Polymorphous light eruption
- Craig A Elmets, MD
Craig A Elmets, MD
- Section Editor — Photodermatology
- Professor and Chair of Dermatology
- University of Alabama at Birmingham
- Section Editors
- Robert P Dellavalle, MD, PhD, MSPH
Robert P Dellavalle, MD, PhD, MSPH
- Section Editor — Dermatology
- Professor of Dermatology and Public Health
- Denver VA Medical Center, University of Colorado School of Medicine and Colorado School of Public Health
- Jeffrey Callen, MD, FACP, FAAD
Jeffrey Callen, MD, FACP, FAAD
- Editor-in-Chief — Dermatology
- Section Editor — Skin and Systemic Disease
- Professor of Medicine
- University of Louisville School of Medicine
Polymorphous light eruption (PMLE) is the most common idiopathic photodermatosis; it is sometimes called "sun poisoning" or "sun allergy." PMLE usually presents as a pruritic rash in sun-exposed areas hours to days after sun exposure and persists for several days before subsiding. Juvenile spring eruption is a variant of PMLE. (See 'Juvenile spring eruption (PMLE variant)' below.)
An overview of cutaneous photosensitivity and a review of other photodermatoses are presented separately. (See "Overview of cutaneous photosensitivity: Photobiology, patient evaluation, and photoprotection" and "Photosensitivity disorders (photodermatoses): Clinical manifestations, diagnosis, and treatment".)
The onset of polymorphous light eruption (PMLE) typically occurs within the first three decades of life, and a female preponderance is reported [1,2]. Fair-skinned individuals are the most commonly affected, although PMLE can develop in individuals of all ethnicities and skin types . It occurs more frequently in temperate areas. Several studies have indicated that the prevalence of PMLE is directly related to the latitude, ranging from 1 percent in Singapore to 20 percent in Sweden [1,2,4-6].
Both ultraviolet A (UVA) and ultraviolet B (UVB) radiation, and occasionally visible light, have been implicated in the development of polymorphous light eruption (PMLE) . In most studies, a higher proportion of patients develops the disease in response to UVA than UVB . The eruption may be influenced by the dose and frequency of the UV radiation as well as by the extent and site of irradiated skin . PMLE occurring after exposure to UVC radiation generated from welding arcs has been reported . (See "Overview of cutaneous photosensitivity: Photobiology, patient evaluation, and photoprotection", section on 'Phototesting'.)
Patients with PMLE appear to have a genetic susceptibility, as evidenced by increased concordance in monozygotic twins . In addition, a positive family history is present in 15 to 46 percent of cases [4,11]. Genetic modeling of PMLE in families with photosensitivity disorders suggests a dominant mode of inheritance with low penetrance . No gene locus has been associated with PMLE. Candidate gene analysis has been inconclusive despite investigating IL-10, FCGR2A, SELE, ICAM-1, IL1-alpha, IL1-beta, IL1RN, and TNF-alpha .
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- CLINICAL MANIFESTATIONS
- Skin hardening effect
- Differential diagnosis
- Preventive measures
- - Sun protection
- - Systemic photoprotection
- - Photohardening
- - Other
- - Patients with mild to moderate eruption
- - Patients with severe eruption
- JUVENILE SPRING ERUPTION (PMLE VARIANT)
- SUMMARY AND RECOMMENDATIONS