Dermatitis, Allergic Contact

Article Author:
Patrick Murphy
Article Editor:
Amber Atwater
Updated:
10/27/2018 12:31:29 PM
PubMed Link:
Dermatitis, Allergic Contact

Introduction

Allergic contact dermatitis (ACD) is a type 4 or delayed-type, hypersensitivity response (DTH) by an individual’s immune system to a small molecule (< 500 daltons), or hapten, that contacts a sensitized individual’s skin.[1] The initial or induction phase of ACD occurs when the hapten combines with a protein to form a complex that leads to the expansion of an allergen-specific T cell population; this process is known as sensitization. During the elicitation phase, re-exposure to the antigen leads to the development of dermatitis. ACD accounts for 20% of contact dermatoses, and allergens differ greatly based upon geography, personal habits and hobbies, and often, the types of preservatives that are legally permissible, such as quaternium-15 in the United States but not Europe.[2]

Etiology

Allergic contact dermatitis (ACD) is an inflammatory disease of the skin that is caused by a type 4 hypersensitivity reaction. It results from contact of an offending chemical or antigen with the skin.[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.

Epidemiology

Allergic contact dermatitis (ACD) is an inflammatory disease of the skin that is common in the general population. It has no preference for gender and affects children and adults the same. Although the precise incidence and prevalence of allergic contact dermatitis are not well established, 20% of dermatitis in children is a result of this disease. It is also the most common type of occupational skin disease.[4]

Pathophysiology

The pathophysiology of allergic contact dermatitis (ACD) begins with the contact of the allergen to the skin. The allergin penetrates that stratum corneum and travels down to the basal layer where it is taken up by Langerhans cells.[5] The antigens are subsequently processed by these cells and displayed on the surface. As part of the skin's normal immunity, Langerhans cells migrate towards regional lymph nodes. The antigens taken up by the Langerhans cells come in contact with the adjacent T-lymphocytes. Because of the process of clonal expansion as well as cytokine-induced proliferation, antigen-specific T lymphocytes are created. These lymphocytes may then traverse through the blood and into the epidermis. This process collectively is known as the sensitization phase of allergic contact dermatitis.[6] The elicitation phase is what occurs in allergic contact dermatitis 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.[7] This, in turn, creates a localized inflammatory response.

Histopathology

The diagnosis of allergic contact dermatitis (ACD) is usually established by a combination of history and physical, clinical presentation, and a positive patch test. If further evaluation is required, a skin biopsy of an affected area of skin will demonstrate intracellular and epidermal edema, known as spongiosis, along with mononuclear infiltrates throughout the epidermis and dermis that are made up primarily of T-cells.[8]

Toxicokinetics

The intensity of the inflammatory response in allergic contact dermatitis (ACD) 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.[9]

History and Physical

Allergic contact dermatitis (ACD) can present on physical exam as acute or chronic. Acute ACD is typically characterized by an erythematous, eczematous, or vesicular dermatitis. Although ACD may present with a localized, well-demarcated skin eruption, 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. [10] Additionally, in cases where an allergen is consumed systemically, a more diffuse cutaneous reaction may occur. Chronic ACD more commonly presents with lichenification, fissuring, and scales. [11] Acute ACD often responds well to allergen avoidance and immunosuppression with steroids (topical or oral) if necessary, but it may follow a prolonged and self-limited course of up to 4 weeks.

Evaluation

A good clinical evaluation of allergic contact dermatitis (ACD) involves a detailed history and physical. The morphology and location of the dermatitis is often the best indicator of the offending agent. Patch testing can be performed to help confirm the diagnosis. If the diagnosis is still not certain, a skin biopsy usually demonstrates spongiosis and a mononuclear infiltrate.[12]

Treatment / Management

The most definitive treatment of allergic contact dermatitis (ACD) is the identification and removal of the offending agent. With intense reactions like bullae formation in acute ACD, cold compresses are extremely helpful.[1] These should be applied every 15 to 30 minutes for up to 3 days or until bullae begin resolving and itching decreases. Cool baths with or without colloidal oatmeal have been shown to be effective against diffuse inflammation. Additionally, calamine lotion can be used for itching, and hydroxyzine or diphenhydramine may be used to control itching and improve sleep. Group I-IV topical steroids can help treat erythema and itching. [13] If ACD involves a delicate area such as skin folds or eyelids, topical calcineurin inhibitors may also be effective. Systemic steroids are often required in severe reactions, and a slow taper can be helpful in avoiding a flare, as is often required for poison ivy. If the allergen is identified, strict avoidance is necessary to prevent recurrence.[3]

In cases of chronic or recalcitrant ACD, patch testing is the gold standard in identifying the causative agent.[5] 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. In addition, 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.

