8% of 108 patients
in Italy (Fargnoli etal. 2019; FDA 2019a).
lizumab 100mg) vs 3% (placebo) (Agache etal.
2020). Injection site reactions were also a prob-
lem for patients receiving 300mg mepolizumab
for the treatment for HES.Six per cent of patients
receiving 300mg of mepolizumab experienced
hypersensitivity reactions manifested by itch,
rashes, ushing, fatigue, hypertension, a warm
sensation in the trunk and neck, cold extremities,
dyspnoea, and stridor; half of which were on the
same day of dosing (Agache etal. 2020; Albers
etal. 2019).
Reslizumab and Benralizumab, however, have
had cases of anaphylaxis during their phase 3
clinical trials (FitzGerald etal. 2016; Castro etal.
2015). Although the incidence is low, 0.3% and
3% respectively, it has prompted a black box
warning advising in-ofce administration and
close monitoring thereafter (Agache etal. 2020).
3.6 Anti-IL-6 (Tocilizumab)
Tocilizumab is an IL-6 blocking agent approved
for use in rheumatoid arthritis, giant cell arteritis,
juvenile idiopathic arthritis (JIA), and treatment
of chimeric antigen receptor (CAR) T cellinduced severe or life-threatening cytokine
release syndrome.
3.5 Anti-IL-5 (Mepolizumab,
Reslizumab,
andBenralizumab)
IL5 is essential for the maturation, differentiation, and activation of eosinophils. Hence, anti IL5 mAbs are used to treat eosinophilic disorders,
namely eosinophilic asthma, eosinophilic granulomatosis with polyangiitis (EGPA), and hypereosinophilic syndrome (HES). Currently, there are
three licensed anti-IL5 mAbs: mepolizumab,
reslizumab, and benralizumab (Agache et al.
2020).
In their phase 3 clinical trials for patients with
eosinophilic asthma, there was no increase in signicant hypersensitivity reactions that were
reported compared to placebo, although more
injection site reactions were reported, 8% (mepo-
Hypersensitivity Reactions
ISRs have been reported in up to 10% of patients
with subcutaneous Tocilizumab, while infusion
reactions have been reported in about 7–8% when
given intravenously with symptoms including
hypertension, headache, rash, urticaria, and pruritis (Burmester etal. 2014). These events were
not treatment limiting (FDA 2019a).
Hypersensitivity reactions resulting in treat-
ment discontinuation have been reported in 0.1–
0.7% in clinical trials on rheumatoid arthritis. In
post-marketing surveillance, these hypersensitivity reactions, including anaphylaxis and death,
have occurred in patients treated with a range of
doses, with or without concomitant therapies and
in patients who received premedication. They
have also been reported as early as the rst infusion, although most commonly after the third or
fourth infusion. As such, it is recommended that
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intravenous use should only be infused by a
healthcare professional with appropriate medical
support to manage anaphylaxis (FDA 2019a).
In addition, few isolated reports of suspected
Drug Rash with Eosinophilia and Systemic
Symptoms (DRESS) or eosinophilia have
emerged (Zuelgaray etal. 2017; Massolino etal.
2018) with one unconrmed case of Stevens-
Johnson syndrome (Villiger etal. 2016) and one
case of acute generalised exanthematous pustulosis (Izquierdo etal. 2012).
O-Target Inammatory Cutaneous
Eruptions
At least eight cases of psoriasiform eruptions
have been reported with tocilizumab. Latency
was 10days to 84weeks and was independent of
underlying disease activity (Hayakawa et al.
2019). In some cases, psoriasiform eruption was
triggered upon withdrawal of tocilizumab, leading authors to suggest that a rebound in IL-6 may
result in downstream differentiation of Th17 cells
resulting in psoriasis (Saito etal. 2020). However,
reports also exist of developing psoriasiform
eruptions while on treatment for which the exact
mechanisms are unknown (Hayakawa et al.
2019). Of these cases, four required discontinua-
tion while four were successfully continued on
treatment with improvement of rash with topical
treatment. One patient had dose intensication
together with topical steroid therapy with resolution of rash (Hayakawa etal. 2019). Other reports
include palmoplantar pustulosis (Sparsa et al.
