ORIGINAL ARTICLE

Pediatric Dermatology 1–8, 2017

Psoriasis and Psoriasiform Eruptions in

Pediatric Patients with Inflammatory Bowel
Disease Treated with Anti–Tumor Necrosis
Factor Alpha Agents
Joshua B. Eickstaedt, M.D.,* Luke Killpack, D.O.,† Jeanne Tung, M.D.,‡ Dawn Davis, M.D.,¶
Jennifer L. Hand, M.D.,¶,#,** and Megha M. Tollefson, M.D.¶

*Division of Hospital Internal Medicine, Mayo Clinic, Rochester, Minnesota, †LewisGale Hospital Montgomery,
Blacksburg, Virginia, ‡Division of Pediatric Gastroenterology and Hepatology and Departments of ¶Dermatology,
#Clinical Genomics and **Pediatrics and Adolescent Medicine, Mayo Clinic, Rochester, Minnesota

Abstract
Background: Anti–tumor necrosis factor alpha (TNF-a) agents are used to
treat a variety of autoimmune and inflammatory conditions, including psoriasis.
Paradoxically, numerous reports have documented new-onset or exacerbation
of psoriasis or psoriasiform skin lesions (PSO) in patients treated with these
agents for conditions other than PSO—particularly in adults with inflammatory
bowel disease (IBD). Not much is known regarding similar cases in children.
Methods: A retrospective chart review was performed on children younger than
19 years of age with IBD seen at the Mayo Clinic between 2003 and 2015 who
developed new-onset or recurrent PSO while undergoing anti-TNF-a therapy.
Results: Fourteen children developed PSO while undergoing anti-TNF-a
therapy for IBD. All three anti-TNF-a agents (infliximab, adalimumab, cer-
tolizumab) used to treat IBD in this series led to induction or recurrence of PSO
lesions. The median time to development of PSO was 11 months (range 0–48
mos), the median age was 15 years (range 12.5–17.5 yrs), and 57% of patients
were male. IBD activity was quiescent in 93% of cases at PSO onset. Seven
patients (50%) discontinued their initial anti-TNF-a therapy because of their skin
disease. Ultimately, four patients (29%) had to discontinue all anti-TNF-a
therapy to induce PSO resolution.
Conclusion: TNF-a antagonist–induced PSO in children with IBD is a rarely
reported adverse reaction. PSO onset has a variable latency, but usually occurs
during IBD remission, with a slight male bias. Nearly half of patients required a
change in their initial anti-TNF-a agent despite conventional skin-directed thera-
pies, and one-third of patients discontinued all anti-TNF-a therapy because of PSO.

Address correspondence to Megha Tollefson, M.D., Depart-

ment of Dermatology, Mayo Clinic, 200 First Street SW, Rochester,
MN 55905, or e-mail: Tollefson.Megha@mayo.edu.

