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Chapter 91. Abnormal Responses to Ultraviolet Radiation: Idiopathic, Probably Immunologic, and Photoexacerbated

Travis W. Vandergriff; Paul R. Bergstresser

Abnormal responses to ultraviolet radiation (UVR) exposure divide into four categories (Table 91-1): (1) acquired idiopathic, presumed immunologic; (2) DNA repair defect disorders; (3) chemical and drug photosensitivity, including the porphyrias; and (4) photoexacerbated dermatoses not caused directly by UVR. The first and last categories and an approach to assessing photosensitivity are covered in this chapter. The other categories are covered in other chapters in this book. Diagnosis of photodistributed eruptions is discussed in Box 91-1 and Figure 91-1, and the entities are discussed in the following sections.

Table 91-1 Abnormal Responses to Ultraviolet Irradiation
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Table 91-1 Abnormal Responses to Ultraviolet Irradiation
  • Acquired idiopathic, presumed immunologic photodermatoses
  • Polymorphic light eruption
  • Actinic prurigo
  • Hydroa vacciniforme
  • Chronic actinic dermatitis
  • Solar urticaria
  • DNA repair defect disorders
  • Xeroderma pigmentosum
  • Cockayne syndrome
  • Trichothiodystrophy
  • Bloom syndrome
  • Rothmund–Thomson syndrome (probable)
  • Chemical and drug photosensitivities
  • Exogenous
  • Systemic
  • Topical
  • Endogenous
  • The porphyrias
  • Photoexacerbated dermatoses
Box 91-1 Differential Diagnosis of Polymorphic Light Eruption
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Box 91-1 Differential Diagnosis of Polymorphic Light Eruption
  • USUAL ACUTE FORM
    • Photoexacerbated dermatoses such as atopic or seborrheic dermatitis or acne
    • Solar urticaria
    • Erythropoietic protoporphyria
    • Xeroderma pigmentosum
  • RARE PERSISTENT FORM
    • Jessner lymphocytic infiltrate
Figure 91-1
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Diagnostic algorithm for abnormal responses to ultraviolet radiation.

Polymorphic (Polymorphous) Light Eruption

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Polymorphic Light Eruption at a Glance
  • A common acquired sunlight-induced disorder typically presenting in the spring.
  • Clinical presentation: a pruritic, erythematous, symmetrically distributed, papulovesicular eruption, usually on exposed areas, within hours of exposure to ultraviolet radiation, most commonly sunlight, with full resolution in days to several weeks.
  • Histopathology: epidermal spongiosis with a superficial and deep dermal, perivascular, mainly mononuclear cell infiltrate and papillary dermal edema.
  • Genetics: most likely a genetically determined delayed-type hypersensitivity reaction against UVR-induced cutaneous antigen(s).
  • Therapy: responds to broad-spectrum sunscreen use, oral or topical steroids, and prophylactic low-dose immunosuppressive phototherapy.

Epidemiology

Polymorphic light eruption (PMLE) is common worldwide, but thought to occur more frequently in temperate latitudes and rarely in equatorial latitudes. However, a large-scale cross-sectional study has revealed no latitudinal gradient in Europe.1 This study estimated an overall suspected lifetime prevalence of 18% among Europeans. Previous reports indicate a prevalence of 10%–15% among North Americans2 and southern Britons,3 and 5% among southern Australians.3 Women are affected more than twice as frequently as men.1 Fitzpatrick skin type also influences the risk of developing PMLE, with the highest prevalence in people with skin type I and the lowest prevalence in people with skin type IV or higher.1

Etiology and Pathogenesis

A delayed-type hypersensitivity (DTH) response to a sunlight-induced cutaneous photoantigen was first suggested as the cause of PMLE in 1942, based on the delay ...

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