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A 50-year-old woman presented to the clinic with an abrupt onset of an intensely pruritic rash that extended over the dorsal aspect of both arms (Figure 199-1). The patient notes no new medicines and no recent exposures to any new chemicals. She acknowledged recent time spent outside in the sun. The plaques were photodistributed, with sparing of her watch area. A clinical diagnosis of polymorphous light eruption (PMLE) was made, and the patient was started on oral antihistamines and topical steroids. It was recommended that she minimize her sun exposure.
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Photosensitivity is an abnormal skin response to ultraviolet light that occurs on sun-exposed areas of the skin. There are three common types of photodermatitis:
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UV light radiating from the sun may be categorized into UVA (wavelength 320 to 400 nm), UVB (290 to 320 nm), and UVC (200 to 290 nm). UVC is completely absorbed by the earth's ozone layer and thus does not play a role in photosensitivity. Photosensitivity may be induced by UVA, UVB, or visible light (400 to 760 nm). Longer wavelength light penetrates deeper into the skin. UVA penetrates through to the dermis, but UVB mainly penetrates and affects the epidermis.
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Ultraviolet light has multiple effects on the skin. Notably, it causes DNA damage and has immunosuppressive effects on skin inflammatory cells increasing the risk of carcinogenesis. In patients with photosensitivity, it elicits an inflammatory response in the skin, leading to the development of a photodermatosis.
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PMLE is an idiopathic, delayed-type hypersensitivity reaction to UVA light and, to a lesser extent, UVB light (Figures 199-1 and 199-2). PMLE is the most common photoeruption encountered in clinical practice. The reaction will remit spontaneously with time and absence of sun exposure, but occasionally it will last as long as sun exposure occurs. PMLE usually begins in the first three decades of life and occurs more commonly in women. The rash develops within hours to days after exposure to sunlight and lasts for several days to a week.
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There is a broad range of degrees of photosensitivity with PMLE. Extremely sensitive individuals can tolerate only minutes of exposure, whereas many people have a low sensitivity and require prolonged exposure to sunlight before developing a reaction. It is a recurrent condition that persists for many years in most patients.2
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Phototoxic reactions are the most common drug-induced photoeruptions (Figures 199-3, 199-4, 199-5, 199-6, and 199-7). They are caused by absorption of ultraviolet rays by the causative drug, which releases energy and damages cell membranes, or, in the case of psoralens, DNA. The drugs that most frequently cause phototoxic reactions are NSAIDs, quinolones, tetracyclines, amiodarone, and the phenothiazines3 (Table 199-2). Most of these drugs have at least one resonating double bond or an aromatic ring that can absorb radiant energy. Most compounds are activated by wavelengths within the UVA (320 to 400 nm) range, although some compounds have a peak absorption within the UVB or visible range.
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Phytophotodermatitis are phototoxic reactions to psoralens, which are plant compounds found in limes, celery, figs, and certain drugs. They can cause dramatic inflammation and bullae where the psoralen comes into contact with the skin (Figures 199-5, 199-6, and 199-7). The inflammation is frequently followed by hyperpigmentation.
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Photoallergic eruptions are a lymphocyte-mediated reaction. Photoactivation of a drug or agent results in the development of a metabolite that can bind to proteins in the skin to form a complete antigen. The antigen is presented to lymphocytes by Langerhans cells, causing an inflammatory response and spongiotic dermatitis (eczema). The eruption is characterized by widespread eczema in the photodistribution areas such as the face, upper chest, arms, and back of hands (Figure 199-8). Most photoallergic reactions are caused by topical agents such as antibiotics and halogenated phenolic compounds added to soaps and fragrances.4 Systemic photoallergens such as the phenothiazines, chlorpromazine, sulfa products, and NSAIDs can produce photoallergic reactions, although most of their photosensitive reactions are phototoxic (Table 199-3).
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Unprotected exposure to sunlight and the use of drugs associated with phototoxic and photoallergic eruptions are the main risk factors.
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Most cases of photodermatitis can be diagnosed on the basis of the patient's history. Be sure to review the patient's medications for possible sources.
