Allergic contact dermatitis (ACD) is a T-cell-mediated, delayed-type IV hypersensitivity reaction to exogenous agents.1,2 ACD and irritant contact dermatitis (ICD) frequently exist together, which contributes to the difficulty in measuring the prevalence of ACD on its own. In many European countries, occupational dermatitis has been found to occur in 500 to 1900 workers per year.3
The pathogenesis of ACD is a 2-step process. When an allergen or benign substance contacts skin initially, it goes through the skin via the stratum corneum. During the sensitization phase, the surface of Langerhans cells in the epidermis becomes coated with the allergen. The Langerhans cells move to surrounding lymph nodes, where naive Th1 cells come into contact with this complex of allergen and proteins. The newly sensitized Th1 cells undergo clonal proliferation and produce memory Th1 cells. The second phase of the delayed hypersensitivity reaction occurs once the patient comes in contact with the allergen again. Memory T cells produce a rapid inflammatory response, resulting in spongiosis.3,4
In the adult population, a common cause of ACD is urushiol, a highly allergenic chemical found in various plants including oak, poison ivy, and sumac. In a patch-testing study, nickel and fragrances each triggered ACD in 14% of patients, and neomycin caused ACD in 11% of patients.5 In pediatric patients, contact sensitization often begins in early childhood through exposures to vaccinations, cosmetics, topical medications, and piercings.6 In addition, pediatric patients with atopic dermatitis frequently also present with ACD. At work and home, risk factors for ACD include contact with chemicals in cleaning supplies, nail and hair products, and skin care products.3
ACD can vary in presentation depending on the time course and severity. Acute, mild reactions present with erythema, edema, and pruritus only at the contact points. More severe reactions also involve vesicular lesions that burst and crust afterward. In particular, when a patient comes in contact with poison ivy, the rash that often appears looks like a line of vesicles from the pattern of contact. After chronic exposure to the allergen, the skin thickens and fissures, with an appearance similar to eczema. Particularly in chronic cases, the rash is more widespread although particularly severe in the allergen contact location. Although the hands are most commonly affected by ACD, any exposed areas of the skin are susceptible.3,5
The histology of ACD in its initial stages predominantly consists of spongiotic vesicles in the lower epidermis. In the later stages, spongiosis can be seen throughout the epidermis. In addition, groups of Langerhans cells, lymphocytes, and macrophages cluster around the superficial vessels in the upper dermis. Absence of eosinophils does not exclude ACD, although eosinophilic exocytosis is often seen in ACD. In patients with chronic ACD, epidermal proliferation, scale crust, and papillary fibrosis of the dermis mostly characterize the skin histology, with limited spongiosis and vesicles.7
The differential diagnosis for ACD includes ICD, atopic dermatitis, psoriasis, rosacea, erythroderma, lichen planus, xerotic eczema, stasis dermatitis, and seborrheic dermatitis.3,7 If ACD appears in the groin, it must be distinguished from extramammary Paget disease, Candida, erythrasma, or inverse psoriasis. Due to the preservatives in topical preparations, ACD of the diaper area is often seen and can be distinguished from Candida by its characteristic “satellite lesions.” If ACD appears on the face, particularly in the perioral region, nutritional deficiencies, periorificial dermatitis, or rosacea should be considered. 7
To date, patch testing has been the gold standard of ACD diagnosis. Patch testing involves placing numerous small patches onto the patient’s back; the allergens that produce a more severe ACD reaction than the control irritant are identified as triggers. While the possible causes of ACD are numerous, diagnosis can be reached via allergen testing specifically considering the patient history and rash distribution.1,3 When patch testing does not reveal a specific etiology, skin biopsy can establish a diagnosis. When tinea is in the differential, the periodic acid-Schiff (PAS) stain can help rule out that diagnosis.7
Treatment and prevention of ACD rely on allergen avoidance. However, this often proves to be difficult due to work or environmental situations. In these types of environments, patients need to be counseled into engaging in protective measures; examples of these include using barrier creams or donning appropriate protective equipment.3 When patients still experience ACD despite attempts at avoidance, topical treatments can be pursued. Topical corticosteroids are the first-line treatment for localized ACD.8 However, chronic use can result in skin atrophy. As a result, topical calcineurin inhibitors such as tacrolimus or pimecrolimus are prescribed following brief topical steroid usage in areas with a thin epidermis.3,9 Although rare, chronic ACD may require immunosuppressive treatment with cyclosporine, azathioprine, or mycophenolate.3 Based on the patient’s history (wearing a new necklace), allergic contact dermatitis was suspected. The patient underwent patch testing and was determined to have an ACD reaction to nickel. The patient stopped wearing the necklace and was treated with topical triamcinolone ointment. The patient’s rash resolved within 1 week.
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