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Y.-T. Cho and C.-Y. Chu
ab
c
d
Fig. 2 Clinical features of FDE and GBFDE. Patients
with FDE can present with (a) a solitary lesion consisting
of a well-dened, oval-shaped, red-to-purple patch and
can also present with (b) several discrete well-demarcated
etal. 2019). In another study, the drug naproxen
was demonstrated to be highly and signicantly
associated with FDE on the lips (Ozkaya-Bayazit
2003). However, it should be noted that such
associations might differ in different countries or
different clinical settings.
dusky-red patches. Patients with GBFDE usually present
with multiple variously sized, well-dened erythematous
or hyperpigmented patches with blisters or erosions on the
whole body (c, d)
Patients with GBFDE tend to be older than
those with FDE and SJS/TEN (Paulmann and
Mockenhaupt 2015; Cho et al. 2014). Such
patients usually present with large areas of welldemarcated red-to-purple or hyperpigmented
patches with various extents of blisters or erosions
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147
on the whole body (Fig.2c, d). Sometimes, it is
difcult to differentiate GBFDE from SJS/TEN
based solely on cutaneous presentations. Mucosal
lesions can also be found in 40–50% of GBFDE
patients (Cho et al. 2014). As in FDE, the time
interval between the intake of drugs and the development of lesions in GBFDE is short, with a mean
value of 3days (Cho etal. 2014). There is a lack
of consensus regarding the denition of
GBFDE. Our group has proposed that GBFDE
might be dened as a condition characterized by
widespread blisters and erosions with typical
FDE lesions involving at least 10% of the body
surface area and distributed on at least 3 of 6 different anatomical sites, including the head and
neck, front of the trunk, back, upper extremities,
lower extremities, and genitalia (Cho etal. 2014).
On the other hand, Lipowicz etal. have proposed
that, in order to make a diagnosis of GBFDE, 2 or
3 out of the following criteria should be fullled
(Lipowicz etal. 2013). These criteria include (1)
similar reaction in the past; (2) fewer than two
mucous membranes involved, with the absence of
spots or target lesions; (3) large and welldemarcated blisters and erosions; and (4) lesions
and erosions on at least two different sites of the
body. Although these two denitions are not
exactly the same, suchcriteria may beuseful in
distinguishing GBFDE from localized forms of
FDE and SJS/TEN.
4.2 Dierential Diagnosis
The differential diagnoses of FDE are many and
is dependent on the presentation of FDE
(Paulmann and Mockenhaupt 2015; Shiohara
2009). For a solitary FDE lesion or a limited
number of FDE lesions, differential diagnoses
include contact dermatitis, insect bite reaction,
trauma, lichen planus pigmentosus, urticaria pigmentosa, autoimmune progesterone dermatitis,
and erythema multiforme. For GBFDE, the differential diagnoses include SJS, TEN, burns,
graft-versus-host disease, bullous pemphigoid,
and staphylococcal scalded skin syndrome.
Among these differential diagnoses, distin-
guishing GBFDE from SJS/TEN can be chal-
lenging(Paulmann and Mockenhaupt 2015). The
lesions of FDE or GBFDE usually do not present
with target lesions or spots, which are more frequently seen in SJS/TEN and erythema multiforme (Paulmann and Mockenhaupt 2015;
Lipowicz etal. 2013). In addition to clinical presentations, a histopathological examination may
help to differentiate FDE from other differential
diagnoses.
4.3 Culprit Drugs
The causative medications of FDE and GBFDE
vary among countries due todifferent prescription
patternsand causality is also likely to evolve with
time (Sehgal and Sirvastava 2006; Savin 2001).
Although many medications have been implicated
(Table 1), nonsteroidal anti- inammatory drugs
(NSAIDs), acetaminophen, and antibiotics are the
most commonly reported culprit drugs. NSAIDs
have been reported as the leading causative drugs
in reports from Taiwan (Cho etal. 2014; Lee etal.
2012), Singapore (Heng etal. 2015), Korea (Jung
et al. 2014), and Tunisia (Fadhel et al. 2019).