DOI: 10.1111/pde.13081

© 2017 Wiley Periodicals, Inc. 1

2 Pediatric Dermatology 2017
Tumor necrosis factor alpha (TNF-a) plays a
significant role in the pathogenesis of several diseases,
including psoriasis and inflammatory bowel disease
(IBD) (1). Furthermore, there is a plausible common-
ality between psoriasis and IBD inflammatory path-
ways mediated by TNF-a (2,3). The development of
anti-TNF-a therapies is a significant advance in the
treatment of psoriasis and IBD.
Despite the efficacy of anti-TNF-a therapies, new-
onset or exacerbation of psoriatic skin lesions has
emerged as a paradoxical side effect (4–14). Tillack
et al (4) found that 5% of adults with IBD treated with
infliximab or adalimumab developed psoriasis or
psoriasiform skin lesions (PSO), a rate similar to that
seen in adults treated with anti-TNF-a agents for
rheumatoid arthritis who subsequently develop PSO
(5). The prevalence of skin reactions to anti-TNF-a
agents in children is unknown.
The aim of our study was to further investigate the
natural history of PSO in children with IBD receiving
anti-TNF-a agents proven to be effective in the
induction and maintenance of remission of IBD–
nfliximab, adalimumab, and certolizumab pegol
(CZP) (15–17). We describe 14 cases of new PSO
eruptions due to anti-TNF-a therapy in children being
treated for IBD at our single-center tertiary care center.
METHODS
The Mayo Clinic Institutional Review Board
approved this study. The medical records of patients
younger than 19 years were retrospectively examined
using the Mayo Clinic electronic medical record
(EMR) database. Our initial search began by identi-
fying patients with a diagnosis of IBD using the
International Classification of Diseases, Ninth Revi-
sion, Clinical Modification (ICD-9-CM) codes for
Crohn’s disease (555.x) and ulcerative colitis (556.x).
These cases were then screened for use of anti-TNF-a
agents. To capture patients who developed PSO, we
searched this subset of records for the ICD-9-CM
codes for psoriasis (696.x) and other inflammatory
conditions of the skin (690.x–698.x).
All patients were seen at the Mayo Clinic between
January 2003 and November 2015 in a pediatric IBD
clinic, and a dermatologist diagnosed PSO in all cases.
Biopsies were reviewed, if available, but not required for
inclusion inthe study. A dermatologist (MMT) reviewed
the medical record if the diagnosis of PSO was in
question. Patients with current psoriasis or psoriasis
active within the previous 6 months were excluded.
Data on sex, age at the time of PSO onset, IBD
phenotype, duration of TNF-a antagonist exposure at
the time of skin reaction, prior diagnosis of psoriasis
or eczema, family history of psoriasis or eczema, type
of anti-TNF-a therapy, and anatomic location of the
eruption were abstracted. Records were also reviewed
for therapeutic strategies used to treat PSO and
response to therapy.
RESULTS
We identified 14 cases of new-onset PSO in children
(57% male) undergoing anti-TNF-a therapy for IBD.
Patient characteristics are summarized in Table 1. Of
the 14 identified cases, 12 had Crohn’s disease and 2
had ulcerative colitis. Ninety-three percent of patients
had quiescent IBD activity at the time of PSO onset.
Two patients had a family history of psoriasis, one of
whom also had a personal history of psoriasis.
The median age at the onset of PSO was 15 years
(range 12.5–17.5 yrs). The median latency period
between initiation of anti-TNF-a therapy and onset
of PSO was 11 months (range 3.5–24 mos). Patients
naive to anti-TNF-a therapy had a median latency of
14.5 months (range 4.2–29.2 mos). The median
latency was 6 months (range 2.5–16 mos) for patients
exposed to a second anti-TNF-a agent.
Eighty-five percent of our patients had lesions
consistent with plaque psoriasis and 2 (15%) presented
with palmoplantar pustular psoriasis (Fig. 1). The
scalp (Fig. 2) was the most common area of involve-
ment (46%), followed by the umbilicus (31%) and
extremities (31%). Other involved areas included the
face and postauricular areas (21%). Two patients had
axillary involvement, one had chest and abdominal
involvement, and one had diffuse disease that excluded
the face. In addition to psoriasis, one patient (patient 8)
developed alopecia areata while taking infliximab.
None of the patients received concomitant
immunomodulators at the time of initial presentation
of PSO. All three anti-TNF-a agents (infliximab,
adalimumab, certolizumab) used to treat IBD in this
series were associated with induction or recurrence of
PSO. Initial therapy with infliximab resulted in nine
cases (64%) of psoriatic lesions, and initiation of
adalimumab resulted in two (14%). Additionally,
infliximab was responsible for two cases of anaphy-
laxis and one case of infusion reaction (shortness of
breath, hypoxia, flushing) leading to discontinuation.
The initial TNF-a antagonist was discontinued in
seven patients (50%) because of PSO; all were started
on a secondary anti-TNF-a agent (four on CZP, three
on adalimumab), with recurrence of PSO in three
patients receiving CZP and one receiving adali-
mumab.
TABLE 1. Clinical Characteristics of Patients with Tumor Necrosis Factor Alpha (TNF-a) Antagonist–Induced Psoriasis and Psoriasiform Skin Lesions (PSO)

Time to Therapy for Course of

Dermatologic development IBD activity IBD after psoriasis and
Age, IBD Anti-TNF-a history, of psoriasis, at time of PSO Type of Location of Dermatologic development response to
Case years Sex phenotype agent patient/family months diagnosis psoriasis involvement therapy of psoriasis treatment

