Allergology International 64 (2015) 382e383

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Allergology International
journal homepage: http://www.elsevier.com/locate/alit

Letter to the Editor

Atopic dermatitis exacerbated with ustekinumab in a psoriatic patient

with childhood history of atopy

Dear Editor, revealed normal pulmonary function, fractional exhaled nitric ox-
ide (FeNo) level was low (24 ppb) pointing to the well-controlled
Ustekinumab is a biological agent that is currently approved for asthma (FeNo values range from 22 to 44 ppb). Ustekinumab was
the treatment of moderate to severe plaque psoriasis. It is a mono- stopped again, improvement of AD was achieved after the adminis-
clonal antibody that binds the p40 subunit of IL-12 and IL-23 to tration of the short course of systemic prednisone at 40 mg daily for
limit the progression of the Th1 and Th17 inflammatory immune 6 days followed by 20 mg for 4 days and 10 mg for 4 days. Topical
responses. Recently, it has been suggested that ustekinumab could corticosteroid therapy was needed to control the disease. While
represent a potential treatment for atopic dermatitis (AD).1e3 How- psoriasis was stable no complete remission of AD and no reduction
ever, inadequate response to ustekinumab in AD patients has also of peripheral eosinophilia (1.63  109/L) was observed during 12-
been reported.4 We present a case of paradoxically exacerbated months follow up. The biologic had no impact for the asthma
AD during the ustekinumab treatment for psoriasis. course.
A 21-year-old man with a 7 year history of severe psoriasis re- Our case is particularly interesting because it describes a patient
fractory to conventional systemic treatments and childhood history with remission of psoriasis and flare of AD due to ustekinumab
of atopy (atopic dermatitis-AD, asthma, seasonal rhinitis) was therapy. To our knowledge, ustekinumab has not been reported
treated with ustekinumab. The patient was without major symp- to exacerbate AD. The patient previous has been treated for 18
toms from respiratory system and AD lesions within a period of 5 month without any flare suggesting the eczematous drug eruption
years before the date of starting the treatment. He was taking mon-
telukast, antihistamines, inhaled corticosterois and formoterol for
asthma. Psoriatic lesions and no clinical sings of AD were found
on baseline examination (Fig. 1). Ustekinumab 45 mg (1 injection
at week 0 and week 4, then every 12 weeks) was introduced (ac-
cording to body weight: 76 kg). After 18 months and following
excellent results, the patient decided to discontinue therapy. But
8 months later recurrence of psoriasis was observed and ustekinu-
mab was restarted. The baseline PASI fell from 11,4 to 3,0 after 4
weeks of treatment with ustekinumab, complete remission of pso-
riasis was achieved after 8 weeks of therapy. However, intense
generalized itching occurred since the first dose was administered.
Severe AD appeared on the neck and lower limbs about 6 weeks af-
ter the reintroduction of ustekinumab (Fig. 2). Eczematous drug
eruption and AD exacerbation due to stress, infection, or other
external factors (i.e. topical treatments of psoriasis) was excluded
in the differential diagnosis. Apart from dermatologic findings,
physical examination revealed no abnormalities. Laboratory tests
showed peripheral blood eosinophilia (1,48  109/L, compared to
the baseline of 0,46  109/L, to the 16 weeks of 0,58  109/L, to
the 28 weeks of ustekinumab therapy of 0,67  109/L, and to the
recurrence of psoriasis of 0,66  109/L), as well as abnormal in-
crease in serum allergen-specific immunoglobulin E (sIgE) level
including dog-, cat-, hamster-, and grass pollen-specific IgE. Total
IgE level was 12576 IU/ml (0e100,0 IU/l reference range). Other lab-
oratory data (erythrocyte sedimentation rate, C-reactive protein
level, complete blood count, biochemical parameters of liver and
kidney, urinalysis) were normal at several time points. Spirometry

Peer review under responsibility of Japanese Society of Allergology. Fig. 1. Psoriatic lesions on the head before the initiating ustekinumab therapy.

http://dx.doi.org/10.1016/j.alit.2015.06.003
1323-8930/Copyright © 2015, Japanese Society of Allergology. Production and hosting by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/
licenses/by-nc-nd/4.0/).
 Letter to the Editor / Allergology International 64 (2015) 382e383
Fig. 2. Skin lesions corresponding to atopic dermatitis on the lower limbs after the
reintroduction of ustekinumab for psoriasis relapse.
rather than AD. Drug eruptions are more likely to occur when ther-
apy is interrupted followed by a second exposure. Some authors
have described patients with an eczematous eruption that
appeared after the administration of ustekinumab.5,6 However,
the eczema has lasted during 12-months follow up after the final
dose of ustekinumab, supporting the diagnosis of AD in our patient.
Why ustekinumab has exacerbated AD but not psoriasis para-
doxically is hard to explain. It is uncommon for AD to coexist
with psoriasis.7 Both diseases have distinct genetic mechanisms
with opposing effects in shared pathways influencing epidermal
differentiation and immune response.8 Psoriasis is believed to be
mediated by Th1/Th17 cells and AD by Th2/Th22 cells.9 The Th17
axis is also activated in patients with acute AD and plays some
role in the pathogenesis of the disease.9 Therefore, ustekinumab
could represent a potential treatment for AD. However, this biologic
blocking Th1 inflammatory pathways (IL-12) partially acts as TNF-a
inhibitor and possibly this may result in downregulation of Th1
383
cytokines and manifestation of Th2-associated disease.10 Increased
Th2 activity in the presented patient might has resulted in the pe-
ripheral blood eosinophilia after initiating ustekinumab. Subse-
quently, AD-like skin lesions were induced by the therapy
reintroduction. Therefore, we would like to highlight the possible
connection between the treatment with ustekinumab and the flare
of AD, while psoriasis go into remission.
Conflict of interest
The authors have no conflict of interest to declare.
 ˛ ty *, Alina Skrzypek-Salamon, Hubert Arasiewicz,
Anna Lis-Swie
 ska-Wcisło
Ligia Brzezin
Department of Dermatology, School of Medicine in Katowice, Medical University of
Silesia, Katowice, Poland
* Corresponding author. Department of Dermatology, Medical University of Silesia,
Francuska Str. 20/24, 40-027 Katowice, Poland.
 ˛ ty).
E-mail address: annadlis@neostrada.pl (A. Lis-Swie
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Received 21 April 2015
Received in revised form 4 June 2015
Accepted 5 June 2015
Available online 8 July 2015