Francisco José Navarro Triviño

This multicentre retrospective case series evaluated the safety and effectiveness of dupilumab in nine recipients of solid organ transplants who had severe atopic dermatitis. Treatment resulted in rapid and sustained clinical improvement in most patients, with significant reductions in disease severity, pruritus and quality of life impairment, and minimal adverse events. Importantly, no graft dysfunction or need for immunosuppressive adjustment was observed, supporting dupilumab as a promising therapeutic option in this high-risk population.

Lichen planus (LP) is a chronic inflammatory dermatosis with limited systemic treatment options, and prospective data on oral phosphodiesterase‐4 (PDE4) inhibition are lacking. We conducted a prospective real‐world case series of ten adults with clinically and/or histologically confirmed LP treated with oral roflumilast, assessing disease severity using the Investigator's Global Assessment (IGA), pruritus and sleep disturbance using Numeric Rating Scales (NRS) and quality of life using the Dermatology Life Quality Index (DLQI). At baseline, 90% of patients presented moderate‐to‐severe disease (IGA 3–4). By week 12, 7 of 9 evaluable patients (78%) achieved IGA 0–1, increasing to 6 of 7 evaluable patients (86%) at week 24. Mean pruritus NRS improved from 7.7 to 1.6, sleep disturbance NRS from 7.3 to 2.0 and DLQI from 12.0 to 3.6. Overall, eight patients (80%) achieved at least 75% clinical improvement and six (60%) complete remission. The most frequent adverse events were insomnia (50%) and loose stools (30%), and two patients (20%) discontinued treatment because of adverse events. These preliminary prospective real‐world findings suggest that oral roflumilast may represent a potential therapeutic option for LP and support further controlled studies to define the role of PDE4 inhibition and optimal dosing in this condition.

The OX40-OX40L co-stimulatory pathway has emerged as an important regulator of T-cell persistence and immune memory. While traditionally associated with type 2 inflammation, its role extends across multiple barrier tissues, including the skin and respiratory mucosa, where it integrates epithelial signals with adaptive immune responses. To provide a comprehensive and integrative overview of the OX40-OX40L axis as a shared driver of immune persistence across skin and airway inflammatory diseases and to discuss its therapeutic implications. A narrative review was conducted based on a focused literature search of PubMed, Scopus, and Web of Science up to February 2026. Experimental, translational, and clinical studies addressing OX40-OX40L biology and therapeutic targeting were included. OX40 signaling acts as a late co-stimulatory pathway that sustains effector T-cell survival, promotes tissue-resident memory T-cell formation, and modulates regulatory T-cell function. In barrier tissues, epithelial-derived alarmins such as TSLP and IL-33 induce OX40L expression on antigen-presenting cells, reinforcing type 2-polarized immune responses. This axis contributes to chronic inflammation in atopic dermatitis, asthma, allergic rhinitis, and nasal polyposis, supporting the concept of shared mechanisms of immune persistence across type 2 inflammatory diseases. Beyond type 2 immunity, OX40-OX40L signaling also participates in Th1-, Th17-, and Th22-mediated responses, as well as in autoimmune, fibrosing, and lymphoproliferative disorders. Therapeutic targeting of this pathway, particularly with monoclonal antibodies such as amlitelimab, has demonstrated clinically meaningful efficacy and suggests potential for durable disease modification. The OX40-OX40L axis represents an important immunological pathway linking epithelial activation to adaptive immune memory across barrier tissues. Its role in sustaining immune persistence provides a conceptual framework for understanding chronic inflammatory diseases and supports continued investigation of therapies targeting upstream co-stimulatory pathways.