1 14 Male Crohn’s Infliximab No/No 29 Remission Plaque Scalp, helices, Triamcinolone Infliximab Cleared with
disease periumbilical 0.025%, discontinued, infliximab
calcipotriene, started certolizumab discontinuation
acetic
acid dressings
Certolizumab 3 Axillae, Hydrocortisone Certolizumab Cleared with
lower 2.5% discontinued, started certolizumab
abdomen methotrexate cessation
2 17 Female Crohn’s Infliximab No/No 6 Remission Plaque Axillae, Hydrocortisone Infliximab Cleared with
disease umbilicus, 2.5%, discontinued, infliximab
right ear & triamcinolone started certolizumab discontinuation
nasal ala 0.05%
Certolizumab First Right ear Hydrocortisone Certolizumab Cleared with
treatment 2.5% discontinued, started certolizumab
methotrexate cessation
3 15 Male Crohn’s Infliximab No/No 30 Remission Plaque Scalp, ears, Hydrocortisone Infliximab Improved with
disease neck, 2.5%, tar-based continued topical therapy
preauricular preparation
face
4 16 Male Crohn’s Infliximab No/No 48 Remission Plaque Right arm, Hydrocortisone Infliximab Improved with
disease postauricular 2.5%, then continued topical therapies
triamcinolone
0.1%,
calcipotriene
5 18 Male Crohn’s Adalimumab No/No 2 Remission Plaque Hands, Topical Adalimumab Remission with
disease ankles, feet calcipotriene, increased, topical therapy
liquor carbonis methotrexate and
detergens 20% initiated methotrexate
6 17 Female Crohn’s Adalimumab No/yes, 36 Remission Plaque Scalp, face, Triamcinolone Adalimumab Cleared with
disease psoriasis chest, 0.1%, narrow- discontinued, adalimumab
abdomen, band ultraviolet started 6- discontinuation;
legs light B 39 weekly mercaptopurine, no recurrence on
then switched to certolizumab +
certolizumab + methotrexate
methotrexate
7 13 Male Ulcerative Infliximab Yes, 17 Remission Palmoplantar Hands, Topical Infliximab Improved
colitis eczema/No pustular ankles, corticosteroids, discontinued,
feet bleach baths, started Asacol and
emollients; then 6-mercaptopurine,
Goeckerman then switch to
treatments adalimumab
Adalimumab 6 Plantar foot, left Acitretin 25 mg Adalimumab Intermittent
nail with wet discontinued, started flares, restarted
dressings, topical budesonide Goeckerman
triamcinolone treatments
8 11 Female Infliximab No/No 12 Remission Scalp, hands
Eickstaedt et al: Anti-TNF-a-Induced Psoriasis in IBD 3
TABLE 1. Continued

Time to Therapy for Course of

Dermatologic development IBD activity IBD after psoriasis and
Age, IBD Anti-TNF-a history, of psoriasis, at time of PSO Type of Location of Dermatologic development response to
Case years Sex phenotype agent patient/family months diagnosis psoriasis involvement therapy of psoriasis treatment

Crohn’s Palmoplantar Topical Infliximab Cleared with

disease pustular fluocinonide discontinued, infliximab
started 6- discontinuation;
mercaptopurine and no recurrence
methotrexate, then on adalimumab
switched to
adalimumab
4 Pediatric Dermatology 2017

9 18 Female Crohn’s Adalimumab No/No First Uncontrolled Plaque Diffuse Ears: Adalimumab Cleared with
disease treatment involvement, hydrocortisone discontinued, adalimumab
sparing face valerate 0.2% started certolizumab discontinuation.
Body: + methotrexate
betamethasone
0.05%
Certolizumab 6 Upper and lower Fluocinonide Certolizumab + Resolved
extremities 0.05% twice a methotrexate
day for flares, discontinued, started
calcipotriene ustekinumab
0.005% twice a
day for
maintenance
10 15 Male Ulcerative Infliximab Yes, 24 Remission Plaque Scalp, right ear, Scalp: clobetasol Infliximab Partial
colitis eczema/No face for 2 wks, then continued improvement
fluocinonide and with topical
calcipotriene therapies
twice a day
Face:
pimecrolimus
twice a day
11 18 Female Crohn’s Adalimumab No/No 21 Remission Plaque Umbilicus, right ear Hydrocortisone Adalimumab Resolved
disease lobe and 2.5% ointment continued
postauricular,
trunk
12 15 Male Crohn’s Infliximab No/Yes, 24 Remission Plaque Scalp, right ear Fluocinolone Infliximab Partial
disease eczema under night discontinued, improvement
occlusion, P&S started oral steroids, before
shampoo, then transitioned to adalimumab
clobetasol adalimumab initiation
13 8 Female Crohn’s Infliximab Yes, psoriasis/ 5 Remission Plaque Umbilicus, Body: Infliximab Improved with
disease Yes, psoriasis postauricular hydrocortisone continued intermittent
2.5%, flares that
calcipotriene responded to
0.005% topical
Scalp: therapies
fluocinonide
0.05% twice a
day
 Eickstaedt et al: Anti-TNF-a-Induced Psoriasis in IBD 5

