Skin Disorders Guide

Diagnostic Hallmarks

1. Distribution
   (a) location of the lesions suggests a specific contactant
   (b) unilateral or asymmetrical distribution suggests external causation
2. Shape of the lesions suggests a specific contactant to the clinician
3. Removal of the suspected contactant leads to resolution of the dermatitis
4. Positive patch test

Clinical Presentaion

The lesions of allergic contact dermatitis are quite different in appearance from those of irritant contact dermatitis. Erythema and edema are prominent, and pruritus is often troublesome. In the more acute cases, weeping and crusting will be present, while in chronic cases, scale and fissuring are the dominant findings. In either instance, some minor degree of excoriation may be found. Blistering is seen only in those cases resulting from contact with plants of the poison ivy type.

The distribution and shape of individual lesions may provide clues to the diagnosis of allergic contact dermatitis. Asymmetrically or unilaterally distributed lesions suggest that the eruption was externally caused and thus could be due to a contactant of some sort. The presence of lesions with a nonround (especially linear or angular) configuration is likewise a clue to possible external causation. In many instances the location and shape of a lesion will suggest to the examiner, unaided by patient history, a single, specific contactant.

Course and Prognosis

Removal of the responsible contactant results in spontaneous resolution of lesions over a 7- to IO-day period. Immunologic sensitivity to these contactants remains for many years, and thus reexposure, even to very small concentrations, is rapidly followed by exacerbation of the eczematous changes. Occasionally, the itch-scratch cycle becomes superimposed on allergic contact dermatitis. In such instances, removal of the contactant alone is insufficient to obtain resolution; attention must also be directed toward disruption of the itch-scratch cycle.

Pathophysiology

Allergic contact dermatitis is an immunologic event. The external factor (the antigen) does not itself cause any direct damage. The eczematous change occurs, instead, as a result of the inflammatory response that the antigen provokes. Moreover, development of allergic contact dermatitis requires the presence of a suitably sensitized host. Thus, one’s first exposure is never accompanied by a significant cutaneous reaction, it simply initiates the process of sensitization.

During sensitization the antigen on the skin is intercepted by epidermal dendritic macrophages known as Langerhans cells. Once processed by the Langerhans cells, the antigen is presented to helper T-cell lymphocytes. These cells, in turn, probably through the release of interleukin-2, activate a clone of responder T cells. This process begins in the epidermis but is concluded in the regional lymph nodes that drain the contact site.

At this point the host is primed to react to subsequent antigen reexposure. When contact with the antigen next occurs, these sensitized lymphocytes migrate to the skin where they attack the offending antigen through the creation of a vigorous cell-mediated immune response.

Our understanding of why some substances stimulate this sensitization reaction and others do not is limited. Nevertheless, it is fortunate that of the thousands of substances we contact daily, only a minuscule number have any significant antigenic potential. Molecules that seem to be the most potent antigens are characterized by the presence of one or more chemically active sites that can form stable, covalent bonds with other substances. Small molecules (generally those under 5000 daltons in molecular mass), in themselves, may not be troublesome, but by binding to a carrier protein present in the host these haptens can become antigenic. Larger molecules do not require carrier proteins and can, instead, bind directly to macrophage cell membranes.

The stratum corneum plays an important role in sensitization. Thickly keratinized surfaces such as the palms and soles resist sensitization, whereas skin with a disrupted stratum corneum is rather easily sensitized. Moreover, chemicals that are soluble in the lipid layer of the stratum corneum may possess stronger antigenic potential than do those that are not soluble.

The substances most likely to cause contact dermatitis and the circumstances under which they are most likely to be contacted include the following. For nondermatologic physicians the most widely encountered antigen is probably that of the pentadecylcatechol responsible for poison-ivy-type contact dermatitis. The second most frequent offender is undoubtedly nickel. Nickel is found in most metals used in snaps, buckles, and jewelry. Thus nickel contact dermatitis can be found in association with rings, bracelets, watch bands, earrings, and metal closures used in various types of clothing. Other common causes of allergic contact dermatitis include- reactions to formaldehyde used in the preparation of permanent press clothing, paraphenylenediamine used in dyes, neomycin, benzocaine, parabens, and ethylenediamine used in many topically applied medications, chromates used in cements and cutting oils, uncured epoxy resins used in many industries, several chemicals used in sunscreens, fragrances used in perfumes, permanent wave solutions used by beauty operators, and accelerators and antioxidants used in the manufacture of rubber. Last but not least is the development of contact urticaria (and sometimes anaphylaxis) on exposure to latex.

The antigens account for more than 90% of all instances of allergic contact dermatitis. Note that soaps, detergents, and most types of clothing are not on this list. These latter items are only rarely responsible for allergic reactions and should not be incriminated simply because there is a history of their use.

Therapy

The first step in therapy is the identification of suspected contactants. This identification is often possible simply because the location or shape of the lesions suggest a specific contactants. In more subtle cases, one has to work with statistical probability based on the knowledge of which contactants are among the most frequent offenders. Rarely, in cases of unremitting eczematous disease, even without a history suggesting a contact etiology, there may be justification for the application of screening patch tests in hopes that one or more positive responses will provide at least a clue to the problem.

Once identified, exposure to the contactant needs to be discontinued. In most cases this is not difficult, but in some instances the offending chemical may be found in unsuspected alternative sources, or the chemical may cross-react with other substances.

Treatment of the dermatitis itself depends on the use of steroids. In most instances, topically applied steroids of mid or high potency will suffice. In instances of greater severity, systemically administered steroids may be desirable.