Clinical presentation

This is the commonest photodermatosis, and women are affected twice as frequently as men. Pruritic urticated papules, plaques and vesicles develop on light-exposed skin usually about 24 h after sun or artificial ultraviolet (UV) exposure (Fig. 1). It starts in the spring and may persist throughout the summer. The degree of severity is variable.

Fig. 1 Polymorphic light eruption affecting the lower legs.

Differential diagnosis and management

Photoallergic contact dermatitis, drug-induced photosensitivity and lupus erythematosus may need to be considered in the diagnosis of polymorphic light eruption.

The first-line therapy is to use sunscreens and protective measures. A short course of UV therapy (UVB or PUVA) in the late spring can ‘harden’ the skin so that the patient is able to have a disease-free summer.

Clinical presentation

There is often a long history of a chronic dermatitis that evolves into a photodermatitis, or a photoallergic contact dermatitis may have been present from the outset. Lichenified plaques of chronic dermatitis form on light-exposed sites and beyond, and are worse in the summer, although the eruption tends to become perennial (Fig. 2). The patients are sensitive to the UVA and UVB wavelengths and often to visible light as well. They may also have a contact or photocontact sensitivity to plant sesquiterpene lactones (airborne allergens) or to cosmetic ingredients, although the contribution of this to the overall picture is unclear.

Fig. 2 Chronic actinic dermatitis involving the light-exposed areas of the face.

Differential diagnosis and management

Airborne contact dermatitis or drug-induced photosensitivity may need to be considered, but there is normally little doubt about the diagnosis. Phototesting is helpful.

Light avoidance, sunscreens and topical steroids are used at first in the management of chronic actinic dermatitis. Subsequently, azathioprine, ciclosporin, mycophenolate or systemic steroids may be necessary.

Porphyrias

Porphyrins are important in the formation of haemoglobin, myoglobin and cytochromes. The porphyrias are rare, mostly inherited, metabolic disorders in which deficiencies of enzymes in the porphyrin biosynthetic pathway lead to accumulations of intermediate metabolites (p. 84). The metabolites are detectable in the urine, faeces and blood, are toxic to the nervous system and cause photosensitivity in the skin.

The main cutaneous porphyrias are the following:

Fig. 3 Porphyria cutanea tarda.

Changes can be seen on the dorsal aspects of the hands.

Pellagra

Dietary deficiency of vitamin B3 (nicotinic acid) may give a photosensitive dermatitis in association with diarrhoea and dementia.

Drug induced

Several drugs may produce an eruption in light-exposed areas by either toxic (dose-dependent) or allergic mechanisms. The morphology may be eczematous, blistering (e.g. griseofulvin, p. 17), pigmented (e.g. amiodarone, p. 86) or an exaggerated sunburn reaction. Rarely, photo-onycholysis can occur (e.g. with tetracycline). Common photosensitizing drugs are shown in Box 1.

Topically applied chemicals

The commonest topical photosensitizers (i.e. allergens) are sunscreen agents (e.g. benzophenones), non-steroidal anti-inflammatory drugs (NSAIDs), coal tar derivatives and fragrances. Topical phototoxicity (with an irritant mechanism) is usually due to plant-derived psoralens, as found, for example, in carrot, celery, fennel, parsnip, common rue and giant hogweed. Phytophotodermatitis describes a photocontact dermatitis that results from the local photosensitization of the skin through contact with psoralens from a plant (Fig. 4). In Berloque dermatitis, streaky pigmentation, often on the sides of the neck, results from the application of perfumes containing psoralens, usually oil of Bergamot (p. 107).

Fig. 4 Phytophotodermatitis to common rue.

The patient had been gathering the plant in the bright sunlight and developed an extreme bullous reaction. The mechanism is toxic, i.e. irritant, rather than allergic.