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ALLERGIC CONTACT DERMATITIS


ALLERGIC CONTACT DERMATITIS
Allergic contact dermatitis is one of the rashes most frequently encountered in the clinician’s office. It is responsible for a large proportion of occupationally induced skin disease. Urushiol from the sap of poison ivy, oak, or sumac plants is the most common cause of allergic contact dermatitis in the United States. The clinical morphology, the distribution of the rash, and results from skin patch testing are used to make the diagnosis. Patch testing is performed when the causative agent is unknown. Nickel has been the most frequent cause of positive patch testing in the world for years. Urushiol is not tested clinically, because almost 100% of the population reacts to this chemical.

MORPHOLOGY OF ALLERGIC CONTACT DERMATITIS
MORPHOLOGY OF ALLERGIC CONTACT DERMATITIS

Clinical Findings: Allergic contact dermatitis can manifest in a multitude of ways. The acute form may show linear streaks of juicy papules and vesicles. Variable amounts of surrounding edema can be seen. Edema is much more common in the loose skin around the eyelids and facial region. Chronic allergic contact dermatitis can manifest with red-pink patches and plaques with various amounts of lichenification. There are localized forms and generalized forms. One of the unique forms of allergic contact dermatitis is the scattered generalized form. Pruritus is an almost universal finding, and it can be so severe as to cause excoriations and small ulcerations.
The prototype of allergic contact dermatitis is the reaction to the poison ivy family of plants. After contact with this plant, urushiol resin is absorbed into the skin and initiates the immune system response to cause allergic contact dermatitis. The dose and the duration of contact with the allergen are important influences on the severity of the rash that develops. Between 3 and 14 days after exposure, the patient notices linear juicy papules and vesicles forming at the sites of contact. The most commonly affected areas are the extremities. Air-borne contact dermatitis may be seen from burning of wood with the poison ivy vine present. These reactions are usually seen on skin that was not covered with clothing, and they can be very severe on the face and eyelids, often causing massive swelling and impeding vision.
The location of the dermatitis can be used as a clue to the diagnosis. A nurse with hand dermatitis may be allergic to a component of the gloves being worn occupationally. A young child with a lichenified rash around the umbilicus may be allergic to a metal component of a pant snap or zipper. The most common culprit in these cases is nickel. Finger dermatitis may be caused by the application of acrylic nails or nail polish. Allergic contact dermatitis can also be seen within the oral cavity, most commonly adjacent to dental amalgams or prostheses. Oral allergic contact dermatitis can mimic oral lichen planus. Lichen planus is usually widespread and affects the mucosa and gingiva both adjacent to and distant from any dental restorations.
The diagnosis in all these cases can be made based on patch testing. Chambers loaded with specific concentrations and amounts of known allergens are applied to the back of the individual. The patches are left on for 48 hours and then removed. After an hour, the first reading is made, based on the reaction seen under the chamber. Elevation of the skin or vesiculation is considered to be a positive reaction.
The presence of only macular erythema needs to be interpreted cautiously but can be considered a positive result in certain situations. Pustular reactions are considered to be irritant reactions and not relevant. The patient must come back for a final reading 3 to 7 days after application of the patches. This is the most critical reading and gives the most valuable information.
Pathogenesis: Much is known about the mechanism of allergic contact dermatitis. This form of dermatitis requires a sensitization and elicitation phase for development. During the sensitization phase, the patient is exposed for the first time to the antigen. The antigen is absorbed through the skin and is phagocytosed by an antigen-presenting cell within the epidermis. The antigen-presenting cell internalizes the antigen and processes it within its lysosomal apparatus. The processed antigen is then sent to the cell surface and expressed on a human leukocyte antigen (HLA) molecule. The antigen-presenting cell migrates to the local draining lymph node and presents the antigen in association with the HLA molecule to T cells. The T cells recognize each individual antigen and proliferate locally, resulting in a clone of lymphocytes that recognize that specific antigen; these lymphocytes then remain ready for when the patient comes in contact with the same antigen in the future.
During the elicitation phase, the patient is reexposed to the antigen. The antigen-presenting cells again process the antigen and present it to the newly cloned lymphocytes, which migrate back to the skin and cause the clinical findings of edema, spongiosis, vesicles, and bullae. If the antigen is exposed in a chronic manner, the findings will be less acute in nature, and the typical findings of a chronic dermatitis are seen.
This entire process is dependent on the size and permeability of the antigen, the recognition and processing of the antigen by the antigen-presenting cell, and the complex interactions among multiple T and B cells. Antign-presenting cells and B cells are required for activation of the T cells and propagation of the allergic contact dermatitis.
Histology: The initial finding in acute allergic contact dermatitis is spongiosis of the epidermis with an associated superficial and deep lymphocytic infiltrate with scattered eosinophils. As the rash progresses, the spongiosis can worsen, and intraepidermal vesicles start to form. The vesicles may eventually coalesce into large bullae.
Chronic allergic dermatitis usually shows acanthosis with spongiosis and eosinophils within the infiltrate. A superficial and deep perivascular lymphocytic infiltrate is seen. Excoriations can also be appreciated.
PATCH TESTING AND TYPE IV HYPERSENSITIVITY FOR ALLERGIC CONTACT DERMATITIS
PATCH TESTING AND TYPE IV HYPERSENSITIVITY FOR ALLERGIC CONTACT DERMATITIS

Treatment: Acute localized allergic contact dermatitis can be treated with a potent topical steroid and strict avoidance of the offending agent. Oral sedating antihistamines work better for the pruritus than their non-sedating counterparts do. Soaks that help to dry the dermatitis are helpful and include aluminum acetate (Domeboro’s solution). Because the most common culprit is the poison ivy plant, time should be taken to explain to the patient the appearance and nature of this plant. As a good rule of thumb, if a plant has three leaves, it could be poison ivy: “Leaves of three, let it be.” Allergic contact dermatitis that is widespread or that affects the eyelids, hands, or groin region can be treated with a tapering dose of oral corticosteroid over a 2- to 3-week period. If the steroid is tapered too quickly, the patient may experience a poststeroid flare of their dermatitis, which can be resistant to further corticosteroid therapy.
Patients who do not respond to these measures should undergo patch testing to determine whether another antigen is causing or provoking the dermatitis. Without the use of patch testing, the allergen will remain unknown and the dermatitis will persist. Not infrequently, patients are found to be allergic to a fragrance or preservative that is an ingredient in one of their personal care products. Once they stop using the product, the dermatitis finally resolves.

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