Photoallergic Contact Dermatitis (Chemical photoallegy)

Are You Confident of the Diagnosis?

What should you be alert for in the history?

Be alert for an eruption that is localized to photodistributed areas, but not diffuse. The eruption typically occurs 24-48 hours after sun exposure (range 6-72 hours). Patients typically complain of pruritis/itch. Upon focused questioning, the patient may report exposure to topical agents, including sunscreens, antimicrobials, fragrances, and other personal products.

The reaction may first appear when the patient has extended sun-exposure, such as a beach vacation. The reaction can occur after multiple exposures to both the chemical agent and ultraviolet (UV) radiation. It is almost entirely due to solar radiation in the UVA range.

Characteristic findings on physical examination

Distribution: Areas of exposure to both sun and the chemical, most commonly involving the face (Figure 1).

Figure 1.

Photoallergic contact dermatitis of the face after exposure to oxybenzone.

Morphology: Lesions are routinely present on the dorsum of the hands, but can appear anywhere on sun-exposed skin.

Expected results of diagnostic studies

The diagnosis is based on clinical history and distribution, and confirmed by photo-patch testing. Photo-patch and patch testing are used to make the diagnosis and to exclude allergic contact dermatitis, respectively. Histology may support the diagnosis but usually is not necessary.

Diagnosis confirmation

The differential diagnosis includes polymorphous light eruption, airborne contact dermatitis, irritant or allergic contact dermatitis to other personal products, and less likely phototoxicity secondary to systemic agents, eg, drugs.

Who is at Risk for Developing this Disease?

Anyone may be at risk for developing the disease. Individuals at higher risk include those on vacations with intense sun exposure and outdoor workers.

Pathophysiology

– Chemical absorbs radiation in the UVA range and is converted to a photoallergen, which then triggers a T-cell mediated contact dermatitis.

What is the Cause of the Disease?
Etiology

Photoallergic contact dermatitis is caused by solar radiation combined with chemical exposure.

Common offending agents included in photo-patch testing are: Octinonxate (Octyl Methoxycinnamate), Sulizobenzone (BZP-4), Thiourea (thiocarbamide), Dichlorophene, Triclosan, Hexachlorophene, Chlorhexidine Diacetate, Sandalwood oil, Musk Ambrette, Tribromosalicylanilide, Oxybenzone (BZP-3), Octyl Dimethyl PABA, Bithionol (Thiobia-chlorophenol), Para-aminobenzoic Acid (PABA), Fenticlor (Thiobis-chlorophenol), Octisalate (Octyl Salicylate), Butyl Methoxydibenzoylmethane, Homosalate, Menthyl Anthranilate, Ketoprofen, 2 hydroxy-methoxy methyl benzophenone, and Phenylbenzimidazole

Pathophysiology

– Chemical absorbs radiation in the UVA range and is converted to a photoallergen, which then triggers a T-cell mediated contact dermatitis.

Systemic Implications and Complications

Typically, there are no associated systemic complications. Very rarely, there may be cross-reactivity between PABA and thiazides and/or other para-amino agents, such as sulfonureas, PPD hair color, etc.

Treatment Options

Treatment options include:

-Avoidance of allergen and temporary avoidance of sun exposure, including protective clothing and broad spectrum sunscreen, which do not contain the offending agent.

– Cool soaks and/or compresses as needed.

– Emollients as needed, including Vaseline or Aquaphor ointments, calamine lotion

– Mid to high-potency topical corticosteroids twice a day as needed, eg. Triamcinolone 0.1% ointment, Fluocinonide 0.05% ointment (Lidex), Clobetasol Propionate 0.05% ointment (Clobex, Temovate)

– Antihistamines as needed for itch, e.g. Diphenhydramine (Benadryl) and Hydroxyzine (Atarax)

– Systemic steroids at 1mg/kg/day if necessary with 2-week taper

Optimal Therapeutic Approach for this Disease

Prevention by avoidance of allergen exposures is curative. Recommended measures include short term sun-protection when exposed to allergen, including protective clothing and broad-spectrum sunscreens that do not contain the offending agent. Symptomatic can be obtained with relief with emollients, topical steroids, and anti-histamines. Systemic steroids may be necessary for severe cases. Sensitivity to the sun may take several weeks to abate, especially with photoallergens from sunscreens.

Patient Management

The patient can be followed until lesions clear. Education should be provided for avoidance of future exposures to allergens and cross-reacting substances, and various approaches to photoprotection.

Unusual Clinical Scenarios to Consider in Patient Management

Very rarely, there may be a systemic contact dermatitis secondary to ingestion of photoallergens or drugs with cross-reactivity to the photoallergen. In the case of PABA allergy, this includes thiazides and other para-amino agents, such as sulfonureas, PPD hair color, etc.

What is the Evidence?

Deleo, VA. “Photocontact dermatitis”. Dermatol Ther. vol. 17. 2004. pp. 279-88. (Review of photoallergic and photoirritant contact dermatitis, phytophotodermatitis, and photo-patch testing.)

Lugovic, L, Situm, M, Ozanic-Bulic, S, Sjerobabski-Masnec, I. “Phototoxic and photoallergic skin reactions”. Coll Antropol. vol. 31. 2007. pp. 63-7. (Review of drug-induced photosensitivity, photoallergic and phototoxic reactions.)

Marks, JG, Elsner, P, DeLeo, VA. “Contact & occupational dermatology”. 2002. (Comprehensive practical guide for contact and occupational dermatology, including diagnosis and management of suspected contact and occupational dermatitis.)

Victor, FC, Cohen, DE, Soter, NA. “A 20-year analysis of previous and emerging allergens that elicit photoallergic contact dermatitis”. J Am Acad Dermatol. vol. 62. 2010. pp. 605-10. (Restrospective analysis of 13 years of photo-patch test results.)