Meanwhile, acetaminophen was identied as the
most common culprit drug in one report from
Table 1 List of reported triggers of FDE (Kauppinen and
Stubb 1985; Ozkaya 2008; Lipowicz et al. 2013; Cho
et al. 2014; Lee et al. 2012; Heng et al. 2015; Brahimi
etal. 2010; Savin 2001)
Nonsteroidal anti-inammatory drugs
Paracetamol
Co-trimoxazole
Tetracyclines
Penicillins
Metronidazole
Rifampicin
Erythromycin
Carbocisteine
Pseudoephedrine
Phenolphthalein
Barbiturates
Carbamazepine
Sulfasalazine
Calcium-channel blockers
Angiotensin-converting enzyme inhibitors
Iodinated contrast
Omeprazole
Complementary medicines
a
Most commonly reported drugs
a
a
a
a
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Y.-T. Cho and C.-Y. Chu
France (Brahimi etal. 2010), whereas the antibiotic co- trimoxazole (a combination of sulfamethoxazole and trimethoprim) was the
top-ranked offender for FDE in reports from India
(Sharma etal. 1996), Bangladesh (Rahman 2014),
Pakistan (Mahboob and Haroon 1998), Iran
(Kavoussi et al. 2015), and Turkey (OzkayaBayazit 2003). There is no difference in culprit
drugs between FDE and GBFDE.
a b
c d
4.4 Prognosis
The prognosis of FDE is generally good. Once the
causative drug is suspended, the lesions are usually
self-limiting and will resolve gradually.
Nevertheless, with each repeated exposure, the
number of lesions may increase (Paulmann and
Mockenhaupt 2015). As shown in Fig.3, a patient
with GBFDE presented with widespread red-to-
Fig. 3 Progression of GBFDE after repeated exposure to
the culprit drug. One patient with GBFDE presented with
widespread red-to-purple patches involving the trunk and
buttocks (a, c, e). These lesions recurred and progressed to
become blisters and erosions after reexposure to the culprit drug (b, d, f)
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149
purple patches with erosions (Fig. 3a, c, e). The
area of detachment markedly enlarged the next
timethe FDE recurred(Fig. 3b, d, f). The prognosis
of GBFDE is thought to be better than that of SJS/
TEN by most physicians. However, Lipowics etal.
found in a case-control study of 58 GBFDE patients
matched by age and extent of skin detachment to
170 patients with SJS/TEN that the mortality rate
was slightly but not signicantly lower for patients
with GBFDE (odds ratio 0.6, 95% condence
interval 0.30–1.4) (Lipowicz et al. 2013). Their
results put into question the general belief that
theprognosis ofGBFDE is better thanSJS/TEN.It
is possible that this was due to the fact that the
extent of skin lesions is a severity marker (Pfutze
et al. 2007). Another possible explanation is that
patients with GBFDE are older than those with
SJS/TEN, which may result in greater disease
andtreatment-related morbidity and mortality.
5 Investigations
Conrming the culprit drug is one of the cornerstones of care, as correct identication can prevent recurrences. Oral challenge or provocation
is by far the gold standard to conrm the causative medication (Shiohara 2009). While there is
no standardized method for performing the oral
challenge in patients with FDE, a sub-therapeutic
dose of the suspect drug, such as a dose one-tenth
the size of the therapeutic dose (Shiohara 2009),
or even a full dose of the drug (Phillips et al.
2019), is usually used and is relatively safe in
most of the cases. Besides the dosage, there is
also a lack of standardized protocol with respect
to the timing of the oral provocation. However,
performing the challenge 1–2 months after the
remission of the eruptions is suggested by most
experts (Phillips etal. 2019; Shiohara 2009).
In addition to systemic provocation tests,
patch testing is also a reliable method for determining the possible culprits in patients with
FDE, especially in those patients with multiple
suspected drugs. A positive patch test result can
be obtained in around 40% of the patients
(Phillips et al. 2019; Andrade et al. 2011). In
brief, suspected drugsaremixed in petrolatum or
vehicles with a concentration of 20% (Brockow
etal. 2002) or 30% (Barbaud etal. 2001). Drug
patch tests should be performed at the sites of
previous FDE lesions rather than on the normal
skin on the back. The best timing for performing
a patch test has yet to be determined, however, a
delay of at least 4–6weeks after the resolution of
the lesions is suggested by most experts in order
to avoid false positive reactions, false-negative
reactions, and the aggravation of the disease
(Phillips etal. 2019). Severalfactors may contribute to a false negative drug patch test result.
