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Photosensitivity
is a poorly understood cutaneous reaction to sunlight probably involving
the immune system. It may be idiopathic or occur after exposure
to certain drugs or chemicals, and it is sometimes a feature of
systemic diseases (eg, SLE, porphyria, pellagra, xeroderma pigmentosum).
Diagnosis is clinical. Treatment varies by type.
In addition to the acute and chronic effects of sunlight, a variety of unusual reactions may occur soon after only a brief sun exposure. Unless the cause is obvious, patients with pronounced photosensitivity should be evaluated for systemic or cutaneous disorders associated with light sensitivity such as SLE (see Autoimmune Rheumatic Disorders: Systemic Lupus Erythematosus (SLE)) and porphyria (see Porphyrias). Treatment for chemical photosensitivity is topical corticosteroids and avoidance of the causative substance.
Solar
urticaria:
In certain patients, urticaria develops at a site of sun exposure within a few minutes. Rarely, if large areas are involved, syncope, dizziness, wheezing, and other systemic symptoms may develop. Etiology is unclear but may involve endogenous skin constituents functioning as photoallergens, leading to mast cell degranulation as in other types of urticaria. Solar urticaria can be distinguished from other types of urticaria in that wheals in solar urticaria occur only on exposed skin after ultraviolet (UV) light exposure. Solar urticaria can be classified based on the component of the UV spectrum (UVA, UVB, and visible light) that produces them. Treatment can be difficult and may include H1 blockers, antimalarial drugs, topical corticosteroids, sunscreens, and psoralen UV light (PUVA). The wheals of solar urticaria usually last just minutes to hours, but the disorder is chronic and can wax and wane over years.
Chemical
photosensitivity:
Over 100 substances, ingested or applied topically, are known to predispose to cutaneous reactions following sun exposure. A limited number are responsible for most reactions (see Table 1: Reactions to Sunlight: Some Substances That Sensitize the Skin to Sunlight ). Reactions are divided into phototoxicity and photoallergy.
In phototoxicity, light-absorbing compounds directly generate free radicals and inflammatory mediators, causing tissue damage manifesting as pain and erythema (like sunburn). This reaction does not require prior sun exposure and can appear in any person, although reaction is highly variable. Typical causes of phototoxic reactions include topical (eg, perfumes, coal tar ) or ingested (eg, tetracyclines, psoralen-containing plants) agents. Phototoxic reactions do not generalize to non–sun-exposed skin.
Photoallergy is a type IV (cell-mediated) immune response; light absorption causes structural changes in the drug or substance, allowing it to bind to tissue protein and function as a hapten. Prior exposure is required. Typical causes of photoallergic reactions include aftershave lotions, sunscreens, and sulfonamides. Reaction may extend to non–sun-exposed skin. Symptoms include erythema, pruritus, and sometimes vesicles.
Polymorphous
light eruption:
These eruptions are unusual reactions to light that do not seem to be associated with systemic disease or drugs. Eruptions appear on sun-exposed areas, usually 30 min to several hours after exposure. Lesions are pruritic, erythematous, and often papular but may be papulovesicular or plaquelike. They are most common among women and people from northern climates when first exposed to spring or summer sun than among those exposed to sun year-round. Lesions subside within several days to 1 wk or so. Actinic prurigo is a similar (perhaps related) phenomenon with more nodular-appearing lesions that may persist year-round, worsening with sun exposure.
Diagnosis is made by history, skin findings, and exclusion of other sun-sensitivity disorders. Diagnosis sometimes requires reproduction of the lesions with artificial or natural sunlight when the patient is not using any potentially sensitizing drugs.
Often, lesions are self-limited and spontaneously improve as summer progresses. Treatment is by moderating sun exposure and applying topical corticosteroids. More severely affected patients may benefit from desensitization by graduated exposure to UV light with PUVA (see Psoriasis and Scaling Diseases: Light therapy) or narrow band UVB (312 nm) phototherapy. Those with disabling disease may require a course of oral immunosuppressive therapy such as prednisone , azathioprine , cyclosporine , or hydroxychloroquine .
Last full review/revision August 2007 by Robert J. MacNeal, MD
Content last modified August 2007
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