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Acquired reactive perforating collagenosis is a rare cutaneous disorder characterised by the extrusion of abnormal connective tissue trough epidermidis and/or follicular units. Reactive perforating collagenosis is often associated with systemic diseases in which pruritus is a common symptom (e.g., diabetes and chronic kidney disease). Less commonly, it has been associated with chronic inflammatory dermatoses, including atopic dermatitis, as in this case. In this report, we describe the exceptional case of a 35-year-old man affected by acquired reactive perforating collagenosis associated with atopic dermatitis who was resistant to conventional topical and systemic treatment and experienced complete resolution of clinical signs and symptoms after 12 weeks of treatment with dupilumab. In our patient, the severe pruritus induced by atopic dermatitis likely contributed to the development of acquired perforating collagenosis lesions, which are thought to be a reactive response to chronic scratching and repetitive injury to the skin. Chronic pruritus in atopic dermatitis is known to be driven by type 2 cytokines, including IL-4 and IL-13, and dupilumab, a monoclonal antibody inhibiting IL-4 and IL-13 signalling, has been shown to be effective in the treatment of moderate to severe atopic dermatitis as well as other type 2-driven pruritic dermatological conditions. This case supports the potential use of dupilumab for the treatment of reactive perforating dermatosis.
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http://dx.doi.org/10.1155/2024/6265608 | DOI Listing |
BMB Rep
September 2025
Department of Microbiology, Jeonbuk National University Medical School, Jeonju 54896; Department of R&D, Cutiimunebio Inc., Jeonju 54907, Korea.
Atopic dermatitis (AD) is a chronic dermatological disorder characterized by intense pruritus and eczematous lesions. Repeated topical application of 2,4-dinitrofluorobenzene (DNFB) in NC/Nga mice produces AD-like clinical symptoms that closely resemble human AD. N-Acetyl-L-Alanine (L-NAA), a derivative of L-Alanine, has unknown biological and physiological effects on cutaneous tissue.
View Article and Find Full Text PDFInt Immunopharmacol
September 2025
Clinical Research Center, The Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi 214023, China. Electronic address:
Allergic diseases, characterized by complex pathological mechanisms involving immune dysregulation and chronic inflammation, impose a substantial burden on global health. The Hippo signaling pathway, a highly conserved regulator of cell proliferation, apoptosis, immune homeostasis, and tissue repair, has recently emerged as a pivotal player in allergic disease pathogenesis. This review synthesizes current knowledge on the core components and physiological functions of the Hippo pathway, elucidates its mechanistic roles in major allergic disorders-including allergic asthma, allergic rhinitis, atopic dermatitis, and food allergies-and evaluates the therapeutic potential of targeting this pathway.
View Article and Find Full Text PDFJ Invest Dermatol
September 2025
Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
Allergol Int
September 2025
Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Tokyo, Japan; Faculty of International Liberal Arts, Juntendo University, Tokyo, Japan. Electronic address:
The epidermal immune microenvironment is a multifaceted system in which the interplay between the skin microbiome and antimicrobial peptides plays a pivotal role in sustaining skin homeostasis and preventing dysbiosis. Disruption of these interactions can lead to inflammatory skin conditions such as atopic dermatitis. This review aims to explore the complex mechanisms by which antimicrobial peptides and the skin microbiome communicate within the epidermal immune microenvironment, emphasizing causal dynamics and the dual role of antimicrobial peptides.
View Article and Find Full Text PDFLancet Respir Med
September 2025
Department for Paediatric Pneumology, Allergology, and Neonatology and German Center for Lung Research, Biomedical Research in Endstage and Obstructive Lung Disease, Hannover Medical School, 30625 Hannover, Germany. Electronic address: