The distribution of SACD relates mostly to the site on the shoe where the allergen is located. Vesicular plantar foot dermatitis is associated with mercaptobenzothiazole within foam insoles, whereas thiuram allergy presents on the dorsal foot and is related to glue used to cement the leather before stitching. Box toe allergy on the dorsal toes is often linked to carbamates.
Symptoms of SACD classically present on the dorsal surface of the toes and feet 1 day to 1 week after the secondary exposure. This anatomical location is particularly susceptible owing to the thin stratum corneum of the dorsal foot and the location of allergens in glues used in shoe manufacturing. Unlike the toe web spaces, this area makes direct contact with the shoe at all times. The arch and heel are not typically involved, because there is less direct contact with the shoe and a thicker stratum corneum is present. Therefore, exclusive dorsal toe and instep involvement is a highly specific finding in SACD. The symptoms present bilaterally in most cases; however, unilateral cases have been reported. This patient was especially vulnerable to transepidermal allergen contact because of her exposure to water, heat, pressure, and friction during hiking.[1,7]
The prevalence of SACD is estimated to be 3.3%-11.7% of those who have allergic contact dermatitis. This represents 1.5%-24.2% of those who undergo patch testing for contact dermatitis. The disease has no specific predilection for sex or race, which makes it a diagnostic challenge for physicians.
Depending on the potency of the offending agent and the extent of exposure, symptoms can vary widely in severity and distribution. Classically, SACD presents subacutely as a red, oozing, and blistering inflammatory reaction in areas where the patient was exposed to the etiologic substance. The spectrum of presenting symptoms is also determined by the chronicity of the exposure. An acute manifestation is characterized by eczematous symptoms, whereas chronic exposure leads to a more dried and lichenified appearance, with scaling, cracks, and fissures.[1,4]
Allergic contact dermatitis is a delayed type IV hypersensitivity reaction caused by sensitization and repeated exposure to specific allergens. Upon the original encounter, T-helper 1 cells are sensitized via the innate immunity. The Langerhans and dermal dendritic cells transport the allergen, traveling to the nearest lymph nodes to promote proliferation of antigen-specific T cells. After these sensitized T cells encounter the antigen again, cytokines are released and an inflammatory reaction occurs. Each consecutive exposure results in a more extreme response.
Patch testing is the test of choice in determining the offending allergen and cause of SACD. It works by exposing the patient to a wide variety of suspect allergens to stimulate a type IV hypersensitivity reaction. Confirmation of the etiologic agent is made by examining which allergen patches cause a subsequent eruption. The most common allergens found to cause shoe dermatitis are rubber accelerators, such as mercaptobenzothiazole, carbamates, and thiurams (eg, tetramethylthiuram disulfide). Allergies can also occur because of potassium dichromate in leather and adhesives, diisocyanates for rubber padding, dimethyl fumarate preservative, felt, cork liners, formaldehyde, dyes, asphalt, and tar.[1,4]
Physicians must stay vigilant for associated sequelae. Complications of allergic contact dermatitis can occur owing to a secondary event. Exposed wounds from blisters or excoriations may lead to a secondary infection, which complicates both the prognosis and the diagnosis if discovered late. In addition, a secondary allergic or irritant contact dermatitis reaction may occur in response to creams or oils used in the treatment of the primary allergic disease.
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