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.
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 | HSV, Mycoplasma | Drugs | Drugs |
| Lesions | Typical raised targets, acral | Flat atypical targets, macules, trunk | Confluent erythema, sheets of detachment |
| Detached skin | 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.
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.
Elsewhere in DurgiPedia
- CD8⁺ cytotoxic T cell
- Type IV hypersensitivity (delayed, T cells)
- Apoptosis: the intrinsic and extrinsic pathways
Connections
Microorganisms1
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 (MedlinePlus, US National Library of Medicine, 2025); Skin Conditions (MedlinePlus, US National Library of Medicine, 2025).
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Representative model, for educational purposes only.