Firstly, theoptimal concentration and penetration ability of the patch-tested drug is
unclear.Secondly, patients may react to metabolites of the causative drugs rather than to the
drugs per se. As such the use of a drug patch test
without its metabolites may yield a negative
result (Andrade etal. 2011).
Although lymphocyte transformation test
(LTT) is used to determine drug causality in
many different drug eruptions, including SJS/
TEN, drug reaction with eosinophilia and systemic symptoms (DRESS), maculopapular
eruptions (MPE), and acute generalized exanthematous pustulosis (AGEP) (Pichler and
Tilch 2004), its role in FDE is not yet established (Phillips etal. 2019; Shiohara 2009).
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Y.-T. Cho and C.-Y. Chu
6 Management
There is no consensus regarding the management
of patients with FDE and GBFDE.However, as
with other drug eruptions, the removal of the culprit drugs is the most important step (Paulmann
and Mockenhaupt 2015). In most cases of FDE,
the cutaneous lesionsrapidlyimprove after withdrawal ofthe causative drug. Although there is
still insufcient evidence, some patients may
benet from topical or systemic corticosteroids.
One study from a tertiary hospital in Korea
reported that around 40% of the patients received
no medical treatment, around 43% applied topical corticosteroids, and around 11% received systemic corticosteroids (Jung etal. 2014). All of the
patients in the study recovered well from the
disease.
Patients with GBFDE usually improve after
the discontinuation of the culprits, just like FDE
(Paulmann and Mockenhaupt 2015; Lipowicz
etal. 2013; Cho etal. 2014). However, for patients
with extensive skin detachment, comprehensive
supportive care in a reference center is suggested.
As with SJS/TEN, patients with GBFDE should
be monitored for disease progression, wound
infections, electrolyte imbalance, and possible
deterioration of internal organ function. Mucosal
lesions should also be managed since involvement
of the lips and genitalia is common. Pain control,
the avoidance of trauma and irritation of the
mucosal surfaces are vital in the care of these
patients. In severe mucosal lesions, parenteral
nutrient supplementation and urine catheterization might be needed. Systemic corticosteroids
may be benecial in the management of patients
with GBFDE.According to our own unpublished
data regarding 36 patients with GBFDE, all of
them received systemic corticosteroid treatment,
and there was only 1 mortality during the acute
stage of the disease. Nevertheless, the evidence
remains anecdotal and further investigations are
needed to evaluate the role of systemic corticosteroids in the management of patients with GBFDE.
References
Andrade P, Brinca A, Goncalo M.Patch testing in xed
drug eruptions—a 20-year review. Contact Dermat.
2011;65:195–201.
Barbaud A, Goncalo M, Bruynzeel D, Bircher A,
European Society of Contact Dermatitis. Guidelines
for performing skin tests with drugs in the investigation of cutaneous adverse drug reactions. Contact
Dermat. 2001;45:321–8.
Bourns DC. Unusual effects of antipyrine. Br Med J.
1889;2:818–20.
Brahimi N, Routier E, Raison-Peyron N, Tronquoy AF,
Pouget-Jasson C, Amarger S, et al. A three-yearanalysis of xed drug eruptions in hospital settings in
France. Eur J Dermatol. 2010;20:461–4.
Brockow K, Romano A, Blanca M, Ring J, Pichler W,
Demoly P. General considerations for skin test procedures in the diagnosis of drug hypersensitivity.
Allergy. 2002;57:45–51.
Brocq L. Eruption erythemato-pigmentee xe due
a l’antipyrine. Ann Dermatol Syphiligr (Paris).
1894;5:308–13.
Cho YT, Lin JW, Chen YC, Chang CY, Hsiao CH, Chung
WH, etal. Generalized bullous xed drug eruption is
distinct from Stevens–Johnson syndrome/toxic epidermal necrolysis by immunohistopathological features. J
Am Acad Dermatol. 2014;70:539–48.
Fadhel NB, Chaabane A, Ammar H, Romdhane HB, Soua
Y, Chadli Z, etal. Clinical features, culprit drugs, and
allergology workup in 41 cases of xed drug eruption. Contact Dermat. 2019;81(5):336–40. https://doi.
org/10.1111/cod/13351.
Heng YK, Yew YW, Lim DSY, Lim YL.An update of xed
drug eruptions in Singapore. J Eur Acad Dermatol
Venereol. 2015;29:1539–44.
