Saturday, January 01, 2011
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
- 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.
- Photo patch testing may be necessary in some cases in which the
photosensitizer is delivered topically, as in a sunscreen (see
- 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 (eg,
zinc oxide or titanium dioxide) may be needed. Sunscreens should be
applied every morning and again after swimming, bathing, or
- 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 2-3 times daily after soaks.
- Give oral antihistamines such as hydroxyzine 10-25 mg 4 times
For severe disease, administer a 10-14 day tapering course of
oral prednisone, starting at 1 mg/kg/day (60 mg every morning).
Polymorphous Light Eruption
Polymorphous light eruption (PMLE) 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.
- Maximum sun protection and sun avoidance is
- The acute reaction is usually responsive to a high-potency
topical steroid cream or gel. Reserve systemic steroid therapy for
the most severe exacerbations.
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
- 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.
- 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.
- UVB, narrowband UVB therapy, or photochemotherapy (PUVA)
beginning in the late winter may induce hardening and prevent
springtime flares of PMLE. About 80% of patients can be controlled
- 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.
In severe cases immunosuppressive or immunomodulatory therapy
may be required. Therapeutic options include the following:
- Azathioprine 50-200 mg daily.
- Mycophenolate mofetil 1 g twice daily.
- Cyclosporine A 3-5mg/kg/day.
- Thalidomide 100-200 mg daily. An appropriate pregnancy
prevention program must be used for potentially pregnant
Chronic Actinic Dermatitis
Chronic actinic dermatitis (CAD) 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 PMLE 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
- 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
- Tacrolimus ointment 0.1% applied twice daily to affected facial
skin, and a high- or super-potent topical steroid to affected skin
- Antihistamines, such as hydroxyzine 10-50 mg nightly and doses
during the day as required for pruritus.
- 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.
- 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.
- Azathioprine 50-200 mg daily is a reproducibly effective
therapy and can be used either chronically or annually during
periods of high sun intensity.
- PUVA may be helpful. Start therapy very cautiously (0.1-0.25
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.
- Mycophenolate mofetil 1.0 g twice daily may be effective in
- 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
- 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
- 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.
- 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
- Failure to identify a photoallergen to which the patient
continues to be exposed.
- 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.
- 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
- 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.
- Check appropriate patients with chronic photosensitivity for
systemic lupus erythematosus and porphyria cutanea tarda, with an
ANA, Ro, La, and urine porphyrins.
- 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