ReviewJournal of the European Academy of Dermatology and Venereology : JEADV2020
Clinical and pathogenic aspects of the severe cutaneous adverse reaction epidermal necrolysis (EN).
Review in Journal of the European Academy of Dermatology and Venereology : JEADV, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 48 citations in OpenAlex.
- Trimethoprim/Sulfamethoxazole-Induced Systemic Toxic Epidermal Necrolysis Syndrome: A Case Report.Clinical case reports · 2026Article
- Rapid progression to toxic epidermal necrolysis following switch of PD-1 inhibitors: a case report.Frontiers in medicine · 2026Article
- Differential risk signals of cutaneous adverse drug reactions among β-lactam antibiotics: ceftriaxone shows increased signals for SJS/TEN in clinical and real-world cohorts.Frontiers in medicine · 2026Article
- Attribution of causality in Stevens-Johnson syndrome/toxic epidermal necrolysis.The ocular surface · 2025Review
- [Overview of clinical manifestations, diagnosis and management of acute allergic disorders].Dermatologie (Heidelberg, Germany) · 2025Review
- Predictive value of a severity-of-illness score for toxic epidermal necrolysis (SCORTEN) factors for in-hospital mortality in Stevens-Johnson syndrome/toxic epidermal necrolysis.Frontiers in medicine · 2025Article
- Exploring recent advances in drugs severe cutaneous adverse reactions immunopathology.Allergy · 2025Review
- [Stevens-Johnson syndrome].Dermatologie (Heidelberg, Germany) · 2024Article
- Tumor necrosis factor inhibitors enhance corticosteroid therapy for Stevens-Johnson syndrome and toxic epidermal necrolysis linked to immune checkpoint inhibitors: a prospective study.Frontiers in immunology · 2024Observational
- Immunological Mechanisms in Cutaneous Adverse Drug Reactions.Biomolecules & therapeutics · 2024Review
- Correlations between histopathologic findings, serum biomarker levels, and clinical outcomes in Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN).Scientific reports · 2023Article
- Post-acute phase and sequelae management of epidermal necrolysis: an international, multidisciplinary DELPHI-based consensus.Orphanet journal of rare diseases · 2023Article
- Multidisciplinary Treatment in Toxic Epidermal Necrolysis.International journal of environmental research and public health · 2023Review
- Adalimumab for Sintilimab-Induced Toxic Epidermal Necrolysis in a Patient with Metastatic Gastric Malignancy: A Case Report and Literature Review.Clinical, cosmetic and investigational dermatology · 2023Article
- Accuracy of SCORTEN in predicting mortality in toxic epidermal necrolysis.BMC medical informatics and decision making · 2022Article
- A Review of the Systemic Treatment of Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis.Biomedicines · 2022Review
- Associations ofFrontiers in pharmacology · 2022Article
- Current Perspectives on Severe Drug Eruption.Clinical reviews in allergy & immunology · 2021Review
- Clinical parameters and biological markers associated with acute severe ocular complications in Stevens-Johnson syndrome and toxic epidermal necrolysis.Scientific reports · 2021Article
- Eosinophils in skin diseases.Seminars in immunopathology · 2021Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The severe cutaneous adverse reaction epidermal necrolysis (EN) which includes toxic epidermal necrolysis and the milder Stevens-Johnson syndrome is characterized by epidermal loss due to massive keratinocyte apoptosis and/or necroptosis. EN is often caused by a drug mediating a specific TCR-HLA interaction via the (pro)hapten, pharmacological interaction or altered peptide loading mechanism involving a self-peptide presented by keratinocytes. (Memory) CD8 + T cells are activated and exhibit cytotoxicity against keratinocytes via the perforin/granzyme B and granulysin pathway and Fas/FasL interaction. Alternatively drug-induced annexin release by CD14 + monocytes can induce formyl peptide receptor 1 death of keratinocytes by necroptosis. Subsequent keratinocyte death stimulates local inflammation, activating other immune cells producing pro-inflammatory molecules and downregulating regulatory T cells. Widespread epidermal necrolysis and inflammation can induce life-threatening systemic effects, leading to high mortality rates. Research into genetic susceptibility aims to identify risk factors for eventual prevention of EN. Specific HLA class I alleles show the strongest association with EN, but risk variants have also been identified in genes involved in drug metabolism, cellular drug uptake, peptide presentation and function of CD8 + T cells and other immune cells involved in cytotoxic responses. After the acute phase of EN, long-term symptoms can remain or arise mainly affecting the skin and eyes. Mucosal sequelae are characterized by occlusions and strictures due to adherence of denuded surfaces and fibrosis following mucosal inflammation. In addition, systemic pathology can cause acute and chronic hepatic and renal symptoms. EN has a large psychological impact and strongly affects health-related quality of life among EN survivors.
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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.