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 — General Dermatology
- Professor of Dermatology and Public Health
- University of Colorado School of Medicine
- Colorado School of Public Health
- Chief, Dermatology Service
- US Department of Veterans Affairs
- Eastern Colorado Health Care System
- 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 [2,3]. 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 [2,3,5-7]. However, within Europe, a latitude gradient has not been shown to occur .
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 ultraviolet C 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 [5,13]. Genetic modeling of PMLE in families with photosensitivity disorders suggests a dominant mode of inheritance with low penetrance . A case-control study found a negative association with the GSTP1 allele of glutathione-S-transferase , but a subsequent study was unable to confirm this finding . Candidate gene analysis of interleukin (IL)-10, Fc fragment of IgG receptor (FCGR2A), selectin-E (SELE), intercellular adhesion molecule-1 (ICAM1), IL1A, IL1B, IL1RN, and tumor necrosis factor (TNF)-alpha has been inconclusive .To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
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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