History and exam

Key diagnostic factors

common

recurrent history of lesions following ultraviolet radiation exposure

Occurs annually after the first intensive ultraviolet radiation exposure of the year.

young women and adolescents

PLE is more common in these population groups.[1]​​

family history of PLE

There is a positive famiy history of the condition in about 50% of patients.[15][16]

severe itching

Clinical signs include severe itching.

reduced symptoms over the course of a year

Typical course of disease follows a natural hardening (habituation) over the year, with repetitive sun exposure.

erythematous patches

In sun-exposed areas.

Skin changes last several days and remission occurs spontaneously without leaving any permanent skin changes.

papules

In sun-exposed areas.

Skin changes last several days and remission occurs spontaneously without leaving any permanent skin changes.

plaques

In sun-exposed areas.

Skin changes last several days and remission occurs spontaneously without leaving any permanent skin changes.

vesicles

In sun-exposed areas.

Skin changes last several days and remission occurs spontaneously without leaving any permanent skin changes.

Risk factors

strong

ultraviolet A exposure

Ultraviolet A (UV-A) plays a prominent role in eliciting the symptoms of PLE, by virtue of the fact that PLE symptoms develop after ultraviolet radiation exposure through glass (which only UV-A wavelengths will penetrate), and historically PLE symptoms often appeared despite the use of SPF sunscreens (which only contain ultraviolet B [UV-B] filters).[10][25]

oxidative stress/reactive oxygen species

Triggered by both UV-A and to some extent UV-B exposure, reactive oxygen species are generated by excitation of cellular chromophores within skin. This leads to the induction of proinflammatory molecules, such as interleukins and intercellular adhesion molecules implicated in PLE.[50][51]

family history of PLE

A positive family history is present in up to 50% of cases.[17]

Genetic differences occur in the regulation of specific transcription factors such as AP-2, which are involved in the regulation of oxidative stress responses in human skin, and thus also in the elicitation of PLE.[30]

weak

female sex

Women are more commonly affected by PLE.[1]​​

Estrogens inhibit the release of interleukin-10 (IL-10) from keratinocytes and thus interfere with ultraviolet radiation-induced immunosuppression.[36]

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