Etiology
The most common causes of ACD are the plants of the Rhus genus, poison ivy (toxicodendron radican), poison oak (toxicodendron quercifolium and toxicodendron diversilobum), and poison sumac (toxicodendron vernix), all of which are strong antigens, and require only two exposures to develop sensitization (Jackson Allen, 2006). After the first exposure, the epidermal Langerhan's cells take up the antigen, process it, and deliver it to the draining lymph nodes. T lymphocytes become sensitized to the antigen, cytokines are proliferated, enter the circulatory system, and eventually come in contact with Langerhan's cells in the skin (Graham-Brown & Bourke, 1998). The next time the sensitized person comes in contact with the antigen, inflammatory mediators are released, causing the allergic response. This type of ACD is sometimes called Rhus dermatitis and the oleoresin plant oil, or urushiol (found in leaves, stems, and roots), of the plant embeds in the skin, producing intense inflammation (Jackson Allen, 2006). This triggers an immune response, and the immune system then attacks the skin containing the urushiol. Allergic phytodermatitis occurs after sensitized individuals are exposed to plant allergens (Habif, 2004). Urushiol sensitivity has a familial characteristic and can be a predictor of childhood sensitization. This oil may be contacted directly through contact with the plant or indirectly from clothing, sports equipment, garden tools, and pets. Other allergens include nickel, latex, fragrances, cosmetics, soaps, detergents, jewelry, hair products, deodorant, clothing, cleansers, neomycin, plants, weeds, and foods, among others (Goldsmith, Lazarus, & Tharp, 1997).
Dermatology Nursing © 2010 Jannetti Publications, Inc.
Cite this: Allergic Contact Dermatitis: Poison Ivy - Medscape - Jul 01, 2010.
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