Differential Diagnosis

Morphologically the clinical presentation of allergic contact dermatitis (ACD) is very similar to irritant dermatitis and atopic dermatitis.[14] Other skin conditions that should be ruled out include cellulitis, impetigo, herpes zoster, herpes simplex virus, and fixed drug eruptions.

Treatment Planning

The goal of the treatment of allergic contact dermatitis (ACD) 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 the dermatitis will be increased. Identifying and removing the allergen is the most effective definitive treatment. If bullae formation occurs, wet compressors should be used to decrease the inflammation as topical steroids cannot penetrate them. If the allergen is consumed systemically, diffuse contact dermatitis may occur which may require prednisone. Additionally, strong sensitizers like oleoresin in poison ivy may also require prednisone use. Minimizing the number of topical products used is important for decreasing any subsequent irritant dermatitis. Ointment-based moisturizers and steroids are preferred vehicles of treatment as creams contain a variety of chemicals and preservatives.

Toxicity and Side Effect Management

The most important step in the management of allergic contact dermatitis (ACD) is the removal of the offending agent. Toxicities and adverse effects to monitor are related to the treatment options. It is important 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. Calcineurin inhibitors, although useful, still have a black box warning for skin malignancies and lymphomas. Calamine lotion is effective at decreasing pruritis, but it can also cause significant drying of the skin.

Prognosis

This disease process stays with the affected populations throughout their lives. To avoid symptoms, strict avoidance of the allergen needs to be implemented. Management of the inflammatory response is the essential goal in treatment.[3] This disease may wax and wain overtime, but managing symptoms simply involves decreasing the inflammation.

Complications

Complications associated allergic contact dermatitis (ACD) involve the inflammatory response.[15] The inflammation subsides with the removal of the allergen. If the allergen consumed systemically, diffuse dermatitis may occur, but this condition is not considered a dermatologic emergency.

Postoperative and Rehabilitation Care

Patients with known rubber glove allergies need to make sure to identify their sensitivity to their healthcare professionals so that extra care is taken to ensure that the appropriate glove type is used during all aspects of their management.[2]

Consultations

Unknown causes of allergic contact dermatitis (ACD) may require patch testing. This is best performed by a dermatologist, immunologist, or physician with clinical experience in analyzing and testing allergic contact dermatitis.

Deterrence and Patient Education

Educating patients on allergic contact dermatitis (ACD) involves assisting the patient in identifying their allergic triggers. Patients must then be provided with practical behavioral modifications to help decrease the inflammatory response of this disease. For instance, in professions that require regular use of rubber gloves, it is important that patients can identify the natural rubber allergy and choose a glove type that uses a rubber accelerator (i.e., thiurams, carbamates, mercapto compounds) towards which they do not form a reaction.[15]

Pearls and Other Issues

Cross-sensitization may occur in the population affected by allergic contact dermatitis (ACD). This process occurs when an antigen that is chemically similar to an antigen that had previously been sensitized by the host triggers a contact dermatitis. Additionally, systemically-induced allergic dermatitis may take place when an individual who previously has been sensitized to a contact allergin consumes the allergin by another route (inhalation, ingestion, injection).[1] If a patient fails to improve with these measures, alternative diagnoses must be considered.

Enhancing Healthcare Team Outcomes

An important allergic contact dermatitis (ACD) that healthcare professionals need to be aware of is natural rubber latex allergy; this reaction represents 80% of allergies that are occupationally acquired. [1]This is a type 4 hypersensitivity reaction that occurs toward the accelerators found in the rubber. Patch testing is performed to identify the offending trigger, and efforts need to be made to avoid the trigger for the healthcare team and their patients. This is especially important in patients who have undergone multiple surgical procedures as they are at an increased risk for developing ACD.



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      Contributed by Matilda Nicholas, MD, PhD