Explain the pathogenesis of allergic contact dermatitis (ACD).

ACD is a type IV, delayed, cell-mediated, hypersensitivity reaction. Initially, a low-molecular-weight antigen hapten (<500 Daltons) contacts the skin and forms a hapten–carrier protein complex. This complex then associates itself with an epidermal Langerhans’ cell, which presents the complete antigen to a T-helper cell, causing the release of various mediators. Subsequently, T-cell expansion occurs in regional lymph nodes, producing specific memory and T-effector lymphocytes, which circulate in the general bloodstream. This whole process of sensitization occurs in approximately 5 to 21 days. Upon reexposure to the specific antigen, there is proliferation of activated T cells, mediator release, and migration of cytotoxic T cells, resulting in cutaneous eczematous inflammation at the site of contact. This phase occurs within 48 to 72 hours after exposure. Because many allergens are irritants, preceding irritation is common and may enhance allergen absorption. In contrast to irritant reactions, relatively small concentrations of an allergen can be enough to elicit an inflammatory reaction. Acute ACD may have erythema, edema, and vesicle formation. Chronic ACD reactions are scaly, erythematous, possibly lichenified, and can mimic chronic ICD. Table 9-1 compares ACD and ICD.

Li L, Cruz P: Allergic contact dermatitis: pathophysiology applied to future therapy, Dermatol Thera 17:219–223, 2004.

 

Table 9-1. Comparison of Irritant and Allergic Contact Dermatitis
			IRRITANT		ALLERGIC
	Examples		Water, soap		Nickel, fragrance, hair dye
	Number of compounds		Many		Fewer
	Distribution of reaction		Localized		May spread beyond area of maximal contact and become generalized
	Concentration of agent needed to elicit reaction		High		Can be minute
	Time course		Immediate to late		Sensitization in 2 weeks; elicitation takes 24–72 hrs
	Immunology		Nonspecific		Specific type IV delayed hypersensitivity reaction
	Diagnostic test		None		Patch test