Excerpt from Contact Dermatitis, Allergic


Synonyms, Key Words, and Related Terms: contact hypersensitivity

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Background: The term contact dermatitis sometimes is used incorrectly as a synonym for allergic contact dermatitis (ACD). Contact dermatitis is inflammation of the skin induced by chemicals that directly damage the skin (see Contact Dermatitis, Irritant) and by specific sensitivity in the case of ACD. ACD is inflammation of the skin manifested by varying degrees of erythema, edema, and vesiculation. It is a delayed type of induced sensitivity (allergy) resulting from cutaneous contact with a specific allergen to which the patient has developed a specific sensitivity.

Jadassohn first described ACD in 1895. He developed the patch test to identify the chemicals to which the patient was allergic. Sulzberger popularized patch testing in the US in the 1930s. The Finn chamber was designed in the 1970s; this is the standard method for patch testing individuals to chemicals not found in the thin-layer rapid use epicutaneous (TRUE) test, which became available in the US in the 1990s.

The causes of ACD evolve over time. Mercury compounds once were important causes of ACD but rarely are used as topical medications and, currently, are less common as a cause of ACD. Ethylenediamine, which was present in the original Mycolog cream, declined as a primary cause of ACD once Mycolog cream was reformulated to no longer contain this allergen.

Pathophysiology: Most chemicals able to provoke ACD have small molecules (<500 d). Approximately 3000 chemicals are well documented as specific causes of ACD. The small chemical molecules responsible for ACD must bind to carrier proteins on Langerhans cells, which are situated within the suprabasilar layer of the epidermis. Langerhans cells are the antigen-presenting cells within the skin. Langerhans cells interact with CD4+ T cells (helper T cells). Skin irritation by both nonallergenic and allergenic compounds induces Langerhans cell migration and maturation. In contrast, only allergenic compounds induce CD1a+ CD83+ Langerhans cell migration with partial maturation at subtoxic concentration.

Cytokines also play an important role in ACD because they regulate accessory-adhesion molecules, such as intercellular adhesion molecule 1. Interleukin 8 may be a cytokine indicating ACD, not irritant contact dermatitis. Langerhans cells can migrate from the epidermis to the regional draining lymph nodes. Sensitization to a chemical requires intact lymphatic pathways. The initial sensitization typically takes 10-14 days from initial exposure to a strong contact allergen such as poison ivy. Some individuals develop specific sensitivity to allergens (eg, chromate in cement) following years of chronic low-grade exposure associated with chronic irritant contact dermatitis resulting from the alkaline nature of cement. Once an individual is sensitized to a chemical, ACD develops within hours to several days of exposure.

CD4+ CCR10+ memory T cells persist in the dermis after ACD clinically resolves.

Frequency:

  • In the US: The National Health and Nutritional Examination Survey (NHANES) estimated the prevalence of contact dermatitis to be 13.6 cases per 1000 population using physical examinations by dermatologists of a selected sample of patients. NHANES underreported the prevalence compared with the physical examination findings. The National Ambulatory Medical Care Survey conducted in 1995 estimated 8.4 million outpatient visits to American physicians for contact dermatitis. This was the second most frequent dermatologic diagnosis. Of office visits to dermatologists, 9% are for dermatitis. At a student health center dermatology clinic, 3.1% of patients presented for ACD, and 2.3% presented for irritant contact dermatitis.