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Workup of a Rash from Sunlight

Q. An adult female patient of mine had a pruritic, papulovesicular rash on her arms, legs, and upper trunk that lasted a few days after a springtime weekend trip to the beach this year, and now the rash is recurring in any sun-exposed area when she spends time gardening. We initially discussed that the rash could be related to sunscreen, but the lesions actually seem to improve if she does use sunscreen - and she has never had this on her face, where she applies sunscreen-containing moisturizer daily. (She also wears insect repellent when gardening, and I do not suspect these are insect bites.) The rash lasts for days, and does improve with topical steroids. How would I evaluate this patient for polymorphous light eruption?

A. The diagnosis of PMLE (polymorphous light eruption) is made clinically based on the history and typical morphology of the eruption. There are no diagnostic laboratory tests available for PMLE, although testing may be useful to rule out other systemic causes of photodermatosis such as photosensitive lupus or photoporphyria. In such cases, antinuclear antibody (ANA), anti-Ro (SS-A), and anti-La (SS-B) tests, as well as urine, stool, and blood porphyrin levels may be helpful. Skin biopsy may be helpful in some cases, although findings are characteristic but not diagnostic. Biopsy may, however be useful in excluding other diagnoses.

A brief discussion of characteristics, differential diagnosis, and treament of PLME is in order. A polymorphic light eruption is the most common photodermatosis. Characteristics include:

  • Typically presents with pruritic, (occasionally stinging), commonly symmetrical non-scarring, erythematous papules (most common), papulovesicles, or plaques. As the name implies, clinical manifestations of polymorphous light eruption (PMLE) vary. Different morphologies may appear, but, usually only one morphology dominates in a given individual. In African Americans, a variant of PMLE with pinpoint papules (1-2 mm) can be observed on sun-exposed areas, sparing the face and flexural surfaces.
  • It is light induced and occurs on sun-exposed skin (e.g., upper chest, arms).
  • The onset of the disease is sudden, occurring within hours to days of sun exposure and resolve completely over several days to a week without scarring. Symptoms are typically worse in the spring and early summer and decrease in severity as the summer progresses before disappearing completely in the winter.

Although most authorities now consider UV-A light as the causative factor, UV-B, or even visible light, have been implicated in the development of polymorphous light eruption (PMLE) eruption.

It is important to exclude other photodermatoses when diagnosing this condition. The differential diagnosis includes:

  • Photocontact dermatitis, which occurs 1-2 days after exposure to sun and an inciting agent in a sensitized individual (this can be diagnosed by a photo patch test).
  • Phototoxicity which occurs within hours of sun exposure and is characterized by a sunburned-like appearance which can occur with some medications (e.g. doxycycline)
  • Photosensitive rash in systemic lupus and cutaneous lupus erythematosus
  • Erythropoietic Protoporphyria
  • Juvenile spring eruption which occurs in children and young adults, typically affecting the helices of the ears
  • Actinic prurigo characterized by pruritic papulonodules, cheilitis, crusts, and lichenification, which can occur in both sun exposed and non-exposed areas often first appearing in childhood
  • Chronic actinic dermatitis, which usually occurs in older adults with a male to female predominance characterized by eczematous patches and lichenification in sun exposed areas frequently with palmoplantar involvement


  • Prophylactic therapy including avoiding sun exposure, wearing protective clothing and using sunscreen is the mainstay of therapy in PMLE. Sunscreens with high sun protection factor (SPF) values are not protective against UV-A–induced PMLE.
  • Prophylactic phototherapy or photo chemotherapy at the beginning of spring for several weeks may prevent flare-ups throughout the summer.
  • When preventive measures and light therapy fail, is ineffective or contraindicated, topical corticosteroids may be useful but not without risk. Antihistamines may help with pruritus. Systemic steroids may be needed to suppress acute flares or extensive generalized eruption.
  • Other therapies that have been tried are antimalarials, beta-carotene, nicotinamide, oral vitamin E supplementation (400 IU), azathioprine, and thalidomide.
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