2014) and interstitial granulomatous dermatitis
(Altemir etal. 2020).
3.7 Interleukin 17 Inhibitors
Approved for use in psoriasis, psoriatic arthritis,
and ankylosing spondylitis, the three IL-17 inhibitors available are secukinumab, ixekizumab, and
brodalumab.
Hypersensitivity Reactions
Injection site reactions with anti-IL17 agents are
most seen with Ixekizumab (13–17%) compared
to Secukinumab (0.8–1.3%) and brodalumab
(0.5–1.4%) (Thomaidou and Ramot 2019; Gülsen
etal. 2020). Reports of anaphylaxis are rare but
have been reported with Secukinumab (FDA
2015). No denite cases of anaphylaxis were
reported in the landmark Ixekizumab trials but
were noted in post-marketing surveillance (FDA
2019b). Urticaria was reported in up to 8.8% of
patients in the Japanese Ixekizumab UNCOVER-J
substudy (Saeki etal. 2017).
O-Target Inammatory Cutaneous
Eruptions
Eczematous eruptions are the most reported paradoxical reaction with the IL-17 inhibitors with a
reported incidence of up to 12% in the Phase 3
UNCOVER-J study on ixekizumab and several
reports with secukinumab (Murphy etal. 2022).
There have yet to be reports of eczematous eruptions due to brodalumab which is the latest to be
approved (Murphy etal. 2022). These eczematous eruptions usually occur within 4months of
treatment with morphologies such as atopic dermatitis, eyelid dermatitis, and pompholyx
reported. About half of reported cases required
treatment discontinuation (Murphy etal. 2022).
As eczema is regarded as a Th2-mediated disease, proposed mechanisms include the compensatory increase in the Th2 pathway due to
downregulation of the Th1/Th17 pathway from
IL-17 inhibition (Eyerich etal. 2011).
At least 15 reports of paradoxical psoriasiform eruptions due to IL-17 inhibitors have been
reported (Murphy etal. 2022) with reported morphologies including pustular psoriasis and ares
of pre-existing psoriasis (Dogra et al. 2019).
Psoriasiform paradoxical reactions in the form of
palmoplantar pustulosis have also been reported
in three patients on brodalumab, all of them after
switching from secukinumab due to loss of therapeutic efcacy. It was hypothesised that patients
losing responsiveness to the therapeutic neutralisation of IL17A may become prone to paradoxical activation of neutrophils under IL-17RA
inhibition by brodalumab (Iznardo and Puig
2020).
Other less frequently reported cutaneous reactions with IL-17 inhibitors include sarcoidosislike granulomatous reactions, alopecia areata,
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pyoderma gangrenosum, lichenoid eruptions,
Bechet’s syndrome, hidradenitis suppurativa,
granuloma annulare, lupus-like, vitiligo, erythema multiforme, bullous pemphigoid, and
pemphigus (Murphy etal. 2022).
3.8 Anti IL12/23 Inhibitor
(Ustekinumab)
Ustekinumab inhibits the p40 subunit of IL-12
and IL-23 and is approved for use for psoriasis,
psoriatic arthritis, and inammatory bowel
disease.
Hypersensitivity Reactions
Injection site reactions are reported in about
1–3% of patients on ustekinumab (Thomaidou
and Ramot 2019; Gülsen et al. 2020).
Hypersensitivity reactions including anaphylaxis
and angioedema are rare but have been reported
(Ghosh etal. 2019). In a review on ustekinumab
safety in psoriasis, psoriatic arthritis, and Crohn’s
disease, no serious anaphylactic reactions or
serum sickness-like reactions to ustekinumab
were observed. However, two patients with
Crohn’s disease displayed signs and symptoms of
hypersensitivity including throat tightness, shortness of breath, and ushing after the rst and
only subcutaneous dose, while the second patient
developed chest discomfort, ushing, urticaria,
and fever after initial intravenous administration.
These cases prompted a caution in the FDA label
regarding the possibility of anaphylaxis. In those
cases, symptoms resolved within 1h following
oral corticosteroid and antihistamine treatment
(Ghosh etal. 2019).
