Deciphering Dermatitis
When evaluating a patient with eczematous dermatitis, clinicians rely heavily on clinical history. Is the dermatitis acute or chronic? Is there a childhood or family history of atopy (eczema, asthma, hay fever, food allergies)? Does the patient's occupational or cosmetic history point to potential contact allergen triggers? These questions all get at the same fundamental unknown: is the eczema "intrinsic" or "extrinsic"? Genetic or acquired?
This splitting of eczema into two broad categories—atopic dermatitis (AD) and allergic contact dermatitis (ACD)—is most useful in cases where a patient's dermatitis is strictly due to a delayed-type hypersensitivity reaction to one or more contact allergens. In such cases of "pure" ACD, allergen avoidance can be curative. Clues pointing to ACD include delayed onset (teenage years or adulthood) and a patterned distribution (eg, eyelids for cosmetic dermatitis; periumbilical, ear lobes, or neck for nickel dermatitis).
In contrast, classic AD presents during infancy with recurrent facial dermatitis, morphing during childhood into chronic inflammatory flexural patches and lichenified plaques. It is a T-cell*mdash;driven, chronic inflammatory skin disease with impaired cutaneous barrier function and a prevalence of up to 10% in adults and 25% in children.[1,2]
In many cases, the "AD versus ACD" distinction is an oversimplification.
