Allergic Contact Dermatitis (ACD)
The term contact dermatitis sometimes is used incorrectly as a synonym for allergic contact dermatitis (ACD). Contact dermatitis is inflammation of the skin induced by chemicals that directly damage the skin (see Contact Dermatitis, Irritant) and by specific sensitivity in the case of allergic contact dermatitis. Allergic contact dermatitis is inflammation of the skin manifested by varying degrees of erythema, edema, and vesiculation. It is a delayed type of induced sensitivity (allergy) resulting from cutaneous contact with a specific allergen to which the patient has developed a specific sensitivity.
Jadassohn first described allergic contact dermatitis in 1895. He developed the patch test to identify the chemicals to which the patient was allergic. Sulzberger popularized patch testing in the US in the 1930s. The Finn chamber was designed in the 1970s; this is the standard method for patch testing individuals to chemicals not found in the thin-layer rapid use epicutaneous (TRUE) test, which became available in the United States in the 1990s.
The causes of allergic contact dermatitis evolve over time. Mercury compounds once were important causes of allergic contact dermatitis but rarely are used as topical medications and, currently, are less common as a cause of allergic contact dermatitis. Ethylenediamine, which was present in the original Mycolog cream, declined as a primary cause of allergic contact dermatitis once Mycolog cream was reformulated to no longer contain this allergen.
Jadassohn first described allergic contact dermatitis in 1895. He developed the patch test to identify the chemicals to which the patient was allergic. Sulzberger popularized patch testing in the US in the 1930s. The Finn chamber was designed in the 1970s; this is the standard method for patch testing individuals to chemicals not found in the thin-layer rapid use epicutaneous (TRUE) test, which became available in the United States in the 1990s.
The causes of allergic contact dermatitis evolve over time. Mercury compounds once were important causes of allergic contact dermatitis but rarely are used as topical medications and, currently, are less common as a cause of allergic contact dermatitis. Ethylenediamine, which was present in the original Mycolog cream, declined as a primary cause of allergic contact dermatitis once Mycolog cream was reformulated to no longer contain this allergen.
Pathophysiology
Most chemicals able to provoke allergic contact dermatitis have small molecules (< 500 d). Approximately 3000 chemicals are well documented as specific causes of allergic contact dermatitis. The small chemical molecules responsible for allergic contact dermatitis must bind to carrier proteins on Langerhans cells, which are situated within the suprabasilar layer of the epidermis. Langerhans cells are the antigen-presenting cells within the skin. Langerhans cells interact with CD4+ T cells (helper T cells). Skin irritation by both nonallergenic and allergenic compounds induces Langerhans cell migration and maturation. In contrast, only allergenic compounds induce CD1a+ CD83+ Langerhans cell migration with partial maturation at subtoxic concentration.[1]
Cytokines also play an important role in allergic contact dermatitis because they regulate accessory-adhesion molecules, such as intercellular adhesion molecule 1. Interleukin 8 may be a cytokine indicating allergic contact dermatitis, not irritant contact dermatitis. Langerhans cells can migrate from the epidermis to the regional draining lymph nodes. Sensitization to a chemical requires intact lymphatic pathways. The initial sensitization typically takes 10-14 days from initial exposure to a strong contact allergen such as poison ivy. Some individuals develop specific sensitivity to allergens (eg, chromate in cement) following years of chronic low-grade exposure associated with chronic irritant contact dermatitis resulting from the alkaline nature of cement. Once an individual is sensitized to a chemical, allergic contact dermatitis develops within hours to several days of exposure.
CD4+ CCR10+ memory T cells persist in the dermis after allergic contact dermatitis clinically resolves.
Filaggrin barrier defects that predispose individuals to atopic dermatitis might also predispose them to allergic contact dermatitis by allowing greater penetration of chemical haptens.[2]
Cytokines also play an important role in allergic contact dermatitis because they regulate accessory-adhesion molecules, such as intercellular adhesion molecule 1. Interleukin 8 may be a cytokine indicating allergic contact dermatitis, not irritant contact dermatitis. Langerhans cells can migrate from the epidermis to the regional draining lymph nodes. Sensitization to a chemical requires intact lymphatic pathways. The initial sensitization typically takes 10-14 days from initial exposure to a strong contact allergen such as poison ivy. Some individuals develop specific sensitivity to allergens (eg, chromate in cement) following years of chronic low-grade exposure associated with chronic irritant contact dermatitis resulting from the alkaline nature of cement. Once an individual is sensitized to a chemical, allergic contact dermatitis develops within hours to several days of exposure.
CD4+ CCR10+ memory T cells persist in the dermis after allergic contact dermatitis clinically resolves.
Filaggrin barrier defects that predispose individuals to atopic dermatitis might also predispose them to allergic contact dermatitis by allowing greater penetration of chemical haptens.[2]
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