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# Erythema multiforme, Stevens–Johnson syndrome and TEN

- Lesion

Target spots after a herpes flare are usually erythema multiforme. Skin peeling off after a new drug is Stevens-Johnson or TEN, an emergency.

Updated Nov 12, 2026

## Key points

- Erythema multiforme: target lesions (three zones), acral, often after HSV (also Mycoplasma); minor (little mucosa) and major (mucosa involved).
- SJS and TEN: usually drugs (sulfonamides, anticonvulsants such as carbamazepine, lamotrigine, allopurinol, NSAIDs); fever, mucosal erosions, Nikolsky sign.
- Spectrum by detached skin: SJS under one tenth of body surface, overlap in between, TEN over three tenths.
- Mechanism: drug-specific CD8 T cells and NK cells; granulysin, perforin and Fas ligand kill keratinocytes.
- HLA-B*15:02 and carbamazepine (South-East Asian ancestry), HLA-B*58:01 and allopurinol.
- Histology: interface dermatitis with apoptotic keratinocytes; full-thickness epidermal necrosis in TEN, with sparse inflammation.

## What it is

Erythema multiforme is an uncommon, self-limited hypersensitivity reaction, most often to herpes simplex virus, in which cytotoxic T cells attack keratinocytes and produce target lesions. Stevens-Johnson syndrome and toxic epidermal necrolysis are a separate, drug-induced spectrum of extensive keratinocyte death with mucosal involvement, defined by how much body surface detaches. All share an interface pattern with apoptotic keratinocytes.

## Structure

- Superficial perivascular lymphocytic infiltrate with basal vacuolisation and scattered apoptotic (dyskeratotic) keratinocytes.
- Lymphocytes in the epidermis next to dying keratinocytes (satellite cell necrosis).
- TEN: confluent necrosis of the full epidermis, subepidermal split, little dermal inflammation.
- Frozen section of the blister roof separates TEN from staphylococcal scalded skin syndrome (subcorneal split).

## EM vs SJS vs TEN

| Feature | Erythema multiforme | SJS | TEN |
| --- | --- | --- | --- |
| [Usual trigger](https://durgical.com/en/conditions/erythema-multiforme/) | HSV, Mycoplasma | Drugs | Drugs |
| [Lesions](https://durgical.com/en/conditions/stevens-johnson-syndrome-and-toxic-epidermal-necrolysis/) | Typical raised targets, acral | Flat atypical targets, macules, trunk | Confluent erythema, sheets of detachment |
| [Detached skin](https://durgical.com/en/conditions/stevens-johnson-syndrome-and-toxic-epidermal-necrolysis/) | Minimal | Small fraction | Large fraction |
| Mucosa | Mild or absent (major: present) | Severe | Severe |
| Mortality | Very low | Significant | High |

## Clinical notes

- SJS and TEN are managed like extensive burns: stop the drug, burn unit, eye care.
- Late complications: scarring of the eyes (blindness), mouth, genitals and oesophagus.

## Memory aid

EM is a bullseye painted by herpes; SJS and TEN are the drug's fire, measured by how much skin burns off.

## Test yourself

Think of the answer, then tap the question to see it.

## What is the most common trigger of erythema multiforme?

Herpes simplex virus infection.

## How are SJS and TEN distinguished?

By the percentage of body surface area with epidermal detachment: SJS involves a small fraction, TEN a large fraction, with an overlap category in between.

## Which cells kill keratinocytes in SJS and TEN?

Drug-specific CD8 cytotoxic T cells and NK cells, using granulysin, perforin, granzyme and Fas ligand.

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## Elsewhere in DurgiPedia

- [CD8⁺ cytotoxic T cell](https://durgical.com/en/immunology/cd8-cytotoxic-t-cell/)
- [Type IV hypersensitivity (delayed, T cells)](https://durgical.com/en/immunology/type-iv-hypersensitivity/)
- [Apoptosis: the intrinsic and extrinsic pathways](https://durgical.com/en/general-pathology/apoptosis-the-intrinsic-and-extrinsic-pathways/)

## Connections

## Related 4

- [Lichen planus and interface dermatitis](https://durgical.com/en/general-pathology/lichen-planus-and-interface-dermatitis/)
- [Pemphigus](https://durgical.com/en/general-pathology/pemphigus/)
- [Apoptosis: the intrinsic and extrinsic pathways](https://durgical.com/en/general-pathology/apoptosis-the-intrinsic-and-extrinsic-pathways/)
- [Injury by therapeutic drugs: the classic examples](https://durgical.com/en/general-pathology/injury-by-therapeutic-drugs-the-classic-examples/)

## Related conditions 4

- [Erythema multiforme](https://durgical.com/en/conditions/erythema-multiforme/)
- [Stevens–Johnson syndrome and toxic epidermal necrolysis](https://durgical.com/en/conditions/stevens-johnson-syndrome-and-toxic-epidermal-necrolysis/)
- [Cutaneous drug reactions and DRESS](https://durgical.com/en/conditions/cutaneous-drug-reactions-and-dress/)
- [Genital herpes (herpes simplex infection)](https://durgical.com/en/conditions/genital-herpes/)

## Microorganisms 1

- [Herpes simplex virus 1](https://durgical.com/en/microbiology/herpes-simplex-virus-1/)

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Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Sources: [Blisters](https://medlineplus.gov/blisters.html) (MedlinePlus, US National Library of Medicine, 2025); [Skin Conditions](https://medlineplus.gov/skinconditions.html) (MedlinePlus, US National Library of Medicine, 2025).

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Representative model, for educational purposes only.

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Source: https://durgical.com/en/general-pathology/erythema-multiforme-stevens-johnson-syndrome-and-ten/
License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/general-pathology/erythema-multiforme-stevens-johnson-syndrome-and-ten/
