Case Report: Paradoxical acrodermatitis of Hallopeau-like eruption following anti-IL-17 therapy [version 1; peer review: 2 approved]

Psoriasis is a chronic immune-mediated inflammatory disease. Up to 40% of patients with psoriasis may develop psoriatic arthritis.  Currently, interleukin (IL)-17/IL-23 pathways are identified as key factors in the immunopathogenesis of both conditions. Here we describe the case of a patient who dev...

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Published inF1000 research Vol. 8; p. 336
Main Authors Tadiotto Cicogna, Giulia, Messina, Francesco, Nalotto, Linda, Szekely, Serena, Alaibac, Mauro
Format Journal Article
LanguageEnglish
Published England Faculty of 1000 Ltd 2019
F1000 Research Limited
F1000 Research Ltd
Subjects
Arthritis
Case Report
Case reports
Cytokines
Dermatology
Family medical history
Immunopathogenesis
Inflammatory diseases
Interleukin 1
Interleukin 17
Interleukin 23
Keratosis
Neutrophils
Onycholysis
Pathogenesis
Psoriasis
Psoriatic arthritis
Skin diseases
Tumor necrosis factor
Italy
psoriasis
Acrodermatitis continua of Hallopeau
paradoxical reaction
IL-17
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Summary:Psoriasis is a chronic immune-mediated inflammatory disease. Up to 40% of patients with psoriasis may develop psoriatic arthritis.  Currently, interleukin (IL)-17/IL-23 pathways are identified as key factors in the immunopathogenesis of both conditions. Here we describe the case of a patient who developed psoriasiform skin lesions 10 months after the initiation of anti-IL17 therapy for psoriatic arthritis. The underlying disease had responded well to the therapy, but the patient developed a striking pustular eruption at the fingers with nail involvement, onycholysis, yellow discoloration, and subungual keratosis. Clinical and histological findings were consistent with an acrodermatitis continua of Hallopeau-like eruption. Skin lesions subsided after discontinuation of the responsible anti-IL17 agent. The interpretation of this paradoxical side effect of biological therapies remains unclear but may relate to an unbalanced inflammatory cytokine response induced by the inhibition of TNF activity. It is likely that patients, who are genetically prone, may respond exaggeratedly to a cytokine imbalance. The identification of this kind of patient, in the future, could be useful in order to choose the correct therapy.
Bibliography:ObjectType-Case Study-2
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No competing interests were disclosed.
ISSN:2046-1402
2046-1402
DOI:10.12688/f1000research.18493.1