Clinical Reference / Therapeutic Strategies / Photosensitivity Dermatoses

Photosensitivity Dermatoses

Photosensitive drug eruptions, polymorphous light eruption, chronic actinic dermatitis (CAD -includes the conditions previously called photosensitive eczema, actinic reticuloid and persistent light reaction).

Photosensitivity dermatoses are caused either by an exogenous substance (either topical or systemic), or are idiopathic. These conditions initially present on sun-exposed skin, may be triggered by topical or systemic exposures, and tend to resolve when sun exposure (UV) is avoided. Over time, especially in men, the condition may become more widespread, affecting sun-protected areas; lose its seasonal variation; occur even when the inducing photosensitizer has been stopped; and have a broader wavelength of reactivity. This end stage may also demonstrate histologic features resembling cutaneous T cell lymphoma (so called actinic reticuloid). Currently, this end-stage condition is termed chronic actinic dermatitis, and includes the conditions previously labeled photosensitive eczema, actinic reticuloid, and persistent light reaction. Porphyrias, lupus erythematosus and other photosensitive connective tissue disorders, and pellagrous dermatitis must be ruled out in all patients who develop a chronic course.

Photosensitive Drug Eruptions

Photosensitive drug eruptions may present either as sunburn (a phototoxic response) or photoallergy (an eczematous response). Photoallergic eruptions may be either eczematous or lichenoid histologically. It may be impossible to clearly define the pattern of eruption clinically. The most important part of the treatment is to stop the inciting medication if possible. Since the eruption requires both UV exposure (usually UVA) and the medication, the eruption may not first appear near the time the medication was started.

General Therapy

First Steps

  1. In phototoxic or photoallergic drug reactions, the offending agent, which may include, among other drugs, thiazide diuretics, sulfonamides, quinidine, tetracyclines, captopril, phenothiazines, NSAIDs, and sulfonylureas, must be identified.
  2. Photo patch testing may be necessary in some cases in which the photosensitizer is delivered topically, as in a sunscreen (see below).
  3. Encourage all patients with photosensitivity diseases to use maximal sun protection, which must include an SPF 30 or higher sunscreen with ingredients that shield against both UVB and UVA. In those patients sensitive to visible light, an opaque sunscreen (e.g., zinc oxide or titanium dioxide) may be needed. Sunscreens should be applied every morning and again after swimming, bathing, or extensive sweating.
  4. Therapy of acute photoallergic dermatitis is the same as for acute contact dermatitis, as follows.
    • Prescribe soaks (Burrow solution, 1:10) to be applied 3 times daily for 15–20 minutes to areas of vesiculation, crusting, oozing, and/or secondary infection.
    • Prescribe a high- or superhigh-potency steroid cream or gel to be applied to the rash 2 to 3 times daily after soaks.
    • Give oral antihistamines such as hydroxyzine 10–25 mg 4 times daily.

Additional Steps

For severe disease, administer a 10- to 14-day tapering course of oral prednisone, starting at 1 mg/kg/day (60 mg every morning).

Polymorphous light eruption

Polymorphous light eruption tends to flare each spring, then spontaneously improve in summer and fall as tanning and/or “hardening” occur. For patients who do not develop hardening, all of the ancillary measures described below continue to apply.

First Steps

  1. Maximum sun protection and sun avoidance is essential.
    These recommendations are for patients who have photosensitive skin diseases. Depending on the severity of the photosensitivity, more of the recommendations may need to be followed. The goal is for patients to continue their regular activities (exercise, occupation) while avoiding ultraviolet radiation that triggers their skin conditions. Patients should be counseled that maximizing photoprotection may reduce the amount of medication required to control their diseases. Phototesting to determine the wavelength of sensitivity may be valuable in determining how to apply the steps below:

    • Avoid mid-day sun. All outdoor activities should occur as near to dawn and dusk as possible.
    • If outdoors, activities should occur in shade.
    • Wear protective clothing. Long sleeve shirts, long pants, shirts with necks, and wide brimmed hats are essential. Gloves are recommended, especially when patients are driving. Clothing should be impervious to light (can’t see light through it) or be specially manufactured to block all UV radiation. Such clothing can be obtained from several manufacturers. Clothing may be washed in SunGuard which contains Tinosorb. This will impart an SPF 30 UVB/UVA protection in the clothing for 20 washings.
    • Use a sunblock: Combination sunscreens with agents that protect out into the UVA1 region are essential. Parasol 1789 and Mexoryl are two such chemical agents, and physical blockers zinc oxide and titanium dioxide also screen out these wavelengths. Ombrelle SPF 60 and Anthelios SPF 60 are two such sunscreens. The sunscreen must be applied every day, in adequate amounts to be effective. Repeat application after sweating and every two hours when outdoors.
    • Use UVA shielding: Normal car side windows and to a lesser degree windshields transmit UVA. Windshields are laminated and transmit only wavelengths beyond 370 nm, whereas nonlaminated side windows transmit more UV radiation starting at 310 nm. UVA shields for car, home, and office windows, and filters on the computer screen are recommended for the most sun-sensitive conditions. While patients are driving, they must keep their arms below the side window, and the windows must be kept closed.
  2. The acute reaction is usually responsive to a high-potency topical steroid cream or gel. Reserve systemic steroid therapy for the most severe exacerbations.

