Atopic dermatitis (AD) and contact dermatitis are common eczematous disorders mediated through inflammatory mechanisms. As with other eczematous disorders, they are both characterized by a serous accumulation in the epidermis and a dermal inflammatory infiltrate, expressed clinically as erythema, with or without concomitant edema and/or blistering. AD is a recurrent, hereditary eczematous condition that typically begins in childhood, affecting patients with a personal or family history of hayfever, asthma, and/or chronic dermatitis. Multiple genetic abnormalities render atopics susceptible to flares of disease activity in the presence of environmental triggers including various allergens, as well as climate and temperature change. Exacerbation of AD can, however, occur in the absence of a known environmental stimulus. Contact dermatitis is an inflammatory condition caused by direct skin exposure to an offending chemical with or without a requirement for ultraviolet light. There are two distinct types of contact dermatitis: irritant contact dermatitis (ICD) and allergic contact dermatitis (ACD). ICD is an inflammatory reaction caused by a chemical insult that results in direct cellular injury upon skin contact. The majority of cases of ICD are associated with soaps, detergents, solvents, acids, and alkali. There are two categories of ICD: acute reactions that develop minutes to hours after exposure to a very strong irritant chemical, and cumulative insult reactions, which follow repeated contact with milder irritants. Since ICD is essentially an injury, all individuals will develop an eruption when certain parameters of chemical concentration and frequency of exposure are exceeded. ACD, like AD, is an eczematous disease mediated through immune mechanisms. ACD is an acquired skin disorder that occurs at sites of contact with small chemical haptens in only those individuals who have been previously exposed to, and immunologically sensitized to, a particular chemical. In contrast to ICD, only a small percentage of the population develops an eruption when exposed to chemicals causing ACD. The most common chemical allergens causing the condition in North America include nickel sulfate, found in everything from keys to buttons on clothing, as well as the pentadecylcatechols, the active moiety in plants of the Rhus family, which include poison ivy, poison oak, and poison sumac. Active skin disease, such as ICD or AD, which disturb the integrity of the body’s epidermal barrier, can be predisposing factors for ACD, allowing easier access of potential chemical allergens to the immune system. Despite differing etiologies, AD and contact dermatitis have been the focus of many studies examining the potential association of the two conditions. In the past, it was believed that patients suffering from AD were less likely to suffer from ACD. However, more recent studies indicate that ACD is equally prevalent among atopics and nonatopics. Current research also indicates that AD patients may be more prone to suffer from ICD. Understanding the potential links between AD and contact dermatitis, and the parallel aspects of their pathogenesis, diagnosis, and treatment, can be helpful to clinicians caring for patients suffering from the disorders.
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Jun 1, 2007
Peck Y Ong + 1
Open Access