topical therapy
Improved with
psoriasis and
response to
Course of

treatment

Adalimumab
development
Therapy for

of psoriasis

continued
IBD after

0.1% twice a day

2.5% twice a day

Intergluteal cleft:
hydrocortisone
triamcinolone
Arms and legs:
Dermatologic

Figure 1. Palmar pustular psoriasis in patient 7.

therapy

intergluteal cleft
Knees, elbows,
involvement
Location of
psoriasis
Type of

Plaque
at time of PSO
IBD activity

Remission
diagnosis

Shaded cells denote cases where TNF-a antagonists were discontinued indefinitely.

Figure 2. Plaque psoriasis of the scalp in patient 10.

Ultimately, 10 of 14 patients (71%) were able to

development
of psoriasis,

continue on an anti-TNF-a agent as first- or second-

Time to

months

line therapy with adjunctive use of topical medica-

15

tions. Five of these patients had complete remission of

their skin lesions and the remainder had significant
patient/family
Dermatologic

improvement with topical therapies, which included

history,

topical steroids, calcipotriene, and calcineurin inhibi-

No/No

tors. Two patients received tar-based topical therapy,

and oral acitretin, Goeckerman regimen, and narrow-
Adalimumab
Anti-TNF-a

band ultraviolet B therapy were used in others.