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- The appearance of the PMLE varies from person to person but is consistent in a given patient. Erythematous pruritic papules, sometimes with vesicles, are most common (Figures 199-1 and 199-2). Lesions may coalesce to form plaques. The rash typically involves the V of the neck and the arms, legs, or both. The face, which is exposed to sunlight in both summer and winter, tends to be spared. It tends to present in spring/summer, with the first significant UV exposure of the year. The rash typically develops 1 to 4 days after sun exposure.
- Phototoxic reaction occurs 2 to 6 hours after exposure to sunlight. The eruption typically appears as an exaggerated sunburn, with mild cases causing slight erythema and severe cases causing vesicles or bullae (Figures 199-3, 199-4, 199-5, 199-6, and 199-7).
- Phytophotodermatitis reactions are asymmetric and localized to the area in which the plant psoralen was in contact with the skin. Accompanying hyperpigmentation is a good clue to a phytophotodermatitis reaction (Figures 199-5, 199-6, and 199-7). Ask the patient if he or she had any contact with limes, celery, or figs. Squeezing lime juice into drinks is a particularly common cause of this reaction.
- Photoonycholysis phototoxicity reactions (sun-induced separation of the nail plate from the nail bed) have been reported with the use of tetracycline, psoralen, chloramphenicol, fluoroquinolones, oral contraceptives, quinine, and mercaptopurine. Photoonycholysis may be the only manifestation of phototoxicity in individuals with heavily pigmented skin.
- Photoallergic eruptions are characterized by widespread eczema in the photodistribution areas such as the face, upper chest, arms, and back of hands. They resemble allergic contact dermatitis, but the distribution is mostly limited to sun-exposed areas of the body (Figure 199-8).
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- All photodermatitis reactions occur in sun-exposed areas, such as the face, ears, dorsal forearms, and V-area of the neck and upper chest.
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- Laboratory studies that may be helpful include antinuclear antibody (ANA), anti-Ro (SSA), and anti-La (SSB) titers to rule out lupus and porphyrin studies to exclude porphyria.
- Phototesting can be used to determine a patient's minimal erythema dose to light exposure and help to define the inciting spectrum of a photodermatosis (UVA versus UVB versus visible light). Phototesting involves irradiating the skin with varying doses of UVA, UVB, and visible light through an opaque screen with multiple openings.5 Usually the test is performed on the back. The presence or absence of solar urticaria is recorded within the first hour and the minimal erythema dose is determined after 24 hours.
- Provocative phototesting involves irradiating normal-appearing previously affected skin with the suspected causative light, either by higher doses of UV light or by natural sunlight exposure.5 Provocative phototesting is primarily used for suspected PMLE.
- Photopatch testing is useful when a topical photoallergen is suspected. It is performed by placing two identical sets of potential photoallergens on the patient's back and covering them. After 24 hours, one set is removed and that site is irradiated with UVA. The site is covered again. Twenty-four hours later, both the irradiated and control test sites are assessed for reactions. A reaction to a specific photoallergen in the irradiated site, but not the control site, indicates a photoallergy. A similar reaction in both sites suggests a contact dermatitis.5
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- Punch biopsy of PMLE demonstrates extensive spongiosis and edema of the dermis with a deep lymphohistiocytic infiltrate. In acute phototoxic reactions, necrotic keratinocytes are observed.
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Sun protection is the primary preventative measure for patients with photosensitivity. Patients should avoid exposure to midday sun (between 10:00 am and 3:00 pm). Protective clothing such as long sleeve shirts and broad rim hats should be worn while outdoors. Fabrics that are tightly woven, thick, and/or dark-colored are useful for protection.14 Clothing treated with broad-spectrum UV absorbers is also helpful. Window film that blocks UV and some visible light can be applied to cars or homes.15
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Sunscreen is important for daily use for patients with photosensitivity. Sunscreens are divided into chemical (organic) and physical (inorganic) products. Physical sunscreens block both UV and some visible light (see Table 199-4). Products containing avobenzone or ecamsule offer improved protection against UVA.
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Physical blocker (inorganic) sunscreens, such as titanium dioxide and zinc oxide, work by reflecting and scattering UV and visible light. Older formulations were opaque making them cosmetically less acceptable to patients. Newer nonopaque, micronized formulations of titanium and zinc oxide have been developed but are less capable of scattering visible light and the longer wavelengths of UVA.
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Chemical sunscreens may cause allergic contact dermatitis or photoallergic reactions in some patients. These patients should use titanium dioxide or zinc oxide sunscreens for protection.