O-Target Inammatory Cutaneous
Eruptions
Compared to the anti-TNFs and IL-17 inhibitors,
inammatory cutaneous eruptions have been less
frequently reported despite over a decade of clinical use. These include few of reports of vitiligo,
psoriasis, alopecia areata, eczematous eruptions,
granulomatous eruptions, bullous pemphigoid,
lupus-like reactions and morphoea, with single
reports of hidradenitis suppurativa, frontal bros-
ing alopecia, Well’s syndrome, erythema annulare centrifugum, and linear IgA bullous
dermatosis (Murphy etal. 2022).
Interestingly, ustekinumab has been reported
to be an effective treatment for anti-TNF-related
psoriasiform reactions with a response rate of
75–100% (Tillack et al. 2014; Mazloom et al.
2020).
3.9 Anti-IL23 Inhibitor
(Guselkumab)
As a relatively new biologic, reports on cutaneous adverse reactions to Guselkumab are currently lacking with two reports of an eczematous
eruptions (Truong etal. 2019; Reyn etal. 2019).
It has been postulated that inhibition of TNFα
can lead to an unopposed increase in IFN-a by
plasmacytoid dendritic cells, resulting in
psoriasiform- eczematous skin lesions. As IL-23
induces upregulation of TNF-a through TH17
cells, it has been suggested that guselkumab may
partially act as a TNFα inhibitor, resulting in
increased IFN-a production and an eczematous
skin reaction in predisposed individuals (Reyn
etal. 2019).
3.10 Anti-IgE (Omalizumab)
Omalizumab, a recombinant mAb with 95%
human protein fused with 5% mouse protein, targets free serum IgE, preventing its binding to
basophils and mast cells and with it, downstream
release of pro-inammatory mediators. The main
mechanism of omalizumab (Agache etal. 2021)
is a downregulation of IgE receptors on these
cells and rapid reduction of free levels of IgE,
thus blunting the allergic response. Omalizumab
has been approved for moderate to severe allergic
asthma and refractory chronic spontaneous urticaria (Agache etal. 2020, 2021).
Injection site reactions appear to be the most
common adverse reactions, accounting for 45%
of reports. Anaphylaxis has been reported in 0.1–
0.2% of patients on omalizumab, occurring early
in the treatment, usually within the rst
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K. J. L. Choo and Y. W. Yeo
3 injections (Shankar and Petrov 2013; Cox etal.
2007). The onset of symptoms is typically within
2h of injection. As a result, the FDA has a black
box warning (Cox etal. 2007) recommending inofce monitoring for 2h for the rst 3doses and
30min for subsequent ones. Delayed onset anaphylaxis cases have also been reported among
asthmatic patients receiving omalizumab with
symptoms starting 1-day post-injection (Agache
etal. 2021). Patients are recommended to be provided with and taught how to use adrenaline
autoinjector. A case-control study (Lieberman
etal. 2016) identied prior history of anaphylaxis
to drug, food, or idiopathic increased subsequent
risk of anaphylaxis association with omalizumab
use (OR 8.1; 95% CI, 2.7 to 24.3).
In some cases, skin tests (skin prick and intradermal tests) are positive suggestive of an IgEmediated hypersensitivity reaction.
Desensitisation with omalizumab has been
reported (Owens and Petrov 2012). Some authors
have proposed that the hypersensitivity reactions
may not be due to active drug itself but due to
additives such as polysorbate used to enhance
drug solubility (Bergmann et al. 2020; Perino
et al. 2018). Others have suggested that these
reactions could be a result of IgG antibodies
against omalizumab (Balbino et al. 2020).
However, a post-marketing surveillance study did
not show any correlation between anaphylaxis or
skin test reactivity to the presence of IgE antibody
to Omalizumab (Shankar and Petrov 2013).
4 Management
ofHypersensitivity
(Resuscitation Council 2008). Corticosteroids
(Choo et al. 2013) and antihistamines (H1 and
H2) (Sheikh et al. 2007), although helpful as
adjuncts, should not substitute the prompt administration of adrenaline (Shaker etal. 2020). The
patient should be positioned supine with their
lower limbs elevated. Large bore intravenous
access should be obtained, and isotonic crystalloid administered if hypotension or shock occurs.