Discontinuation of anti-TNF-a therapy was required
agent

in four patients (29%) to induce PSO resolution. Two

patients were switched to methotrexate and one to
phenotype

ustekinumab (a monoclonal antibody against inter-

disease
Crohn’s

leukins 12 and 23). One was started on budesonide for

IBD
TABLE 1. Continued

IBD but also required reinitiation of Goeckerman

treatments.
Male
years Sex

DISCUSSION
Age,

11

The use of TNF-a antagonists continues to increase,

Case

as does the number of reported TNF-a antagonist–

14
6 Pediatric Dermatology 2017
induced PSO cases, although there are only 26
reported cases of TNF-a antagonist–induced PSO in
children, the majority of whom had IBD (6–10). Our
case series of 14 patients adds to the limited pediatric
literature.
Boys accounted for 57% of cases in our study,
which is similar to the 58% in other pediatric case
series and suggests a slight male predominance in
TNF-a antagonist–induced PSO (6–10). There is no
sex bias in non-drug-induced pediatric PSO (18). This
is in contrast to adult IBD cases of TNF-a antago-
nist–induced PSO, in which men were in the minority
and accounted for 42% of cases (19). It is not clear
whether a personal or family history of psoriasis is
associated with a risk of reaction to anti-TNF-a
agents. In our study, only one patient had a personal
history of psoriasis, and two (15%) had a family
history. Sherlock et al (10) reported 18 children with
psoriasiform reactions, of whom 34% had a family
history of psoriasis. Thus there may be a genetic
component to this reaction.
The inclusion of patients with a prior history of
psoriasis is a potential limitation of our study. The
natural history of psoriasis includes spontaneous
relapses and remissions, so distinguishing between
spontaneous and TNF-a antagonist–induced psori-
atic eruptions could prove difficult. Only one of our
patients had a remote history of psoriasis, minimizing
the influence of this potential limitation.
We were unable to describe any similarities or
differences between IBD subtypes and TNF-a antago-
nist-induced PSO, because we only identified two
patients with ulcerative colitis. Interestingly, 93% of
our patients had clinically quiescent IBD at the onset
of PSO. This parallels an adult study in which 88% of
IBD patients were in clinical remission upon onset of
anti-TNF-a-induced PSO (20). Furthermore, the
majority of pediatric IBD patients who developed
cutaneous reactions to anti-TNF-a agents had low
levels of intestinal inflammation, based on fecal
calprotectin levels (11). These findings are interesting
because PSO and IBD are inflammatory conditions
and express the Th17 cytokine, therefore one would
expect the disease severity of each to correlate (4).
In addition, 64% of our cases were due to
infliximab. This is consistent with a recent systematic
review in adults that found 69% of TNF-a antago-
nist–induced PSO resulted from infliximab infusions
(21). Likewise, 75% of the eight previously published
pediatric cases were associated with infliximab (6–9).
The recent case series by Sherlock et al (10) examined
only patients with Crohn’s disease treated with
infliximab, although in a study of patients with
rheumatoid arthritis there was a stronger association
between new-onset PSO and adalimumab than inflix-
imab or etanercept (5). It is possible that PSO is seen
more frequently with infliximab in children with IBD
due to selection bias for treatment, because it is often
selected as the first-line anti-TNF-a agent, although
other factors cannot be excluded, including immuno-
genicity or chemical composition.
The latency period between initiation of anti-
TNF-a therapy and the onset of lesions varied in
our patients, from the first infusion to 48 months after
initiation of treatment, with a mean onset of
20.2 months. Similar findings are seen in adults. Ko
et al (19) and Wollina et al (12) reported a mean anti-
TNF-a–induced PSO onset of 10.5 months (range
0–48 mos) and 9.5 months (range 0–63 mos), respec-
tively. An onset ranging from 1 month to 3 years has
been reported in previous pediatric cases (6–10).
Furthermore, patients exposed to a previous TNF-a
antagonist had a shorter median latency to PSO onset
(6 mos) than anti-TNF-a–naive patients (14 mos). To
our knowledge, this is the first demonstration of
variable latency to PSO onset for naive patients and
those with prior exposure to TNF-a antagonists. The
variable time between initiation of anti-TNF-a ther-
apy and the development of PSO suggests that other
factors, including stress, diet, injury to the skin,
genetic predisposition, and immunogenicity, may
have some effect (14). In the future, sufficiently
powered studies are needed to investigate the under-
lying pathogenesis of this seemingly paradoxical
effect.
Plaque psoriasis is the most common subtype of
PSO in the general pediatric population. Guttate
psoriasis (14%) and sebopsoriasis (8%) are the next
most common, and palmoplantar pustulosis is extre-
mely rare (18). Eighty-five percent of our patients
developed plaque psoriasis while undergoing anti-
TNF-a therapy and the remaining 15% developed
palmoplantar pustular psoriasis; this is similar to the
pediatric literature (6–10). Thus it appears that plaque
psoriasis is commonly seen in classic and TNF-a
antagonist–induced psoriasis, but the aforementioned
studies suggest that palmoplantar psoriasis is more
frequently seen with TNF-a antagonist–induced PSO
and rare in classic psoriatic disease.
Psoriasis in children typically involves the extrem-
ities, including the elbows and knees (60%), scalp
(47%), and trunk (35%), and approximately half of
these children have lesions at more than one anatomic
site (18). In our study, the scalp was most commonly
affected (46%), followed by the umbilicus (31%) and
extremities (31%); 85% of patients had lesions at