Jung JW, Cho SH, Kim KH, Min KU, Kang HR.Clinical
features of xed drug eruption at a tertiary hospital in
Korea. Allergy Asthma Immunol Res. 2014;6:415–20.
Kauppinen K, Stubb S.Fixed eruptions: causative drugs
and challenge tests. Br J Dermatol. 1985;112:575–8.
Kavoussi H, Rezaei M, Derakhshandeh K, Moradi A,
Ebrahimi A, Rashidian H, et al. Clinical features
and drug characteristics of patients with generalized
xed drug eruption in the west of Iran (2005–2014).
Dermatol Res Pract. 2015;2015:236703.
Lee AY.Fixed drug eruptions. Incidence, recognition, and
avoidance. Am J Clin Dermatol. 2000;1:277–85.
Lee CH, Chen YC, Cho YT, Chang CY, Chu CY.Fixed
drug eruption: a retrospective study in a single
referral center in Northern Taiwan. Dermatol Sin.
2012;30:11–5.
Lipowicz S, Sekula P, Ingen-Housz-Oro S, Liss Y,
Sassolas B, Dunant A, etal. Prognosis of generalized
Fixed Drug Eruptions andGeneralized Bullous Fixed Drug Eruptions
https://t.me/medicina_free
151
bullous xed drug eruption: comparison with Stevens–
Johnson syndrome and toxic epidermal necrolysis. Br
J Dermatol. 2013;168:726–32.
Mahboob A, Haroon TS. Drugs causing fixed erup-
tions: a study of 450 cases. Int J Dermatol. 1998;37:
833–8.
Masopust D, Vezys V, Marzo AL, Lwfrancois
L.Preferential localization of effector memory cells in
nonlymphoid tissue. Science. 2001;291:2413–7.
Mizukawa Y, Yamazaki Y, Teraki Y, Hayakawa J,
Hayakawa K, Nuriya H, et al. Direct evidence for
interferon gamma production by effector-memory-
type intraepidermal T cells residing at an effector site
of immunopathology in xed drug eruption. Am J
Pathol. 2002;161:1337–47.
Ozkaya E.Fixed drug eruption: state of the art. J Dtsch
Dermatol Ges. 2008;6:181–8.
Ozkaya-Bayazit E.Specic site involvement in xed drug
eruption. J Am Acad Dermatol. 2003;49:1003–7.
Paulmann M, Mockenhaupt M.Severe drug-induced skin
reactions: clinical features, diagnosis, etiology, and
therapy. J Dtsch Dermatol Ges. 2015;13:625–45.
Pfutze M, Niedermeier A, Hertl M, Eming R.Introducing
a novel autoimmune bullous skin disorder inten-
sity score (ABSIS) in pemphigus. Eur J Dermatol.
2007;17:4–11.
Phillips EJ, Bigliardi P, Bircher AJ, Broyles A, Chang
YS, Chung WH, etal. Controversies in drug allergy:
testing for delayed reactions. J Allery Clin Immunol.
2019;143:66–73.
Pichler WJ, Tilch J. The lymphocyte transformation test
in the diagnosis of drug hypersensitivity. Allergy.
2004;59:809–20.
Rahman MH.Fixed drug eruption in Bangladeshi popu-
lation: conrmed by provocative test. Int J Dermatol.
2014;53:255–8.
Sallusto F, Lenig D, Forster R, Lipp M, Lanzavecchia
A. Two subsets of memory T lymphocytes with
distinct homing potentials and effector functions.
Nature. 1999;401:708–12.
Savin JA. Current causes of xed drug eruption in the
UK.Br J Dermatol. 2001;145:667–8.
Sehgal VN, Sirvastava G. Fixed drug eruption (FDE):
changing scenario of incriminating drugs. Int J
Dermatol. 2006;45:897–908.
Sharma VK, Dhar S, Gill AN. Drug related involvement
of specic sites in xed eruptions: a statistical evaluation. J Dermatol. 1996;23:530–4.
Shiohara T.Fixed drug eruption: pathogenesis and diagnostic
tests. Curr Opin Allergy Clin Immnol. 2009;9:316–21.
Shiohara T, Mizukawa Y. Fixed drug eruption: a disease
mediated by self-inicted responses of intraepidermal
T cells. Eur J Dermatol. 2007;17:201–8.
