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Polymorphous light eruption

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

INTRODUCTION

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".)

EPIDEMIOLOGY

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 [3]. 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].

PATHOGENESIS

Both ultraviolet A (UVA) and ultraviolet B (UVB) radiation, and occasionally visible light, have been implicated in the development of polymorphous light eruption (PMLE) [7]. In most studies, a higher proportion of patients develops the disease in response to UVA than UVB [2]. 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 [8]. PMLE occurring after exposure to UVC radiation generated from welding arcs has been reported [9]. (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 [10]. 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 [12]. 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 [13].

                

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Literature review current through: Nov 2016. | This topic last updated: Mon Sep 21 00:00:00 GMT+00:00 2015.
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