more than one anatomic site. Another case series of
children with IBD treated with infliximab described a
rate of scalp involvement similar to that of our study
(56%) but also found that the postauricular region,
which was characterized separately from the scalp,
was involved in four cases (22%) (10). We found that
three patients (21%) had postauricular involvement.
These combined findings suggest that the scalp is the
most common location of TNF-a antagonist–induced
psoriasis in children, with a unique predilection for
postauricular involvement. As a result, dermatolo-
gists, primary care physicians, and subspecialists
treating patients with anti-TNF-a medications should
suspect this drug-associated complication not only on
the extremities, but also on the scalp, face, postauric-
ular area, and palmar surfaces. These findings may
help in the clinical assessment of drug-induced com-
plications in children with IBD.
Seventy-one percent of our patients were able to
continue anti-TNF-a therapy, as a first- or second-line
agent, with the addition of adjuvant topical therapies
for their psoriatic lesions. This rate is lower than
previously described in the case series by Sherlock et al
(10) and Malkonen et al (11), who reported contin-
uation rates of 77% and 83%, respectively. This
finding may be due to the fact that a significant
proportion, 44% and 30%, respectively, of patients
received concomitant immunomodulation (6-mercap-
topurine, azathioprine, methotrexate, and glucocorti-
coids). None of the patients in our study received
concomitant immunomodulation with initial anti-
TNF-a therapy, although our patients were started
on concomitant immunomodulation for IBD when
their initial anti-TNF-a agent was discontinued.
Furthermore, these studies examined only infliximab.
It is possible that concomitant immunomodulation
decreases the severity of PSO in patients receiving
infliximab, although further studies are needed to
confirm this.
Although there are no universally accepted treat-
ment recommendations for TNF-a antagonist–in-
duced PSO, initial treatments are often similar to
those for any child with psoriasis. A dermatologist
should evaluate all patients undergoing anti-TNF-a
therapy who develop lesions indicative of psoriasis. As
seen in our study and other reported cases, topical
treatment can be effective and thus should be first-line
therapy. This includes topical corticosteroids, vitamin
D analogs, phototherapy, emollients, and keratolytic
therapies. In cases that are refractory or significantly
affect quality of life, cessation of anti-TNF-a therapy
may be necessary. The use of a second anti-TNF-a
agent should be carefully considered since PSO may
Eickstaedt et al: Anti-TNF-a-Induced Psoriasis in IBD 7
reoccur. One of our patients experienced complete
resolution of skin and IBD symptoms after switching
from adalimumab to ustekinumab. Although this
medication is not approved in children, it is often used
to treat plaque psoriasis and can be effective in treating
IBD. In one adult study, nine patients with Crohn’s
disease and severe psoriasiform lesions achieved PSO
resolution when treated with ustekinumab (4).
The exact mechanism leading to the paradoxical
induction or exacerbation of psoriasis is not com-
pletely understood. The most commonly accepted
hypothesis is based on the balance between TNF-a and
interferon alpha (INF-a), the latter of which plasma-
cytoid dendritic cells (pDCs) secrete. TNF-a inhibits
pDC maturation, which decreases INF-a production
(22). Therefore, TNF-a antagonists allow for unregu-
lated pDC maturation and increased production of
INF-a (23). The study by Tillack et al (4) demonstrated
a large number of INF-a-secreting cells in psoriatic
lesions induced by anti-TNF-a therapies which sup-
ports this hypothesis. Further studies are needed to
investigate this hypothesis.
CONCLUSION
Our case series of TNF-a antagonist–induced PSO in
children with IBD is one of the larger studies to
describe this phenomenon and the first to describe PSO
attributable to multiple anti-TNF-a agents in children.
Latency to PSO onset is shorter in patients exposed to
a second or third anti-TNF-a agent. Most patients had
quiescent IBD disease upon PSO onset. There appears
to be a slight male predominance in TNF-a antago-
nist–induced PSO. Plaque psoriasis of multiple ana-
tomic sites, specifically the scalp, is the most common
presentation, and a conventional skin-directed treat-
ment strategy may often be successful in controlling
the disease. The incidence of this seemingly paradox-
ical side effect is likely to increase as the use of these
