Sharon E. Jacob, MD; Andrew D. Breithaupt, BA
Department of Dermatology and Cutaneous Surgery, University of California San Diego, San Diego, California
This article presents the case of a patient with rheumatoid arthritis who was referred to dermatology for what was suspected to be a photosensitivity reaction to hydroxychloroquine, a common culprit in photodrug reactions. Despite the patient’s insistence to the contrary, the cause of her eruption was an airborne allergic contact dermatitis to chemicals she was exposed to during her longtime hobby of soap-making. This case serves as an important illustration of the anatomical differences between eruptions occurring in exposed and photodistributed areas. This article also discusses the causes of dermatitis that may mimic photodrug reactions. (J Clin Aesthetic Dermatol. 2009;2(9):44–45.)
A 66-year-old woman with debilitating rheumatoid arthritis was referred to the authors’ clinic by the rheumatology department to rule out a photodrug reaction (Figure 1). The patient had recently had hydroxy-chloroquine added to her current regimen of gold and several months later began to develop symmetrical swelling of the face, neck, and antecubital fossa, which she attributed to the medication.
Further questioning of the patient revealed that one of her hobbies was crafting homemade soaps. Careful physical examination of the patient revealed eczematous, scaly, red, coalescing papules and plaques involving the entire anterior neck, including the submandibular area—an area that would normally be protected by anatomy in photo-distributed dermatitis.
The patient was patch tested with a modified North American Contact Dermatitis Group (NACDG) standard series (based on her exposures) in addition to serial dilutions of hydroxychloroquine, gold thiosulfate, gold maleate, and her personal hygiene products, including the products she used in the manufacturing of her homemade soaps. She had multiple positive reactions, including those to Myroxylon pereirae (also known as balsam of Peru, BOP), fragrance mix 1, Lavandula angustifolia, and fragments of her homemade essential oil soaps. Reactions to the medications were negative.
She immediately improved after fragrance avoidance was implemented and she discontinued her soap-making practices. She was able to restart the hydroxychloroquine and again achieved good control of her rheumatoid arthritis with no reccurrence of the dermatitis.
The distinction between photodistributed and exposed area dermatitis can be a very difficult one to make. Meticulous inspection of the distribution of an eruption is critical to diagnosis. Exposed area dermatitis involves the areas usually anatomically spared in photodistributed dermatitis, such as behind the ears (Wilkinson’s triangle), nasolabial folds, and under the chin. This crucial distinction is often overlooked by medical professionals when evaluating dermatitis. In fact, Darvay et al reviewed 15 years of referrals for photosensitivity and found that of the 2,715 patients patch tested, only 62 (2.3%) exhibited a photoallergic reaction. The majority of these reactions were to ultraviolet (UV) filters, most of which are no longer used in today’s sunscreens.
Due to the areas affected, namely the face, neck, and arms, allergic contact dermatitis (ACD) to personal hygiene products (cosmetics, fragrances, and lotions) can mimic photosensitivity.[2,3] Because the chemicals in cosmetics tend to cause a chronic eczematous dermatitis rather than an acute vesicular eruption and the fact that more than half of reported cases of cosmetic ACD involve the face and periocular area,[5,6] making the distinction between ACD and photodrug reactions can be difficult. A careful history and physical examination, along with a low threshold of suspicion to use patch testing, are critical for proper diagnosis.
Eruptions in an exposed distribution mimicking photodistributed dermatitis may also be the result of airborne substances—in this case, the fumes produced from the patient’s soap-making practices. Airborne contact dermatitis occurs mostly from plants and chemicals encountered in the occupational setting, and the offending chemicals and routes of exposure vary tremendously. Pesticides, industrial chemicals,[9,10] and synthetic resins are just some of the examples of contact allergens encountered in the workplace. Airborne allergens also have been reported to be a trigger of atopic dermatitis, but may rarely be suspected by the practitioner.
On the other hand, the foremost example of airborne ACD to plants is to the pollen from the Compositae plant family (e.g., ragweed, feverfew, chrysanthemum, daisy, and blanket flowers). Recently, a Dutch group demonstrated that airborne parthenolide is the offending allergen in patients with ACD. A seasonal pattern starting in the summer and disappearing by late autumn can be a key clue to diagnosis. Classically, Compositae dermatitis involves the face, the “V” of the neck, hands, and forearms. Involvement of the eyelids and Wilkinson’s triangle is a key feature enabling the clinician to distinguish Compositae dermatitis from photosensitivity.
The patient in the case described was referred for a photodistributed drug eruption, when, in fact, the dermatitis was in exposed areas (the submandibular area being the key clue). A careful inspection of any dermatitis suspected to be photodistributed should be performed to ensure that there is sparing of areas “photo-protected” by anatomy, with common causes of contact dermatitis always being ruled out. Despite the patient’s insistence that the causal agent was her medications and not her long-time use of certain products and soap-making ingredients, the authors tested her products and found them indeed to be the culprit. It is important to listen to the patient, but to screen what is heard in the selection of the patch-test allergens. Unless physical examination is striking for a photodrug reaction, one should always be cognizant of and try to rule out more common reactions.
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