Supplemental oxygen should be given to patients
with respiratory distress. Serum tryptase levels
measured within 30–120min of the anaphylactic
reactions, if elevated, carry a high positive predictive value (Buka etal. 2017).
hypersensitivity reactions with the following
medications (Picard and Galvão 2017):
1. Acetylsalicylic acid can be used for ushing.
2. Meperidine for chills and/or rigors.
3. Acetaminophen for fever.
4. Salbutamol or montelukast for bronchospasm.
4.2 Local/Injection Site Reactions
Most injection site reactions are mild and do not
necessitate treatment discontinuation. Reports
also suggest that at least in some patients, the
severity of ISRs may improve with continuation
of injections and only in severe cases does treatment need to be discontinued (Murdaca et al.
2013).
tions include the following (Thomaidou and
Ramot 2019):
Reactions toMonoclonal
Antibodies Biologic Agents
4.1 Acute Management
Once a hypersensitivity reaction has occurred,
the priority is to stabilise the patient by immediately stopping the infusion, followed swiftly by
an assessment of vital signs.
In the event of an anaphylactic shock, intramuscular doses of adrenaline should be administered and advanced cardiac life support initiated
1. Patient education and training on the correct
2. Ensuring the medication is at room tempera-
3. Appropriate choice of injection sites, rotating
4. Applying cold compresses to the injection site
5. Symptomatic treatment with oral antihista-
Symptomatic relief can be provided for milder
Measures that may reduce injection site reac-
injection technique.
ture prior to injection.
the sites.
afterwards.
mines, topical steroids, and oral analgesic
agents as required.
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4.3 O-Target Inammatory
Cutaneous Eruptions
Management of off-target inammatory cutaneous eruptions and paradoxical reactions remains
challenging and requires close collaboration with
the primary prescribing physician and the dermatologist. Several treatment algorithms have been
proposed, particularly for anti-TNF-induced psoriasis/psoriasiform eruption (Navarro and Daudén
2014; Li et al. 2019; Mazloom et al. 2020).
Factors that need to be considered include, rstly,
the severity of the reaction as assessed by body
surface area, disease-specic severity scores such
as Psoriasis Activity and Severity Index (PASI),
dermatological life quality index (DLQI), or
involvement of special sites such as palmoplantar
pustulosis. Secondly, the control of the underlying condition for which the biologic is indicated
and thirdly, if there are alternative biologic
classes that have been shown to be effective for
the underlying condition.
For example, if the psoriasiform reaction is
mild and the underlying condition is well controlled on the anti-TNF agent then consideration
may be given to either continue on (“treat
through”) or switch to an alternative anti-TNF
agent, bearing in mind that these paradoxical
reactions are a class effect. In moderate to severe
cases, consideration may be made to switch to a
biologic of a different class except in cases where
the primary condition is well controlled in conditions where anti-TNF therapy is currently preferred, such as in uveitis, and the anti-TNF agent
is deemed critical in disease control (Li et al.
2019).
In patients whom a “treat through” strategy is
employed, the efcacy of topical therapy alone
has been reported to be between 28% and 63.5%
in various cohorts (Mazloom et al. 2020). In
moderate to severe cases, the addition of traditional systemic agents such as methotrexate,
cyclosporine, acitretin, or phototherapy has been
reported to be effective in a subset of patients (Li
etal. 2019; Mazloom etal. 2020).
Despite this, reports on paradoxical psoriasiform lesions have suggested that 41–50% of
patients required treatment discontinuation.
Discontinuation resulted in psoriasis resolution
(47.7%) more often than switching to another
anti-TNF agent (36.7%), or continuing (32.9%)
TNF-alpha therapy (Brown etal. 2017), supporting the consideration of switching biologic class
in moderate to severe paradoxical reactions
where alternatives are available. Furthermore,
rechallenge with an anti-TNF agent has been
associated with a 50% recurrence rate of paradoxical psoriasis (Mazloom etal. 2020). Several
studies have shown benet in switching to other
non-TNF biologics. Reports have shown promising results with the use of ustekinumab in the
management of paradoxical psoriasis due to antiTNFs with response rates up to 75–100% (Tillack
etal. 2014; Mazloom etal. 2020).
