Polymorphic light eruption is the most common photodermatosis with a female preponderance typically presenting in the spring.
Clinical presentation: A pruritic, erythematous, symmetrically distributed, eruption of variable interindividual morphology (in most cases papular) on sun-exposed skin areas, within hours to days of exposure, with full resolution in several days.
Histopathology: Epidermal spongiosis with a superficial and deep dermal, perivascular, mixed-cell infiltrate and papillary dermal edema.
Etiology and Pathogenesis: A resistance to ultraviolet (UV)-induced immune suppression with subsequent delayed-type hypersensitivity reaction against UV-induced antigen(s).
Prevention and Therapy: Responds to broad-spectrum sunscreen use, oral or topical steroids, and prophylactic low-dose immunosuppressive phototherapy.
Polymorphic light eruption (PMLE) is the most common photodermatosis, with a high prevalence, particularly among young women, in temperate climates. As the name of the condition implies, itchy lesions of variable morphology appear on sun-exposed skin after the first exposure to an intense dose of sunlight in spring or early summer. The exact etiology and pathogenesis of PMLE is unknown, but a resistance to ultraviolet (UV)-induced immune suppression (a physiologic phenomenon in healthy individuals) and a subsequent immune reaction to UV-modified elements in the skin are suggested.
Clinical symptoms of PMLE were first described under the term of Prurigo aestivalis in 1888 by Hutchinson.1,2 In 1942, Epstein suggested a photoallergic pathophysiology for photodermatoses.2 In 1984, Moncada and colleagues found a predominance of T-helper (Th) cells and cells expressing high levels of Ia antigens in the dermal cell infiltrate of PMLE, suggesting that an abnormal immune response is responsible for the pathophysiology of the disease.3 Consistently, histologic features with an early influx of CD4+ T lymphocytes, followed by CD8+ T cells in established lesions, were described in PMLE by Norris and colleagues, pointing to a cellular-mediated immune response.4
PMLE has a wide geographic distribution, but is described as being seen more frequently in temperate latitudes and rarely in equatorial latitudes. The incidence rate of PMLE in the United Kingdom has been described as being approximately 15%, compared with less than 5% in Australia.5 However, a recent large-scale cross-sectional study with individuals residing from the Mediterranean to Scandinavia found no correlation between PMLE incidence and increasing latitude, with an average prevalence of PMLE in 18% of Europeans.6 PMLE occurs in all skin types and racial groups.7,8 Similar to many autoimmune disorders PMLE usually has its onset within the first 3 decades of life and affects females approximately 4 times more often than males.8-10 Symptoms also may begin in early childhood or late adulthood, but onset during childhood is less commonly seen in PMLE than for instance in other photodermatoses like actinic prurigo.7 Fitzpatrick skin type is described to influence the risk of developing PMLE. In a pan-European study of PMLE patients with skin types I ...