In some cases, a diffuse or widespread rash may be seen in response to systemic exposure to an allergen to which the patient was previously sensitized with a topical agent. This is referred to as autoeczematization or an “id” reaction. This secondary dermatitis presents distally to the original dermatitis within 1 or more weeks following the initial onset. There is a range of morphologic presentations, although it is usually symmetrical with areas of erythematous papules and vesicles. Although the pathogenesis remains unclear, id reactions are seen in the context of contact dermatitis and underlying infections.26–28
Despite similar manifestations as an eczematous rash, there are notable differences among these disease processes (Table 1). Conceptualizing the physiologic processes of these entities may be useful in understanding the differences. Briefly, the mechanism driving the development of AD primarily involves an endogenous problem of epithelial cell dysfunction.15 Conversely, ICD and ACD are more consistent with exogenous exposure to an irritant. Although allergens are highly diverse, fragrances and preservatives are most common.29,30
Whereas the direct effects of the irritant primarily drive ICD, ACD is a delayed-type hypersensitivity reaction caused by prior sensitization and exposure to the allergen of interest. A thorough history and physical examination can provide further insight into these conditions. For instance, individuals with AD may describe its onset during childhood with recurrent episodes following an age-dependent pattern throughout their lifetime. In contrast, patients with contact dermatitis may describe its onset following an acute incident, such as exposure to strong irritants or after employment at a new job where certain hygiene practices are common.
Relying on the clinical morphology alone may not be enough to distinguish ICD from ACD. As such, understanding the area of distribution, duration of onset, and associated symptoms may aid in diagnosis. Both ICD and ACD present as sharply demarcated areas, but diffuse involvement of the distal skin can be seen in ACD. The timeline from exposure to the symptom onset is another distinguishing characteristic. In cases of ICD, symptoms present in minutes to hours. In ACD, onset is delayed and may occur up to 72 hours following repeated exposure. Patients with ICD typically manifest with a burning sensation, whereas pruritus is observed in ACD. When ICD and ACD cannot be distinguished clinically, patch testing is necessary (the criterion standard for the diagnosis of ACD).31
The goals of treatment are to resolve the current skin eruption, relieve symptoms, treat the underlying epithelial dysfunction, and engage in maintenance therapy to reduce the risk of future symptoms. In all cases, education is the cornerstone of management to identify and avoid known exacerbating factors. In the case of ICD and ACD, protective equipment such as gloves should be used when working with known irritants.32 General care includes a regular skin care routine and the use of moisturizers to protect against dry skin.33–35 Using moisturizers reduces xerosis, pruritus, erythema, fissuring, and lichenification, thereby lessening the severity of disease.36 In AD, moisturizers are associated with extension to the time of flare, a reduction in the number of flares, and less corticosteroid required to achieve control.37,38 Although various formulations exist, including ointments and creams, no particular preparation has been shown to be significantly more effective.
Steroid-sparing therapies include topical calcineurin inhibitors such as pimecrolimus 1% cream for mild or moderate disease and tacrolimus 0.03% to 0.1% ointment for moderate to severe disease.43,45,46 Common adverse reactions associated with topical calcineurin inhibitors include local stinging and/or burning. In addition, topical calcineurin inhibitors contain a black box warning for increased lymphoma risk,47 but postmarketing surveillance since the early 2000s has not substantiated this risk. Recent developments in topical therapies for the treatment of mild to moderate AD include crisaborole 2% ointment.36,48 Intermittent use of these topical agents can be continued after the initial rash has been resolved, once or twice per week. Proactive use of mild-potency topical corticosteroids or topical calcineurin inhibitors once or twice per week is recommended to reduce the recurrence of flares.36
Systemic therapies (such as systemic steroids) are occasionally used in AD and ACD but not typically in ICD. Systemic corticosteroids are reserved for cases that involve greater than 10% of the body surface area.41 In ACD, systemic corticosteroids are used in cases of severe poison ivy, disseminated ACD, or failure of topical therapies.49 In AD, systemic steroids are reserved for acute, severe exacerbations as bridge therapy to topical corticosteroids. However, systemic corticosteroids are not recommended as a long-term treatment for dermatitis.
Narrowband UV-B phototherapy or psoralen and UV-A may be used in cases of AD and ACD. In particular, the use of narrowband UV-B phototherapy in patients with moderate to severe AD has resulted in significant clinical improvement.50 However, its utility is limited by patient adherence, owing to the frequency of treatments and sparse location of treatment facilities.
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