Photodermatoses are skin diseases that are precipitated or aggravated by exposure to sunlight. They may be precipitated by one or a combination of different wavelengths of light: ultraviolet A (UVA 320–400 nm), UVB (290–320 nm) and visible light (400–750 nm). Photodermatoses can be idiopathic, inherited or secondary to other causes (Table 40.1). They affect exposed skin such as the face, anterior neck, upper chest wall, dorsum of the hands; photoprotected skin including behind the ears is usually spared (Table 40.2).

The onset of the rash following light exposure can be immediate or delayed. Patients with immediate photosensitivity usually present with an urticarial rash. Patients with delayed photosensitivity present with blistering, papules, increased freckling and/or eczematous rash.

Certain inflammatory skin diseases can be exacerbated by sunlight (e.g. rosacea, cutaneous discoid lupus erythematosus) or improved with sunlight (e.g. psoriasis).

Individuals with severe photodermatoses may develop vitamin D insufficiency or deficiency as a result of decreased sunlight exposure.

Polymorphic Light Eruption (Figure 40.2)

Polymorphic light eruption (PLE) is one of the most common photodermatoses, usually occurring at the beginning of spring and resolving by autumn. Itchy erythematous papules, plaques and vesicles on exposed skin appear about 1 day following exposure to bright sunlight.

Treatment includes sun protection (clothing, broad spectrum sunscreen) and moderately potent topical corticosteroids. Severe cases benefit from a 1-week course of oral prednisolone 20 mg/day at the onset of the rash. Narrowband UVB or psoralen plus UVA (PUVA) treatment at the beginning of spring can desensitise and ‘harden’ the skin to decrease the severity of PLE.