Shiohara T, Mizukawa Y, Teraki Y. Pathophysiology of
xed drug eruption: the role of skin-resident T cells.
Curr Opin Allergy Clin Immunol. 2002;2:317–23.
Teraki Y, Moriya N, Shiohara T. Drug-induced expres-
sion of intercellular adhesion molecule-1 on lesional
keratinocytes in xed drug eruption. Am J Pathol.
1994;145:550–60.
Lichenoid Drug Eruptions
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YeeKiatHeng andYenLooLim
1 Introduction
Lichenoid disorders are inammatory dermatoses
characterised clinically by at-topped, pruritic,
papular lesions and histologically by a band-like
inltrate of lymphocytes in the papillary dermis.
Lichen planus (LP) is the most typical and wellrecognised of the lichenoid dermatoses and presents with rm, shiny, polygonal, 1–3mm papules
with a red to violaceous colour and overlying ne
white lines known as Wickham’s striae. Greybrown pigmented macules may result upon resolution of primary lesions. On mucosal surfaces,
Wickham’s striae are also often seen (Tziotzios
etal. 2018; Shiohara and Mizukawa 2018).
LP-like or lichenoid drug eruptions (LDE)
may be difcult to distinguish clinically and histologically from classic LP (Tziotzios etal. 2018;
Shiohara and Mizukawa 2018; Ardern-Jones and
Lee 2016). Identication of a drug cause may be
difcult as the latency period between drug
administration and onset of rash is variable and
may be prolonged, up to several months or even
years (Halevy and Shai 1993). Furthermore, resolution of the rash after discontinuation of the
causative drug may take weeks to months (Halevy
and Shai 1993), adding to the uncertainty of the
diagnosis. Causality may be conrmed by re-
Y. K. Heng (*) · Y. L. Lim
National Skin Centre, Singapore, Singapore
e-mail: ykheng@nsc.com.sg; yllim@nsc.com.sg
exposure to the drug, but may not be acceptable
to the patient.
2 Epidemiology
LDE is generally uncommon though specic
reports on incidence rates are lacking. In fact, most
epidemiological studies on cutaneous adverse
drug reactions (CADRs) do not mention LDE.One
study reported that LDE accounted for only 4% of
all CADRs in a tertiary hospital in India (Qayoom
etal. 2015). Approximately 10% of all LP cases
are drug induced (Ardern-Jones and Lee 2016).
Age of presentation does not differ much
between LDE and LP, reportedly ranging from 44
to 66years for LDE (Halevy and Shai 1993; Lage
etal. 2012; Fessa etal. 2012; West etal. 1990)
and 47 to 50 years for LP (Lage et al. 2012).
Paediatric LDE is rare (Payette etal. 2015) but
may result from childhood vaccinations. There is
reportedly no gender bias (Tziotzios etal. 2018).
3 Description ofFeatures
Clinical and histological features which distinguish LDE from LP are summarised in Table1.
LDE tends to present with LP-like lesions
(Fig. 1) which are more generalised, polymorphous, lack Wickham’s striae and have a more
eczematous or psoriasiform appearance (Fig.2).
© Springer Nature Switzerland AG 2022
H. Y. Lee, D. Creamer (eds.), Drug Eruptions, Updates in Clinical Dermatology,
https://doi.org/10.1007/978-3-031-09388-3_12
153
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Table 1 Clinical and histological differences between
lichen planus and lichenoid drug eruption
Classical
Lichenoid drug
–
Clinical
Mean age of
onset
Latency period Months–years Not relevant
Distribution More generalised,
Morphology Similar to LP but
Wickham striae Less common Common
Photodistribution Common Uncommon
Mucous
membranes
Nail involvement Rare Common
Histological
– Focal
– Numerous
– Cytoid bodies in
– Varying degree of
– Deep perivascular
Adapted from references (Tziotzios etal. 2018; Shiohara
and Mizukawa 2018; Lage etal. 2012)
eruption
65years 50years
including trunk
Symmetric
with more
‘eczematous’ or
‘psoriasiform’
features
Usually spared Common
parakeratosis and
focal interruption
of the granular
layer
clusters of
apoptotic
keratinocytes
cornied,
granular and
upper spinous
layers
eosinophilic and/
or plasma cell
inltrates
inltrate may be
present
idiopathic lichen
planus
Predilection for
wrists, exor
areas of
forearms, lower
legs, genitalia
Shiny, attopped,
polygonal
violaceous
papules
Parakeratosis
uncommon
Few clusters of
apoptotic
keratinocytes
Cytoid bodies in
lower spinous
layers
Eosinophils and
plasma cells
uncommon
Dense band-like
inltrate of
lymphocytes in
papillary dermis
Y. K. Heng and Y. L. Lim
Fig. 1 Lichen planus-like papules and plaques on the
dorsal hand and forearm
Fig. 2 Lichenoid drug eruption with a more polymorphous appearance with mixture of LP-like and eczematous papules and plaques
Photodistribution is more common in LDE and
may be a useful diagnostic clue (Shiohara and
Mizukawa 2018). Mucosal involvement (Fig.3)
is less common in LDE than in LP (Shiohara and
Mizukawa 2018).