Alternative Steps

  1. Tacrolimus ointment 0.1% applied to the eruption twice daily may be effective and safe for facial skin where long-term topical steroid therapy is less ideal.
  2. UVB, NBUVB, or PUVA therapy beginning in the late winter may induce hardening and prevent springtime flares of PMLE. About 80% of patients can be controlled with phototherapy.
  3. Hydroxychloroquine 200 mg once or twice daily may be tried starting in late winter and continuing until mid to late fall. The onset of benefit is 3–6 weeks after the medication is initiated, so treatment must be started a month or so before spring. Chloroquine 250 mg daily, or the addition of quinacrine 100 mg daily to the hydroxychloroquine, may be used in patients failing hydroxychloroquine treatment alone.

Subsequent Steps

In severe cases immunosuppressive or immunomodulatory therapy may be required. Therapeutic options include the following:

  1. Azathioprine 50–200 mg daily.
  2. Mycophenolate mofetil 1 g twice daily
  3. Cyclosporine A 3–5mg/kg/day.
  4. Thalidomide 100–200 mg daily. An appropriate pregnancy prevention program must be used for potentially pregnant women.

Chronic actinic dermatitis

Chronic actinic dermatitis is a persistent photosensitivity disorder in which patients respond abnormally to UVA, UVB, and sometimes to visible irradiation. The disorder is pruritic, and results in thick, lichenified photodistributed plaques. It may develop in persons with polymorphous light eruption or in those who have had a photosensitive drug eruption (from either a topical or systemic photosensitizer). CAD may occur in persons with dark skin (skin types 4, 5, 6) who are unaccustomed to being photosensitive.

First Steps

  1. Avoidance of all UV irradiation is critical. Maximum sun protection is essential. Patients with CAD may need to have their house and car windows covered with UVA shielding.
  2. Tacrolimus ointment 0.1% applied twice daily to affected facial skin, and a high- or super-potent topical steroid to affected skin elsewhere.
  3. Antihistamines, such as hydroxyzine 10–50 mg nightly and doses during the day as required for pruritus.

Alternative Steps

  1. For severe flares, prednisone 60 mg daily in a single dose may be used for brief periods (a few weeks) and rapidly tapered, so that the total course is less than 1 month.
  2. Hydroxychloroquine 200 mg once or twice daily may be added to topical therapy outlined above. Chloroquine 250 mg daily may be used if hydroxychloroquine is ineffective.

Subsequent Steps

  1. Azathioprine 50–200 mg daily is a reproducibly effective therapy and can be used either chronically or annually during periods of high sun intensity.
  2. Photochemotherapy (PUVA) may be helpful. Start therapy very cautiously (0.1 to 0.25 J/cm2) to limited parts of the body to avoid disease flares. The dosage can be slowly increased thereafter. Maintenance therapy (1-2 times per week) is needed even with clearing.
  3. Mycophenolate mofetil 1.0 g twice daily may be effective in refractory cases.
  4. Thalidomide 50–200 mg daily can control severe disease, and may be added to the above regimens. Thalidomide is a potent teratogen. Female patients must be enrolled in an appropriate pregnancy prevention program.
  5. Cyclosporine 2–5 mg/kg/day is effective in the most severe cases and is useful for rapid control of the most difficult symptoms. However, patients rapidly relapse after discontinuation, thus another approach such as azathioprine, thalidomide or mycophenolate mofetil may be required for chronic control.

Phototesting (photopatch testing and photosensitivity determinations)

  1. Photoallergens are found in cosmetics, herbal shampoos, household soaps, foods, sunscreens, and drugs. Photopatch testing performed by experts in this technique (usually in a tertiary care facility) may be necessary to identify the offending agent.
  2. Light testing with artificial light sources to delineate the sensitivity spectrum may help establish a correct diagnosis and facilitate more precise use of sunscreens and more accurate patient education.


  1. Failure to identify a photoallergen to which the patient continues to be exposed.
  2. Inadequate patient education, inappropriate (insufficient) sunscreen application, and the use of a sunscreen with insufficient SPF or spectrum are common causes for photosensitivity patients to fail to improve.
  3. Sunscreen agents themselves can be sensitizing. This may be extremely confusing if superimposed on the underlying disease. P-Aminobenzoic acids (PABAs) are implicated, although benzophenone, avobenzone, and other sunscreens also cause allergic contact dermatitis.
  4. Patients with persistent light reactions are often chronically depressed; physicians must be aware of the social consequences of a disease that banishes patients to the night.
  5. Check appropriate patients with chronic photosensitivity for systemic lupus erythematosus and porphyria cutanea tarda, with an ANA, Ro, La, and urine porphyrins.
  6. Chronic actinic dermatitis may mimic the Sézary syndrome variant of cutaneous T-cell lymphoma. A skin biopsy and examination of the blood for T cell gene rearrangements should be performed when appropriate.