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EN is often caused by a drug mediating a specific TCR\u2010HLA interaction via the (pro)hapten, pharmacological interaction or altered peptide loading mechanism involving a self\u2010peptide presented by keratinocytes. (Memory) CD8\u00a0+\u00a0T cells are activated and exhibit cytotoxicity against keratinocytes via the perforin\/granzyme B and granulysin pathway and Fas\/FasL interaction. Alternatively drug\u2010induced annexin release by CD14\u00a0+\u00a0monocytes can induce formyl peptide receptor 1 death of keratinocytes by necroptosis. Subsequent keratinocyte death stimulates local inflammation, activating other immune cells producing pro\u2010inflammatory molecules and downregulating regulatory T cells. Widespread epidermal necrolysis and inflammation can induce life\u2010threatening 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\u00a0+\u00a0T cells and other immune cells involved in cytotoxic responses. After the acute phase of EN, long\u2010term 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\u2010related quality of life among EN survivors.<\/jats:p>","DOI":"10.1111\/jdv.16339","type":"journal-article","created":{"date-parts":[[2020,3,12]],"date-time":"2020-03-12T14:26:30Z","timestamp":1584023190000},"page":"1957-1971","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":46,"title":["Clinical and pathogenic aspects of the severe cutaneous adverse reaction epidermal necrolysis (EN)"],"prefix":"10.1111","volume":"34","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0243-7826","authenticated-orcid":false,"given":"E.C.","family":"Kuijper","sequence":"first","affiliation":[{"name":"Department of Dermatology Leiden University Medical Centre Leiden The 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