Chronic spontaneous urticaria (CSU) remains difficult to manage in patients refractory to antihistamines and omalizumab. Although dupilumab has recently been approved and incorporated into international guidelines, real-world evidence remains limited, particularly in treatment-refractory populations. We conducted a multicentre ambispective cohort study across 16 Spanish hospitals including adults with CSU, with or without concomitant chronic inducible urticaria, treated with dupilumab and followed for ≥4 weeks. The primary outcome was well-controlled disease within 24 weeks (Urticaria Control Test ≥12 and Urticaria Activity Score over 7 days≤6). Fiftyone patients were included; 92.0% had previously received omalizumab. At week 24, 69.7% (23/33) achieved well-controlled disease and 39.4% (13/33) complete control. Among patients with available week-52 data, 90.5% (19/21) and 61.9% (13/21), respectively, achieved these outcomes. Concomitant therapy use declined from 94.1% at baseline to 55.6% at week 52. Among omalizumab-experienced patients evaluable at week 24, dupilumab response was lower in prior nonresponders than in those with at least partial response to omalizumab (40% vs 85%, p=0.011). Atopic comorbidities were associated with greater UAS7 reduction (p=0.018). Dupilumab was well tolerated, with mostly mild adverse events. In routine clinical practice, dupilumab provides effective disease control in patients with difficult-totreat CSU, including most omalizumab-experienced individuals.

Head and neck atopic dermatitis represents a common and clinically challenging phenotype of atopic dermatitis, characterized by anatomical selectivity, chronicity, and variable therapeutic response. Increasing evidence indicates that head and neck atopic dermatitis is not merely a regional extension of generalized disease, but a distinct phenotype shaped by the convergence of regional barrier fragility, a lipid-rich sebaceous microenvironment, microbiome imbalance, particularly involving Malassezia species, and a mixed immune signature integrating type 2, type 17, and type 22 inflammatory pathways. These factors promote persistent inflammation, psoriasiform features, and relative treatment refractoriness in the head and neck region. The clinical relevance of this phenotype has increased in the era of targeted therapies, as persistent or de novo facial involvement has been reported during biologic treatment, most notably with interleukin-4Rα blockade. Dupilumab-associated head and neck dermatitis exemplifies a pathway shift characterized by suppression of type 2 inflammation alongside exaggerated interleukin-22 and aryl hydrocarbon receptor-driven epithelial stress responses, providing mechanistic insight into paradoxical inflammation and incomplete regional control. Advances in immunobiology are beginning to translate into more tailored therapeutic strategies. Interleukin-13-selective biologics, systemic and topical Janus kinase inhibitors, and emerging agents targeting tissue-resident memory T-cell pathways offer new opportunities to address the dominant inflammatory circuits active in this region. Although comparative data remain limited, these approaches raise the possibility of improved control in selected patients with difficult-to-treat head and neck involvement. This review synthesizes current evidence on the pathogenic hallmarks of head and neck atopic dermatitis, integrates emerging mechanistic and clinical data, and discusses evolving therapeutic strategies aimed at phenotype-driven region-specific management of this complex manifestation of atopic dermatitis.

Background: Dyshidrotic eczema (DE), also termed acute and recurrent vesicular dermatitis, is a vesicular clinical pattern of hand eczema (HE) with heterogeneous aetiologies. Objectives: To characterise the clinical‐allergological profile of patients with DE and to compare it with non‐DE HE subtypes. Methods: A multicentre, retrospective, observational study was conducted using data from the Spanish Contact Dermatitis Registry (2019–2024). Results: Of 4378 patients with HE, 559 were diagnosed with DE. A longer median disease duration (24 vs. 14 months) and more frequent palmoplantar involvement (16% vs. 7%) were observed in DE compared with non‐DE HE. At least one positive patch test was identified in 43% of DE versus 52% in non‐DE HE. Although overall sensitisation patterns were largely comparable, DE showed lower sensitisation rates to 2‐HEMA, carba mix and thiuram mix. Occupational factors were less frequently implicated in DE (9% vs. 29%) compared with non‐DE HE. Conclusions: Despite a high overall frequency of contact allergen sensitisation, the pattern of findings suggests that the dyshidrotic phenotype may follow a clinical course less dependent on external or occupational triggers, pointing towards a relatively greater contribution of endogenous factors compared with other HE subtypes.

