Contact Dermatitis and Related Conditions
DEFINITION
Contact dermatitis is an acute or chronic immunologic (allergic) or nonimmunologic (irritant) inflammation of the skin usually caused by contact with chemicals but occasionally by biologic or physical agents.1 Of the more than 85,000 chemicals in our environment, many can be irritants and more than 4350 have been identified as contact allergens. The potential for these substances to cause contact dermatitis varies greatly, and the severity of the dermatitis or eczema, the most common clinical expression, ranges from a mild, short-lived condition to a severe, persistent, job-threatening disease.
PREVALENCE AND RISK FACTORS
The prevalence of contact dermatitis in the general U.S. population has been variably estimated between 1.5% and 5.4%. Contact dermatitis is the third most common reason for patients to seek consultation with a dermatologist, accounting for 9.2 million visits in 2004. It also accounts for 95% of all reported occupational skin diseases.1
Exogenous and endogenous risk factors are listed in Boxes 1 and 2, respectively. Although genetics, gender, and age can be risk factors, the inherent nature, toxicity, and degree of cutaneous exposure to chemicals are probably more important. A history of atopic dermatitis is linked to an increased susceptibility to irritant dermatitis because of a lower threshold for skin irritation, impaired skin barrier function, and slower healing process.2 Wet work and chemical exposure are major precipitating factors for the development of irritant contact dermatitis (ICD) in patients with atopic eczema. Although atopic patients downregulate Th1 cells with a decreased propensity to contact sensitization, allergic contact dermatitis (ACD) is often seen in patients with atopic eczema, and nickel sensitization is increased in atopic patients.3 Other skin conditions with the highest risk of ACD include stasis dermatitis,1 hand and foot eczemas, and chronic actinic dermatitis.1
Irritant Contact Dermatitis
Irritants cause as much as 80% of cases of contact dermatitis. ICD follows exposure to chemical or physical substances capable of direct damage to the skin.1,2
There are two major types of ICD. Chronic cumulative (traumiterative, marginal) ICD is the type of contact dermatitis most commonly encountered in clinical practice. Cumulative ICD develops as a result of repeated insults to the skin, where the chemicals involved are often multiple and weak.3 The most common irritants include soap, detergents, surfactants, organic solvents, and oils (Box 3).1 Dry skin with a glazed, parched appearance may be the initial sign; erythema, hyperkeratosis, and fissuring can supervene.3 The second major type is acute ICD, which generally results from a single skin exposure to a strong irritant or caustic chemical (alkalis and acids). Most cases are the result of occupational accidents. Depending on the type of exposure to the irritant, the patient can develop erythema, edema, vesicles, and tissue necrosis.1
Allergic Contact Dermatitis
Pathogenesis
ACD is a T cell delayed-type (type IV) hypersensitivity reaction that arises from direct skin exposure to an exogenous allergen. These allergens are low-molecular-weight (<500 Da) lipophilic chemicals called haptens that penetrate the skin and covalently bind to carrier proteins to become fully immunogenic. The new antigen-protein complex is processed by Langerhans cells in the epidermis and then travels to the regional draining lymph nodes and is presented to naïve Th1 cells. There, cytokines such as interleukin 2 and interferon-γ are secreted, leading to clonal proliferation of the newly sensitized memory Th1 cells in the paracortical region of the lymph nodes and are released into the circulation. This is the sensitization phase, which takes 5 to 21 days. On re-exposure to the same antigen, the elicitation phase, the previously sensitized person elicits a clinical dermatitis, usually after 12 to 48 hours.1,3
Clinical Features
The clinical features of ACD are often indistinguishable from those of ICD. In the acute stage, erythematous papules, oozing vesicles, and crusted lesions predominate; these can occur anywhere but are best visualized on the palms, sides of the fingers, periungual areas, and soles. Frequently occurring or persistent episodes of acute contact dermatitis often become chronic, with thickening associated with lichenification, scaling, and fissuring. Postinflammatory hyperpigmentation or hypopigmentation can occur. Pruritus is a hallmark of most forms of contact dermatitis.1 Major causes of ACD are listed in Box 4.
Systemic Contact Dermatitis
Systemic reactivation of ACD, or systemic contact dermatitis (SCD), occurs when persons with contact allergy to a hapten are exposed systemically to the same hapten via the oral, subcutaneous, transcutaneous, intravenous, inhalation, intra-articular, or intravesical route.1,3,5
Clinical features of SCD include flare-up of sites of previous dermatitis or of prior positive patch tests and development of dermatitis in previously unaffected areas, such as vesicular hand eczema, flexural dermatitis, nonspecific maculopapular eruptions, vasculitis-like lesions, and the baboon syndrome,3 which is a well-demarcated eruption on the buttocks, genital area, and inner thighs. Associated systemic symptoms of headache, nausea, vomiting, arthralgias, and diarrhea can accompany the cutaneous findings.
DIAGNOSIS
Diagnostic history and physical examination clues are discussed in the overview of ICD and ACD. The appearance of the lesions often corresponds to whether the patient’s dermatitis is acute or chronic at the time of presentation. Most of the diagnostic discussion focuses on ACD, which is easier to diagnose than ICD. A summary of the diagnostic workup is listed in Box 5. The differential diagnosis of contact dermatitis is listed in Box 6.
