External Agents

Most topical photosensitizers produce photoallergic reactions with at least some element of phototoxicity as well.

Photoallergy is difficult to confirm without photopatch testing (see Iableiii30:1). Soap photoallergy (Fig.,,30-4) is less common now than it once was, because halogenated salicylanilides were removed from the market. Ihe fragrance musk ambrette has become an important cause of photoallergic dermatitis.

Clinically, photoallergic contact dermatitis appears eczematous, whereas acute phototoxic contact dermatitis is edematous or bullous. Erythema is common to both. Occasionally, photoallergy lingers for months or even years without further exposure to the allergen ("persistent light reactor").

Topical phototoxic agents include tars and psoralens. Psoralens are found in many plants and a few colognes. Acute phototoxic dermatitis typically is followed by striking hyperpigmentation with bizarre configurations ( e.g., berlock dermatitis [see Fig 2.4.-5] and phytophotodermatitis). Phytophoto-dermatitis is due to oils from plants such as lime, celery, parsnip, corn, parsley, buttercup, and carrot.

Actinic reticuloid resembles the persistent light reactor state but gives different phototest results (see Tabje 30Z1.) and resembles cutaneous lymphoma histologically. TREATMENT

1. The patient should avoid sunlight (even glass-filtered sunlight) and strong fluorescent lighting, if possible. Topical sunscreens as a rule are only partially effective, especially in chronic cases. The patient should select a sunscreen with the highest SPF that does not irritate, preferably one that also screens out ultraviolet A. Many sunscreens contain PABA or PABA ester (padimate). It should be noted that PABA itself occasionally causes photoallergic reactions.

2. Topical corticosteroids may give some symptomatic relief, and, if severe, systemic corticosteroids may be necessary.

3. The patient should avoid further exposure to the photosensitizer.

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