The Triggers of Systemic Contact Dermatitis

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. Patients with AD are more likely to develop contact allergies due to immune dysregulation and skin barrier disruption,^[3] with one study showing ACD in 25% of AD patients.^[4] Furthermore, contact dermatitis can masquerade as AD, as illustrated by a recent case series of children misdiagnosed with AD who had developed chronic ACD to methylisothiazolinone-a biocide and preservative found in baby wipes, paint, and "homemade slime."^[5]

Add to this picture the concept of systemic contact dermatitis (SCD): eczema triggered by inhaled or ingested allergens. SCD occurs when skin-sensitized patients are reexposed to a triggering allergen such as Compositae, balsam of Peru, or nickel through the respiratory or gastrointestinal tracts. Flares tend to be severe, widespread, and chronic.

Risk Factors for SCD

What are the risk factors for developing SCD? To address this important question, Scott and colleagues^[6] first identified 23 allergens known to cause SCD via a type IV (delayed) hypersensitivity reaction. They divided these into four broad groups: plant derivatives, metals, steroids, and miscellaneous (dibucaine, ethylenediamine, parabens, propylene glycol).

Next, they performed a retrospective cohort review of 2416 patients who were patch tested for suspected ACD over a 15-year period. Of this group, 457 patients (18.9%) had AD (defined as a history of childhood flexural dermatitis). Patients with AD were further stratified by age (younger or older than 18 years), presence or absence of respiratory atopy, and occupation (wet or dry work).^[7]

The study's patch test cohort had the following main characteristics:

278 out of 457 patients with AD also had respiratory atopy (60.8%)
Patients with AD were more likely to have positive patch tests to SCD-linked allergens if they also had respiratory atopy (odds ratio [OR], 1.28)
Patients without AD had similar patch test results whether or not they had respiratory atopy
In younger patients with AD (< age 18 years), those with concurrent respiratory atopy were most likely to have positive patch tests to SCD-linked allergens (OR, 2.33)
In patients with both AD and respiratory atopy, an occupational history of wet work (eg, hairdresser) versus dry work increased the likelihood of a positive patch test result (OR, 1.47)

Viewpoint

Because of its widespread distribution, severity, and chronicity, SCD can mimic an atopic flare. Patients with treatment-resistant AD should be patch tested for contact allergen triggers, remembering that allergen exposure can occur through inhalation or ingestion.

Based on the observations of Scott and colleagues, younger patients with both AD and respiratory atopy are most likely to have positive patch test results to at least one of the 23 allergens identified in this study as being associated with SCD. Occupational wet work also increases the likelihood of being sensitized to these allergens.^[8]

Do positive patch test results predict the true risk of developing SCD? Not necessarily, as this study was limited by a retrospective design. A prospective study linking positive patch tests to clinically confirmed eczema flares that improve upon allergen avoidance would be far more informative. Nevertheless, these results offer a tantalizing first step. If we can identify those atopic patients who are most likely to develop SCD, then we'll be in a better position to offer targeted patch testing in the future.

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