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Polymorphous light eruption

Craig A Elmets, MD
Section Editors
Robert P Dellavalle, MD, PhD, MSPH
Jeffrey Callen, MD, FACP, FAAD
Deputy Editor
Rosamaria Corona, MD, DSc


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 [1]. 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 [4]. 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 [8].


Both ultraviolet A (UVA) and ultraviolet B (UVB) radiation, and occasionally visible light, have been implicated in the development of polymorphous light eruption (PMLE) [9]. In most studies, a higher proportion of patients develops the disease in response to UVA than UVB [3]. 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 [10]. PMLE occurring after exposure to ultraviolet C radiation generated from welding arcs has been reported [11]. (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 [12]. 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 [14]. A case-control study found a negative association with the GSTP1 allele of glutathione-S-transferase [15], but a subsequent study was unable to confirm this finding [16]. 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 [17].


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Literature review current through: Jul 2017. | This topic last updated: Jul 10, 2017.
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