Psoriasis and atopic dermatitis (AD) are traditionally viewed as distinct inflammatory skin diseases driven by type 17 and type 2 immune pathways, respectively. Increasing use of targeted therapies has revealed a treatment‐associated phenotype switch between these conditions, the so‐called ‘flip‐flop’ phenomenon, characterized by sustained emergence of eczematous features in patients treated for psoriasis or psoriasiform disease in those treated for AD. Robust real‐world data on this entity remain limited. Objectives: To characterize treatment‐associated phenotype switching between psoriasis and AD in a large real‐world cohort, focusing on clinical features, implicated therapies, management strategies and outcomes. Methods: We conducted a retrospective, multicentre, multinational observational study across 17 dermatology centres in six countries. Patients with psoriasis or AD who developed a clinician‐defined, persistent phenotype switch temporally associated with systemic or biologic therapy and requiring treatment modification were included. Demographic, clinical, therapeutic and outcome data were collected and analysed descriptively. Results: A total of 148 patients were included: 101 (68.2%) developed eczematous features while treated for psoriasis (PsO → eczematous), and 47 (31.8%) developed psoriasiform disease while treated for AD (AD → psoriasiform). PsO → eczematous patients were older and had more cardiometabolic comorbidities, whereas atopic comorbidities were more frequent in the AD → psoriasiform group. PsO → eczematous switches occurred mainly under interleukin (IL)‐17 and IL‐23 inhibitors, while AD → psoriasiform switches occurred exclusively during biologic therapies targeting type 2 inflammation, predominantly dupilumab. Treatment was modified in all patients. Janus kinase (JAK) inhibitors were the most frequently used strategy in both switch directions, particularly in PsO → eczematous cases. Marked clinical improvement was observed across phenotypes following therapeutic adjustment. Conclusions: Treatment‐associated phenotype switching between psoriasis and AD is a reproducible, bidirectional and clinically relevant real‐world phenomenon reflecting immune plasticity rather than paradoxical disease induction. Recognition of this entity is essential to guide appropriate therapeutic adaptation, with JAK inhibitors emerging as a commonly effective management option.

Zusammenfassung: Die atopische Dermatitis ist die häufigste chronisch‐entzündliche Hauterkrankung. Die klassische Definition beruht auf den ekzematischen Läsionen und dem schubförmigen Verlauf. In den letzten zehn Jahren hat sich jedoch zunehmend herausgestellt, dass diese Erkrankung wesentlich heterogener ist als bisher angenommen – sowohl bezüglich des klinischen Bildes als auch der zugrundeliegenden molekularen und immunologischen Mechanismen. Dieser kurze Review untersucht das in ständiger Entwicklung befindliche Rahmenkonzept für die Analyse der atopischen Dermatitis. Dieses umfasst das klinische Bild (Phänotyp), das Immunpolarisationsprofil (Immunotyp) sowie Faktoren im Hintergrund mit Bezug zur Erkrankung und ihrem Kontext, die sie prägen. Dieser Review will zeigen, wie die Heterogenität den Schweregrad der Erkrankung, die Progression und das Ansprechen auf die Therapie beeinflusst, insbesondere im Zusammenhang mit den immer stärker individualisierten Behandlungsstrategien. Durch Synthese der derzeit verfügbaren wissenschaftlichen und klinischen Erkenntnisse stellt dieser Review für klinisch Tätige einen praktischen Leitfaden für das komplexe Spektrum der AD und deren zugrundeliegende therapeutische Zielstrukturen zur Verfügung. Für das Verständnis des Krankheitsverlaufs und die Optimierung der Therapie ist es entscheidend, die multidimensionale Variabilität der Erkrankung zu erkennen und richtig zu interpretieren.