Differential diagnoses to consider include
LP-like contact dermatitis [e.g. to methacrylic acid
esters (Kawamura etal. 1996) and dimethyl fumarates (Guillet et al. 2009)], lichenoid keratosis
(Pitney et al. 2016), paraneoplastic pemphigus
(Tey and Tang 2009; Lim etal. 2018) drug-induced
subacute cutaneous lupus (Crowson and Magro
1999), dermatomyositis (Al-Najjar et al. 1985),
graft-versus-host disease (Hymes etal. 2006) and
secondary syphilis (Tang etal. 2004).
Lichenoid Drug Eruptions
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Fig. 3 White plaques with lace-like pattern and erosions
on the buccal mucosa
4 Drug Causality
155
1981), chloroquine (Savage 1958)] were well-
recognised to cause LDE but have become less
commonly used.
Relatively new drugs which affect the immune
system have now been reported to cause
LDE.These include vaccines, for example, hepatitis B (Saywell et al. 1997; Rebora et al. 1999;
Ferrando et al. 1998; Calista and Morri 2004;
Schupp and Vente 1999; Limas and Limas 2002;
Al-Khenaizan 2001) and human papillomavirus
vaccines (Laschinger etal. 2015), interferon (IFN)
therapy (Bush etal. 2017) and anti-HIV therapy
[e.g. efavirenz (Baumrin et al. 2018), tenofovir
(Gupta et al. 2015)]. In recent years, biological
therapies [e.g. tumour necrosis factor [TNF] inhibitors (Inoue et al. 2017; El Habr et al. 2014; De
Simone etal. 2008; Darrigade etal. 2016; Andrade
etal. 2015; Utsu etal. 2012; Gonzalez etal. 2018)],
targeted oncological drugs [e.g. imatinib
(Sendagorta etal. 2009; Gómez Fernández etal.
2010; Sudha etal. 2011; Ena etal. 2004; Dalmau
et al. 2006; Pascual et al. 2006; Lim and Muir
2002; Kawakami etal. 2009; Kuraishi etal. 2010)]
and immune checkpoint inhibitors (Hwang etal.
2016; Cogen et al. 2018; Min Lee et al. 2018;
Coleman etal. 2019; Curry et al. 2017; Shi etal.
2016; Obara etal. 2018; Biolo etal. 2019; Siegel
etal. 2018; Coscarart etal. 2019) have featured as
new and emerging causes of LDE.
Arsenic was the rst drug reported to cause LDE
in 1929 (Almeyda and Levantine 1971). Since
then, LDE has been reported to a long and growing list of drugs (Table2). Many commonly used
drugs, for example, beta-blockers, thiazide
diuretics, angiotensin-converting enzyme inhibitors and non-steroidal anti-inammatory drugs
(NSAIDs), are now recognised to cause
LDE. Drugs which have been recognised to be
associated with LDE at certain anatomical locations, for example, sun-exposed areas or mucosa,
are listed in Table3.
Older drugs such as gold (Penneys et al. 1974,
Glenert 1984, Russell et al. 1997), penicillamine
(Seehafer et al. 1981) and anti- malarials [e.g.
quinine (Dawson 1986), quinacrine (Bauer
4.1 Biologics
While TNF-inhibitors have well-known clinical
efcacy in treating inammatory conditions, it is
now recognised that they may cause paradoxical
inammatory skin reactions (e.g. psoriasis).
