Photosensitivity is a cutaneous reaction to sunlight 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 disorders (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 less common reactions may occur after 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 Systemic Lupus Erythematosus (SLE)) and porphyria (see Porphyrias).
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 causes them (and thus how such exposures could be subsequently prevented or minimized). If necessary, patients can be tested by exposing part of the skin to natural light or artificial light at particular wavelengths (phototesting). Treatment can be difficult and may include H1 blockers, antimalarial drugs, topical corticosteroids, sunscreens, and psoralen plus ultraviolet A (PUVA) light. The wheals of solar urticaria usually last just minutes to hours, but the disorder is chronic and can wax and wane over years.
Over 100 substances, ingested or applied topically, are known to predispose to cutaneous reactions after sun exposure. A limited number are responsible for most reactions (see Table 1: Some Substances That Sensitize the Skin to Sunlight). Reactions are divided into phototoxicity and photoallergy. Phototesting can help confirm the diagnosis. Treatment for chemical photosensitivity is topical corticosteroids and avoidance of the causative substance.
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, furocoumarin-containing plants [such as limes, celery, and parsley], drugs used for photodynamic therapy) or ingested (eg, tetracyclines, diuretics) 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, making the complex allergenic. Prior exposure to the allergen 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; however, sometimes eruptions do not appear for up to several days. Lesions are pruritic, erythematous, and often papular but may be papulovesicular or plaquelike. They are more 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 often subside within several days to weeks.
Diagnosis is made by history, skin findings, and exclusion of other sun-sensitivity disorders. Diagnosis sometimes requires reproduction of the lesions with phototesting when the patient is not using any potentially photosensitizing 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 psoralen plus ultraviolet A (PUVA―see Phototherapy) or narrowband UVB (312 nm) phototherapy. Patients with disabling disease may require a course of oral immunosuppressive therapy such as prednisone, azathioprine, cyclosporine, or hydroxychloroquine.
Last full review/revision March 2014 by Robert J. MacNeal, MD
Content last modified April 2014