biologic agents increases. For this reason, it is imper-
ative to remain vigilant for this adverse reaction.
REFERENCES
1. Breese EJ, Michie CA, Nicholls SW et al. Tumor
necrosis factor alpha-producing cells in the intestinal
mucosa of children with inflammatory bowel disease.
Gastroenterology 1994;106:1455–1466.
2. Cohen AD, Dreiher J, Birkenfeld S et al. Psoriasis
associated with ulcerative colitis and Crohn’s disease.
J Eur Acad Dermatol Venereol 2009;23:561–565.
3. Najarian DJ, Gottlieb AB. Connections between pso-
riasis and Crohn’s disease. J Am Acad Dermatol
2003;48:805–821.
8 Pediatric Dermatology 2017
4. Tillack C, Ehmann LM, Friedrich M et al. Anti-TNF
antibody-induced psoriasiform skin lesions in patients
with inflammatory bowel disease are characterised by
interferon-c-expressing Th1 cells and IL-17A/IL-22-
expressing Th17 cells and respond to anti-IL-12/IL-23
antibody treatment. Gut 2014;63:567–577.
5. Harrison MJ, Avnon L, Freud T et al. Rates of new-
onset psoriasis in patients with rheumatoid arthritis
receiving anti-tumour necrosis factor alpha therapy:
results from the British Society for Rheumatology
Biologics Register. Ann Rheum Dis 2009;68:209–215.
6. Perman MJ, Lovell DJ, Denson LA et al. Five cases of
anti-tumor necrosis factor alpha-induced psoriasis pre-
senting with severe scalp involvement in children.
Pediatr Dermatol 2012;29:454–459.
7. Peek R, Scott-Jupp R, Strike H et al. Psoriasis after
treatment of juvenile idiopathic arthritis with etaner-
cept. Ann Rheum Dis 2006;65:1259.
8. Pourciau C, Shwayder T. Occurrence of pustular
psoriasis after treatment of Crohn disease with inflix-
imab. Pediatr Dermatol 2010;27:539–540.
9. Avila Alvarez A, Garc
ıa-Alonso L, Solar Boga A et al.
Flexural psoriasis induced by infliximab and adali-
mumab in a patient with Crohn’s disease. An Pediatr
(Barc) 2009;70:278–281.
10. Sherlock ME, Walters T, Tabbers MM et al. Inflix-
imab-induced psoriasis and psoriasiform skin lesions in
pediatric Crohn disease and a potential association with
IL-23 receptor polymorphisms. J Pediatr Gastroenterol
Nutr 2013;56:
512–518.
11. M€alk€onen T, Wikstrom A, Heiskanen K et al. Skin
reactions during anti-TNF-a therapy for pediatric
inflammatory bowel disease: a 2-year prospective study.
Inflamm Bowel Dis 2014;20:1309–1315.
12. Wollina U, Hansel G, Koch A et al. Tumor necrosis
factor-alpha inhibitor-induced psoriasis or psoriasiform
exanthemata: first 120 cases from the literature includ-
ing a series of six new patients. Am J Clin Dermatol
2008;9:1–14.
13. Cohen JD, Bournerias I, Buffard V et al. Psoriasis
induced by tumor necrosis factor-a antagonist therapy:
a case series. J Rheumatol 2007;34:380–385.
14. Cullen G, Kroshinsky D, Cheifetz AS et al. Psoriasis
associated with anti-tumour necrosis factor therapy in
inflammatory bowel disease: a new series and a review
of 120 cases from the literature. Aliment Pharmacol
Ther 2011;34:1318–1327.
15. Colombel JF, Sandborn WJ, Rutgeerts P et al. Adal-
imumab for maintenance of clinical response and
remission in patients with Crohn’s disease: the
CHARM trial. Gastroenterology 2007;132:52–65.
16. Hanauer SB, Feagan BG, Lichtenstein GR et al.
Maintenance infliximab for Crohn’s disease: the
ACCENT I randomised trial. Lancet 2002;359:1541–
1549.
17. Schreiber S, Khaliq-Kareemi M, Lawrance IC et al.
Maintenance therapy with certolizumab pegol for
Crohn’s disease. N Engl J Med 2007;357:239–250.
18. Tollefson MM, Crowson CS, McEvoy MT et al.
Incidence of psoriasis in children: a population-based
study. J Am Acad Dermatol 2010;62:979–987.
19. Ko JM, Gottlieb AB, Kerbleski JF. Induction and
exacerbation of psoriasis with TNF-blockade therapy: a
review and analysis of 127 cases. J Dermatolog Treat
2009;20:100–108.
20. Fr
eling E, Baumann C, Cuny JF et al. Cumulative
incidence of, risk factors for, and outcome of derma-
tological complications of anti-TNF therapy in inflam-
matory bowel disease: a 14-year experience. Am J
Gastroenterol 2015;110:1186–1196.
21. Denadai R, Teixeira FV, Steinwurz F et al. Induction
or exacerbation of psoriatic lesions during anti-TNF-a
therapy for inflammatory bowel disease: a systematic
literature review based on 222 cases. J Crohns Colitis
2013;7:517–524.
22. de Gannes GC, Ghoreishi M, Pope J et al. Psoriasis and
pustular dermatitis triggered by TNF-a inhibitors in
patients with rheumatologic conditions. Arch Dermatol
2007;143:223–231.
23. Nestle FO, Gilliet M. Defining upstream elements of
psoriasis pathogenesis: an emerging role for interferon
alpha. J Invest Dermatol 2005;125:xiv–xxv.