Numerous cases of LDE due to anti-TNFs have
been reported (Inoue etal. 2017; El Habr etal.
2014; De Simone et al. 2008; Darrigade et al.
2016; Andrade et al. 2015; Utsu et al. 2012;
Gonzalez et al. 2018). Interestingly, LDE has
been reported to develop in a patient after switching from iniximab to its biosimilar, suggesting
possibly different immunogenicity of the biosimilar drug (Gonzalez etal. 2018). Change in therapeutic class of biologics may still re-elicit the
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Table 2 Drugs implicated in lichenoid drug eruptions
Drugs implicated in lichenoid drug eruptions
Well-recognised causes Less well-recognised causes Newer drugs
Anti-malarials [e.g. quinine
(Dawson 1986), quinacrine (Bauer
1981), chloroquine (Savage 1958)]
Golda (Penneys et al. 1974; Glenert
1984; Russell etal. 1997)
Penicillamine (Seehafer etal.
1981)
Beta-blockers [e.g. labetalol (Fessa
etal. 2012; Gange and Jones 1978),
propranolol (Massa etal. 1991)]
Thiazide diuretics (Harber etal.
1959)
NSAIDs [e.g. naproxen (Güneş
etal. 2006), acetylsalicylic acid
(Ruiz Villaverde etal. 2003),
ibuprofen (Hamburger and Potts
1983), indomethacin (Hamburger
and Potts 1983)]
ACE inhibitors [e.g. captopril (West
etal. 1990; Firth and Reade 1989),
enalapril (Kanwar etal. 1993)]
Diuretics [e.g. frusemide (West etal.
1990), spironolactone (Downham
1978)]
Calcium channel blockers [e.g.
diltiazem (Kubo etal. 2010),
nifedipine (Leibovici etal. 1988)]
HMG-CoA reductase inhibitors [e.g.
pravastatin (Pua etal. 2006), lovastatin
(Sebök etal. 2004), uvastatin (Sebök
etal. 2004)]
Anti-diabetic medication [e.g.
chlorpropamide (Barnett and Barnett
1984), tolazamide (Barnett and Barnett
1984), glimepiride (Hammami etal.
2015)]
Vaccines [e.g. inuenza (Sato etal.
2010), hepatitis B (Saywell etal. 1997;
Rebora etal. 1999; Ferrando etal.
1998; Calista and Morri 2004; Schupp
and Vente 1999; Limas and Limas
2002; Al-Khenaizan 2001), human
papillomavirus (Laschinger etal.
2015)]
Immunomodulatory drugs [e.g.
anakinra (Vila etal. 2005),
immunoglobulin (Yockey and Ahmed
1997), interferon-α (Bush etal. 2017),
leunomide (May etal. 2017),
mesalazine (Alstead etal. 1991),
sulfasalazine (Ghosh etal. 2013)]
Immune checkpoint inhibitors
(Hwang etal. 2016; Cogen etal.
2018; Min Lee etal. 2018; Coleman
etal. 2019; Curry etal. 2017; Shi
etal. 2016; Obara etal. 2018; Biolo
etal. 2019; Siegel etal. 2018;
Coscarart etal. 2019) (e.g.
pembrolizumab, nivolumab,
ipilimumab)
Targeted oncologic drugs [e.g.
imatinib (Sendagorta etal. 2009;
Gómez Fernández etal. 2010; Sudha
etal. 2011; Ena etal. 2004; Dalmau
etal. 2006; Pascual etal. 2006; Lim
and Muir 2002; Kawakami etal.
2009; Kuraishi etal. 2010)]
Anti-TNFα (Inoue etal. 2017) [e.g.
adalimumab (Inoue etal. 2017; El
Habr etal. 2014; De Simone etal.
2008; Darrigade etal. 2016; Andrade
etal. 2015), etanercept (Utsu etal.
2012), iniximab (Darrigade etal.
2016; Andrade etal. 2015), iniximab
biosimilar (Gonzalez etal. 2018)]
Anti- IL17 drugs [e.g. secukinumab
(Maglie etal. 2018; Thompson etal.
2016; Komori etal. 2017)]
Anti-CD20 drugs (Kuten-Shorrer
etal. 2014; Bakkour and Coulson
2012; O'Connor etal. 2017) (e.g.
rituximab)
Y. K. Heng and Y. L. Lim
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