ArticleJournal of the European Academy of Dermatology and Venereology : JEADV2025
IL-6 levels dominate the serum cytokine signature of severe epidermolysis bullosa: A prospective cohort study.
Article in Journal of the European Academy of Dermatology and Venereology : JEADV, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Tissue and systemic inflammation in dystrophic epidermolysis bullosa: a systematic review and meta-analysis.Orphanet journal of rare diseases · 2025Pooled it
- A Mechanistic Map of the Phenotypic Complexity in Recessive Dystrophic Epidermolysis Bullosa Provides Basis for Therapeutic Target Discovery and Drug Repurposing.International journal of molecular sciences · 2026Article
- Contribution of HMGB1 to keratinocyte inflammation in recessive dystrophic epidermolysis bullosa.JID innovations : skin science from molecules to population health · 2026Article
- A Single Center Retrospective Chart Review of Monitoring Laboratory Tests in Recessive Dystrophic Epidermolysis Bullosa.Pediatric dermatology · 2026Article
- Updates in the Treatment of Pain and Pruritus in Epidermolysis Bullosa.Pediatric dermatology · 2026Review
- Selected Vascular, Inflammatory, and Lipid Parameters in Patients with Selected Keratinization Disorders: Preliminary Data from a Retrospective Observational Study.Journal of clinical medicine · 2026Article
- Interplay between iron metabolism, inflammation, and EPO-ERFE-hepcidin axis in RDEB-associated chronic anemia.Blood advances · 2025Article
- Prevalence and Mechanisms of Itch in Chronic Wounds: A Narrative Review.Journal of clinical medicine · 2025Review
- Systems immunology integrates the complex endotypes of recessive dystrophic epidermolysis bullosa.Nature communications · 2025Article
- IL-6 levels dominate the serum cytokine signature of severe epidermolysis bullosa: A prospective cohort study.Journal of the European Academy of Dermatology and Venereology : JEADV · 2025Article
- Systemic treatment of recessive dystrophic epidermolysis bullosa with mesenchymal stromal cells: a scoping review of the literature and conclusions for future clinical research.The Journal of dermatological treatment · 2024Article
- Unveiling the value of C-reactive protein as a severity biomarker and the IL4/IL13 pathway as a therapeutic target in recessive dystrophic epidermolysis bullosa: A multiparametric cross-sectional study.Experimental dermatology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
backgroundSystemic inflammation is considered a major player in the pathogenesis of epidermolysis bullosa (EB), but its pattern has only been described in small heterogeneous cohorts. There is controversy if and how systemic inflammation should be therapeutically targeted.
methodsWe examined serum proinflammatory, anti-inflammatory, and itch related cytokines in a paediatric cohort of 29 patients with junctional and dystrophic EB. The cytokine that emerged as the most relevant was measured in a validation cohort of 42 patients during follow-up visits over 2 years.
resultsIL-6 showed the most consistent and highest aberration dominating systemic inflammation. IL-6 correlated with wound body surface area (BSA) in both, finding and validation cohorts. Patients with less than 3% wound BSA had normal IL-6, while IL-6 levels significantly increased at more than 5% and 10% of wound BSA. TGF-β was only marginally elevated in patients with severe recessive dystrophic EB, while TNF-α, IFN-γ and IL-1β varied inconsistently. Patients reporting itch showed elevations in type 2 immunity (IgE, TSLP, IL4 and/or IL-31, respectively).
conclusionsOur data suggest a dominant skin barrier and wound healing inflammatory pattern in junctional and dystrophic EB that depends on the wound area and not on the EB type. In EB, itch mediators may be similar to other pruritic disorders.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.