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1 Introduction

Polymorphous light eruption (PMLE) is the most common of the immunologically mediated (formerly categorized as idiopathic) photodermatoses. The prevalence of PMLE ranges from 10 to 20 %, depending on the geographic location [1]. Onset is typically within the first three decades of life [2–5]. Females are two to three times more affected than males [2–5].

2 Clinical Features

PMLE lesions can present as non-scarring, erythematous, pruritic papules, vesicles, papulovesicles, plaques, or nodules [1]. Pinpoint variant of PMLE is the most common morphology seen in individuals with skin phototypes IV–VI (Figs. 47.1 and 47.2) [3]. Pinpoint PMLE is characterized by the development of pinpoint papules, 1–2 mm, on sun-exposed areas minutes or hours after ultraviolet radiation [6]. PMLE has a predilection for the arms, forearms, hands, head, and neck region.

Fig. 47.1
figure 1

Pinpoint papules due to PMLE located on the cheek and perioral skin in an African American male (Photograph reprinted with written permission from the Journal of Drugs in Dermatology)

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Fig. 47.2
figure 2

Pinpoint papules due to PMLE on the cheek of an African American male (Photograph reprinted with written permission from the Journal of Drugs in Dermatology)

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3 Natural History and Prognosis

PMLE lesions present hours to days after ultraviolet (UV) light exposure. The lesions and usually last over 1–7 days and completely resolve without scarring [3]. PMLE typically begins in the spring, improving by late summer with “hardening” due to increased tolerance of the skin [4]. These patients have decreased ability to be locally suppressed upon exposure to UV, which explains the “hardening” response seen clinically [5].

4 Histopathological Features

Histology of the skin lesion is considered nonspecific, revealing superficial and deep dermal inflammatory cell infiltrates [1]. Variable epidermal changes can occur that range from mild spongiosis to acanthosis [1].

5 Diagnosis and Differential Diagnosis

Diagnosis of PMLE is typically made through history, morphology of lesions, and clinical course; phototesting and photopatch testing are not routinely performed [6]. Selected laboratory examinations such as antinuclear antibody (ANA), anti-Ro (SSA), anti-La (SSB), plasma porphyrin levels, and in some cases biopsy of persistent lesions may assist in making the diagnosis [2]. Differential diagnoses include, but are not limited to, systemic lupus erythematosus, eczema, erythropoietic protoporphyria, solar urticaria, and actinic prurigo.

6 Treatment

Prevention is essential with sun avoidance, utilization of broad spectrum sunscreen, and photoprotective clothing [7]. Additionally, light tolerance or “hardening” can be accelerated using narrowband UVB phototherapy or, less commonly, psoralen plus UVA (PUVA) before the sunny period of the year [7]. Other treatment modalities include topical corticosteroids and antimalarials. Systemic corticosteroids may rarely be required in the setting of acute exacerbation of the disease or during a brief winter vacation to a sunny locale [8].