Allergic Contact Dermatitis

Etiology

Allergic contact dermatitis is an inflammatory disease of the skin that is caused by a type 4 hypersensitivity reaction. It results from the contact of an offending chemical or antigen with the skin, and the subsequent T-cell mediated response.[3] Morphology and location of the dermatitis are often the best indicators of the offending agent. For instance, when found around the wrist, it may indicate an allergic response to a bracelet or watchband.

Poison ivy is a common cause of ACD and presents as linear streaks where the plant comes into contact with the skin.

Nickel is another common cause of ACD and presents as dermatitis where necklaces and earrings containing nickel are worn.

Rubber gloves are also a common cause of chronic dermatitis.

Other agents include hair dyes, textile chemicals, preservatives, fragrances, sunscreens, and photo allergens.

Epidemiology

Allergic contact dermatitis is an inflammatory disease of the skin that is common in the general population. It is the most common type of occupational skin disease.[4]

The disorder is more common in women than in men. In the elderly, the condition often correlates with topical medications.

Pathophysiology

The pathophysiology of allergic contact dermatitis starts with the contact of the allergen to the skin. This allergen penetrates that stratum corneum of the skin and is taken up by Langerhans cells.[5] [6] The antigens subsequently undergo processing by these cells and get displayed on their surface. Langerhans cells then migrate towards regional lymph nodes. The antigens taken up by these cells come in contact with the adjacent T-lymphocytes. Due to the process of clonal expansion as well as cytokine-induced proliferation, antigen-specific T lymphocytes get created. These lymphocytes may then travel through the blood and into the epidermis. This process collectively is known as the sensitization phase of allergic contact dermatitis. The elicitation phase is what occurs after reexposure to the antigen takes place. The Langerhans cells containing the antigen interacts with the antigen-specific T-lymphocytes for that antigen, which triggers a cytokine-induced proliferation process. This proliferation, in turn, creates a localized inflammatory response.

Histopathology

The diagnosis of allergic contact dermatitis is usually established by a combination of history and physical examination, clinical presentation, and a positive patch test. If further evaluation is required, a skin biopsy of an affected area of skin will typically demonstrate spongiosis. However, this finding is unlikely to facilitate differentiation of ACD from other eczematous dermatologic disorders. [7]

Toxicokinetics

The intensity of the inflammatory response in allergic contact dermatitis is dependent on both the sensitizing ability of the allergen and the concentration of the allergen present. Poison ivy is an example of a strong sensitizer that can create an intense inflammatory response, even in small concentrations.[8]

History and Physical

Obtain a thorough history of occupation, hobbies,  medications, lifestyle, use of fragrances, and perfumes. 

Allergic contact dermatitis can present on physical exam as acute or chronic. Acute ACD characteristically presents as an erythematous, eczematous, or vesicular dermatitis. Although ACD may present with a localized, well-demarcated skin eruption most commonly on the hands or face, it can also be more widespread. For example, rinse-off products such as shampoo or body wash may come into contact with many parts of the body, leading to a more diffuse presentation.[9] Additionally, in cases where the patient systemically consumes an allergen, a more diffuse cutaneous reaction may occur. Chronic ACD more commonly presents with lichenification, fissuring, and scale.[10] 

Evaluation

A good clinical evaluation of allergic contact dermatitis involves a detailed history and physical. The morphology and location of the dermatitis is often the best indicator of the offending agent. Patch testing is the gold standard to confirm the diagnosis and should be performed when ACD is suspected in patients with persistent symptoms. Patch testing can help determine the allergen to avoid future exposure. While patch testing is easy to perform, the test may be over-utilized, leading to higher costs for the patient. If the diagnosis is still not certain, a skin biopsy usually demonstrates spongiosis.[11]

One should always rule out tinea as a cause of dermatitis.

Treatment / Management

The only definitive treatment of ACD is the identification and removal of the offending agent, and all patients with suspected or confirmed ACD should be advised of this. First-line medical therapy includes topical steroids when ACD is confined to less than 20% of the body, and oral corticosteroids when greater than 20% of the body is involved.  If ACD involves a delicate area such as skin folds or eyelids, topical calcineurin inhibitors or PDE4 inhibitors may also be effective. Upon identification of the allergen, strict avoidance is necessary to prevent a recurrence.[12] Symptomatic management includes oral antihistamines, topical hydrocortisone, and cool water soaks. Vesicles should not be ruptured as there is a risk of infection. The use of moisturizers is a recommended adjunct.

For severe cases, topical immunomodulators like tacrolimus may be beneficial. Some patients may benefit from phototherapy using UV A plus psoralen. Rarely in severe cases, one may require immunosuppressive agents like mycophenolate.

In cases of chronic or recalcitrant ACD, use patch testing to identifying the causative agent.[13] Successful patch testing requires several components: choice of appropriate chemicals for testing, a positive patch test to relevant allergens, and patient counseling of patch test results. Additionally, the American Contact Dermatitis Society’s Contact Allergen Management Program (CAMP) can be utilized to generate a “safe list” of products that do not contain the patient’s allergens. In the case where allergens are unavoidable, systemic therapy may be necessary.[14]

Differential Diagnosis

Morphologically the clinical presentation of allergic contact dermatitis is very similar to irritant contact dermatitis and atopic dermatitis.[15] Other skin conditions that should be ruled out include drug eruptions, scabies, urticarial bullous pemphigoid, urticaria, psoriasis, seborrheic dermatitis, periorificial dermatitis, and rosacea. 

Treatment Planning

The goal of the treatment of allergic contact dermatitis is to decrease the inflammatory response that is triggered by the type 4 hypersensitivity reaction. Reactions caused by strong sensitizers may require quicker and more aggressive treatment as the intensity of dermatitis will increase. Identifying and removing the allergen is the most effective definitive treatment. Ointment-based moisturizers and steroids are preferred vehicles of treatment as creams contain a variety of chemicals and preservatives.[16]

Toxicity and Adverse Effect Management

The most important step in the management of allergic contact dermatitis is the removal of the offending agent. Toxicities and adverse effects to monitor are related to the treatment options. It is crucial to control the strength of the topical steroids to appropriate dosages as the most common adverse effect of these medications is thinning of the skin.[16]

Prognosis

This disease stays with the affected populations throughout their lives. Strict avoidance of the allergen needs to be the implemented strategy. Management of the inflammatory response is the essential goal in treatment.[12]

The longer a person has ACD, the more time it will take to resolve.

Complications

Complications associated with allergic contact dermatitis (ACD) involve the inflammatory response.[4] The inflammation subsides with the removal of the allergen. If the allergen is consumed systemically, diffuse dermatitis might occur, but this condition is not considered a dermatologic emergency.