While most patients experience resolution of
paradoxical psoriasiform eruptions, up to 46% of
patients may experience improvement but incomplete resolution of psoriasis despite discontinuation. Those with more severe reactions such as
generalised pustular psoriasis may also be more
likely to have persistent disease despite discontinuation with only 27.3% experiencing resolution in the systematic review by Brown et al.
(2017). Thus, it is important to counsel patients
regarding the possibility of persistent skin
disease.
4.4 Diagnostic Evaluation
ofHypersensitivity Reactions
The rst question to address in the diagnostic
evaluation of mAbs hypersensitivity reaction,
like any drug hypersensitivity reaction, is whether
the benet of continuing the mAbs outweighs the
risk of harm of testing. If a safe and equally efcacious alternative treatment is available, the best
solution would be to switch out of the culprit
mAb. To date, there is a lack of data on the extent
of cross reactivity between mAbs of the same
class. Extrapolating from other drugs, one could
logically speculate some degree of cross reactivity in mAbs that share similar chemical structures
or similar target specicity.
However, if both patient and clinician are keen
to pursue diagnostic evaluation of a mAbs hyper-
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Table 2 Brown grading system of the severity of hypersensitivity reactions
Brown
classication
Severity
grading Description
1 Mild reactions: symptoms and signs
limited to the skin, e.g. urticaria,
angioedema, ushing, pruritus
2 Moderate reactions: symptoms and
signs that involve the respiratory,
gastrointestinal, and cardiovascular
system without hypotension, e.g.
dyspnoea, wheezing, cough, chest
tightness, presyncope, abdominal pain,
nausea, vomiting, diarrhoea
3 Severe impairment of cardiovascular or
neurologic system, e.g. hypotension,
collapse, hypoxia, cyanosis, seizure,
confusion, syncope
sensitivity reaction, then the goal of such evaluations is threefold: to determine its main
mechanism of action, the severity of the index
reaction, and the culprit drug.
The Brown classication system (Brown
2004) has been utilised in grading the severity of
hypersensitivity reactions (see Table2).
Drug causality may be deduced from a detailed
clinical history from the patient and/or observers
as well as scrutiny of his/her drug chart. In some
cases, it is straightforward with only one mAbs
administered. In cases where multiple mAbs are
given in succession, skin tests may be helpful to
identify the culprit agent. However, there are several limitations to skin tests (Brown etal. 2017)
namely:
1. Immediate reading of skin prick and intrader-
mal tests are useful only in type I IgEmediated reactions.
2. To date, mAbs skin tests are not fully vali-
dated and their sensitivity, specicity, negative and positive predictive values are
extrapolated from small cohort studies.
3. Data on non-irritating concentration for skin
tests have not been determined for all mAbs.
4. As small aliquots of mAbs are not available,
the entire dose/vial may need to be used, making testing prohibitively expensive.
Table 3 Published non-irritating concentration for skin
tests
Monoclonal
antibodies SPT IDT
Adalimumab 40mg/ml (neat) 0.4mg/ml (1/100
dilution)
Etanercept 50mg/ml (neat) or
25mg/ml (1:2)
Iniximab 10mg/ml (neat) 1mg/ml (1/10
Omalizumab 125mg/ml (neat) or
0.00125mg/ml
(1/100,000
a
dilution)
Rituximab 10mg/ml (neat) 1mg/ml (1/10
Tocilizumab 20mg/ml (neat) 20mg/ml (neat)
a
Based on ENDA/EAACI Drug Allergy Interest Group
position paper (Brockow etal. 2013), with permission
0.5mg/ml (1/100
a
dilution)
dilution) or
10mg/ml (neat)
0.00125mg/ml
(1/100,000
dilution)
dilution), 10mg/
ml (neat)
a
A positive skin test at non-irritating concentrations of mAbs (see Table3) strongly suggests
type I IgE-mediated hypersensitivity reactions
(Picard and Galvão 2017). As re-exposure carries
the risk of anaphylaxis, it should only be carried
out via the process of desensitisation.
For non-IgE-mediated reactions, the method
of re-exposure should be based on the severity of
the index hypersensitivity reactions (Fouda and
Bavbek 2020). Patients with mild (Brown’s class
I) reactions may attempt a challenge test with the
culprit mAbs. Re-exposure for severe (Brown’s
class III) non-IgE-mediated reactions should
only be performed via the desensitisation protocol. In patients with moderate severity reactions,
the decision to challenge vs desensitise could be
made on a case-by-case basis, considering the
risk of provoking a recurrent reaction and its
impact on the patient.
