Acta Dermato-Venereologica 99-12CompleteContent | Page 9
CLINICAL REPORT
1071
Acquired Cold Urticaria vs. Autoinflammatory Diseases, Genetic
and Clinical Profile and Differential Diagnosis: Study of a Cohort
of Patients in a Tertiary Reference Centre
Gustavo DEZA 1 , Anna MENSA-VILARÓ 2,3 , Alvaro MARCH-RODRIGUEZ 1 , Silvia SÁNCHEZ 1 , Ramon M. PUJOL 1 , Juan I.
ARÓSTEGUI 2–4# and Ana M. GIMÉNEZ-ARNAU 1#
Department of Dermatology, Hospital del Mar – Institut Mar d’Investigacions Mèdiques, Universitat Autònoma de Barcelona (UAB), 2 Department
of Immunology, Hospital Clínic, 3 Institut d’Investigacions Biomèdiques August Pi i Sunyer, and 4 University of Barcelona, Barcelona, Spain
#
These authors contributed equally to this work.
1
Acquired cold urticaria (ACU) is characterized by the
development of itchy wheals after cold exposure. Ge-
neralized urticarial skin rashes triggered by cold ex-
posure characterize certain monogenic autoinflamma-
tory diseases (AIDs). The objective of this study is to
investigate the presence of variants in genes causing
AIDs that present with cold-induced urticarial skin
rashes in patients clinically diagnosed with ACU, in or-
der to look for susceptibility factors for the disease.
Fifty patients with primary ACU were studied. Germ-
line and post-zygotic variants on the NLRP3, NLRP12,
NLRC4 and PLCG2 genes were investigated using next-
generation sequencing technology. Seven patients
(14%) carried 8 heterozygous germline variants in the
following genes: NLRP3 (n = 1), NLRP12 (n = 3), NLRC4
(n = 1), PLCG2 (n = 3). No pathogenic or likely pathoge-
nic variants were detected, and deep analyses of the
sequences obtained did not identify any post-zygotic
variant. In conclusion, ACU is not related to post-zy-
gotic or germline pathogenic variants in the NLRP3,
NLRP12, NLRC4 and PLCG2 genes.
Key words: autoinflammatory diseases; cold urticaria; genetic
variant; urticaria; urticarial skin rash.
Accepted Aug 12, 2019; E-published Aug 13, 2019
Acta Derm Venereol 2019; 99: 1071–1077.
Corr: Ana M. Giménez-Arnau, Department of Dermatology, Hospital del
Mar – Institut Mar d’Investigacions Mèdiques, Universitat Autònoma de
Barcelona (UAB), Passeig Marítim, 25–29, ES-08003 Barcelona, Spain.
E-mail: [email protected], [email protected]
C
old urticaria is a physical urticaria characterized by
the development of itchy wheals and/or angioedema
after direct contact between the skin and cold air, liquids
and/or objects (1–3). Its diagnosis is usually supported
by cold-contact stimulation tests (CSTs), in which an
immediate wheal is induced after the application of a
cold stimulus to the skin (1). Cold urticaria syndromes
are very heterogeneous and can be classified into acqui-
red and familial disorders (3). Acquired cold urticaria
(ACU) are further divided into 2 subgroups: (i) primary
(“idiopathic”) and (ii) secondary ACU, depending on
the presence of an underlying disease or factor associa-
ted with the induction of the cold urticaria symptoms.
A particular subtype of ACU, known as atypical ACU,
SIGNIFICANCE
Acquired cold urticaria represents a subtype of inducible
urticaria characterized by the development of itchy wheals
after cold exposure. Generalized cold-induced urticarial
rashes are also seen in certain monogenic autoinflamma-
tory diseases. In the present study, we demonstrated that
acquired cold urticaria is not related to the presence of
germline and post-zygotic pathogenic variants on genes
causing autoinflammatory diseases that present with cold-
induced urticarial skin rashes (i.e. NLRP3, NLRP12, NLRC4
and PLCG2 genes). However, the presence of cold urticaria
in addition to systemic manifestations, family history and/
or laboratory abnormalities should alert physicians to the
potential diagnosis of a monogenic autoinflammatory di-
sease.
is characterized by the negative responses after CSTs,
and therefore, its diagnosis is established mainly on the
basis of a detailed clinical history (3). ACU most fre-
quently affects young adults, although up to 15–25% of
patients may show an onset of symptoms before the age
of 18 years (2, 4), with recent evidence suggesting that
paediatric-onset patients might exhibit distinctive clinical
features (2). Its symptoms are usually limited to cold-
exposed skin areas and typically appear a few minutes
after exposure to cold air, liquids and/or solids. Exten-
sive cold contact may occasionally result in generalized
symptoms, including headache, dyspnoea, hypotension
or loss of consciousness (1, 5). It is known that ACU is
caused by the release of histamine, leukotrienes, platelet
activating factor and other proinflammatory mast-cell
mediators (3–6). However, the complete pathophysiology
of the disease, particularly the atypical ACU, remains
undetermined (2).
Autoinflammatory diseases (AIDs) are a group of
inherited conditions of innate immunity characterized
by seemingly unprovoked and recurrent episodes of
sterile inflammation. The main subgroups among AIDs
are the inflammasomopathies, which are characterized
by a dysfunction of the inflammasome, a cytosolic
multiprotein complex regulating the pyroptosis and the
release of caspase-1 activation-dependent inflammatory
cytokines (7). From a clinical point of view, patients with
This is an open access article under the CC BY-NC license. www.medicaljournals.se/acta
Journal Compilation © 2019 Acta Dermato-Venereologica.
doi: 10.2340/00015555-3292
Acta Derm Venereol 2019; 99: 1071–1077