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PhotodermatosisCommonICD-10 L56.4

Polymorphic light eruption

PMLE · PLE · polymorphous light eruption · benign summer light eruption · juvenile spring eruption (variant)

Polymorphic light eruption is the commonest idiopathic photodermatosis in the UK, affecting up to 15-20% of pale-skinned adults. It is characterised by a delayed (hours to days) pruritic papular, vesicular or plaque-like eruption on sun-exposed skin within 24-48 hours of UV (mostly UV-A) exposure, particularly in spring / early summer. It is a major DDx for lupus, photoaggravated dermatoses, drug-induced photosensitivity and lentigo maligna in older patients with persistent photo-distributed pigmentation.

CurrentLast reviewed 16 May 2026

Pathogenesis

  • Delayed type-IV-like hypersensitivity to a photo-induced antigen.
  • UV-A (320-400 nm) primary; some UV-B contribution.
  • Genetic susceptibility: increased frequency in Northern European populations.
  • Female > male (3:1); peak 20-40 years; often improves with age.
  • Mechanism: failure of the immunosuppression-of-sun-exposed-skin that protects most individuals from PLE-like reactions.

Clinical features

  • Onset hours to 2 days after first significant sun exposure of spring / early summer.
  • Distribution: sun-exposed sites — usually V of neck, dorsal arms, forearms, dorsal hands; spares habitually-exposed face / hands.
  • Lesion morphology monomorphic within an individual but variable between patients ("polymorphic" between patients):
    • Itchy erythematous papules (most common).
    • Vesicles / vesiculobullae.
    • Plaques.
    • Erythema multiforme-like (rare).
  • Improves within 7-10 days of further sun avoidance / minimal exposure.
  • Phenomenon of "hardening" — repeated low-grade sun exposure improves tolerance, hence improvement with summer-long exposure.
  • Juvenile spring eruption: variant on ears in children.
  • Actinic prurigo: distinct entity in Native American populations; chronic, scarring.

Differentials

  • Lupus erythematosus (SCLE, ACLE) — photo-distributed; persistent; ANA / Ro / La positive.
  • Phototoxic drug eruption — drug history (thiazides, amiodarone, fluoroquinolones, NSAIDs, tetracyclines, retinoids).
  • Photoallergic dermatitis — contact + UV; patch / photo-patch testing.
  • Solar urticaria — wheals appear within minutes; resolves <1 hour.
  • Erythropoietic protoporphyria, porphyria cutanea tarda — chronic photosensitivity.
  • Chronic actinic dermatitis — elderly; chronic; sun-exposed eczematised plaques.
  • Hydroa vacciniforme — childhood; vesicular; scarring.
  • Phytophotodermatitis — streaky linear pattern.
  • Lentigo maligna — persistent pigmented patch in older patient (biopsy if unsure).

Investigations

  • Clinical diagnosis usually adequate.
  • Skin biopsy in atypical / chronic / persistent cases: non-specific superficial / deep perivascular lymphocytic infiltrate, dermal oedema.
  • Provocation phototesting: confirm by exposure of unaffected skin to MED (minimal erythema dose) UV-A / UV-B in specialist photobiology unit.
  • Photo-patch testing: if photoallergic contact dermatitis suspected.
  • Bloods: ANA, ENA (Ro / La), dsDNA, complement, FBC, LFT to exclude lupus.
  • Porphyrin screen if porphyria suspected.
  • Drug history.

Management

  • Photoprotection:
    • Broad-spectrum (UV-A + UV-B) high-SPF 50 mineral sunscreen.
    • UV-protective clothing, wide-brimmed hat.
    • Avoid intense midday sun (10:00-15:00).
  • Hardening / desensitisation:
    • Gradual incremental sun exposure from early spring.
    • Prophylactic narrowband UVB / PUVA in late winter / early spring (specialist) — induces tolerance.
  • Acute eruption:
    • Cool compresses, calamine.
    • Mid-potency topical corticosteroids for 3-5 days.
    • Sedating antihistamines for itch.
    • Short course of oral prednisolone (20-30 mg / day, 3-5 days) for severe attack.
  • Refractory / severe:
    • Hydroxychloroquine 400 mg OD spring / summer.
    • Polypodium leucotomos extract — oral antioxidant supplement; some RCT evidence.
    • Nicotinamide.
    • Azathioprine, ciclosporin in extreme cases.
  • Counsel:
    • Often spontaneous improvement with age.
    • Hardening makes summer better than spring.
    • Vitamin D supplementation given strict photoprotection.

References

  1. Honigsmann H. Polymorphous light eruption. Photodermatol Photoimmunol Photomed. 2008;24:155-161.
  2. Gruber-Wackernagel A et al. Polymorphic light eruption: clinic, pathogenesis, and treatment. Dermatol Clin. 2014;32:315-334.
  3. Lehmann P, Schwarz T. Photodermatoses: diagnosis and treatment. Dtsch Arztebl Int. 2011;108:135-141.
  4. British Association of Dermatologists. Polymorphic light eruption — patient information leaflet. London: BAD; 2024.

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