4.5 Desensitisation
The best reported desensitisation protocol for
mAbs is the 12 steps protocol developed at
Brigham and Women’s Hospital (see Table 4)
(Brennan etal. 2009; Castells etal. 2008; Isabwe
et al. 2017). It should only be performed by
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Table 4 Example of an iniximab desensitisation protocol (12step/3bag) protocol (taken from Picard and Galvao
etal.) (Picard and Galvão 2017), with permission
Drug: iniximab
Target dose: 400mg
Volume (ml)
Bag
Solution 1250 0.016 9.25 0.148
Solution 2250 0.16 18.75 3
Solution 3250 1.587 250 396.75
per bag
Concentration (mg/
ml) per bag
Amount (ml) of
bag infused
Dose infused
(mg) per bag
297
Step Solution Rate (ml/h) Time (min) Volume infused
(ml)
1 1 2 15 0.5 0.008 0.008
2 1 5 15 1.25 0.02 0.028
3 1 10 15 2.5 0.02 0068
4 1 20 15 5 0.08 0.148
5 2 5 15 1.25 0.20 0.348
6 2 10 15 2.5 0.40 0.748
7 2 20 15 5 0.80 1.548
8 2 40 15 10 1.6 3.148
9 3 10 15 2.5 3.969 7.117
10 3 20 15 5 7.937 15.054
11 3 40 15 10 15.874 30.928
12 3 80 174.4 232.5 369.072 400
Total time (h)=5.7h
trained clinicians and a facility equipped to treat
anaphylactic patients. About 30% of patients suffer breakthrough reactions, usually during the
last step, and these are generally mild (Makowska
the step when breakthrough reactions occur and
limiting the nal infusion rates to 40–60ml/h and
using a 4bag/16step desensitisation protocol in
patients with very low threshold.
Dose infused
(mg) per step
Cumulative
dose (mg)
and Lewandowska-Polak 2020). When a breakthrough reaction occurs, the infusion should be
halted, and the patient’s symptoms treated.
4.6 Challenge
Depending on the symptoms, H1 and H2 antihistamines, inhaled beta agonists, intravenous uids, montelukast, and corticosteroids could be
used. Intramuscular adrenaline should be available on site and used if indicated, although this
happens rarely (Brennan etal. 2009). Once the
symptoms resolve, the infusion is resumed where
it is stopped and most patient are able to com-
There is no standardised protocol for mAbs challenge test. One review suggests starting the mAb
infusion at one-tenth of the target infusion rate
for 15min and if tolerated, to increase the rate to
its target according to the manufacturer’s instructions or regular infusion protocol (Picard and
Galvão 2017).
plete the protocol. Premedications can be considered in patients requiring subsequent
desensitisation if they experience breakthrough
4.7 Premedication
reaction with it before. Other interventions that
could prevent breakthrough reactions include coadministration of normal saline at rates between
100 and 250ml/h in parallel to the desensitisation
protocol, adding an intermediate step just before
Premedication, typically administered 30–60min
prior, can be used as an adjunct to desensitisation
and should be tailored to the patient’s index or
breakthrough reactions (Chung 2008). H1 and
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K. J. L. Choo and Y. W. Yeo
H2 antihistamines are given for cutaneous symptoms, montelukast for respiratory bronchospasm,
paracetamol, corticosteroid, and nonsteroidal
anti-inammatory drugs to prevent fever, and
aspirin to prevent ushing (Chung 2008). A
short-acting benzodiazepam such as lorazepam
can be prescribed to alleviate anxiety associated
with desensitisation.
5 Conclusion
The use of mAbs has increased exponentially,
covering a myriad of indications. This is likely to
continue to grow in the future. While these drugs
have given hope to many patients with previously
intractable diseases, like all medications, they
come with potential adverse reactions which is
important for medical practitioners to be aware of
and familiar with. While more varied types of
mAbs are being discovered with a variety of
modes of action, they share certain common
characteristics and knowledge of rst principles
can help to predict and prepare for potential
adverse reactions for improved patient
outcomes.
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