Like contact dermatitis, contact urticaria, or hives, which result from the dilation of the small blood vessels in the skin and leakage of fluid into the surrounding tissue, may be triggered by direct contact with allergenic substances or, more commonly, through direct contact with various irritating agents. Sometimes called welts or wheals, hives are pinkish swellings of the skin and mucous membranes that are usually very itchy and generally last no more than twenty-four hours, often fading somewhere up to six hours after first developing. Ordinary hives range in size from half an inch to twelve inches or more in diameter. Extremely large, swollen hives are called angioedema and may extend the length of an entire extremity or swell the entire face.
Despite the fact that all the chemical mediators responsible for contact urticaria have yet to be identified, histamine is believed to play a major role in the production of the itching, redness, and swelling seen in this condition. In nonallergic cases of contact urticaria, the provocative agent somehow induces the direct release of histamine (and other agents) from mast cells and basophils. IgE, the same antibody involved in triggering attacks of asthma and allergic rhinitis, is believed to be responsible for doing so in allergic cases.
As in the case of irritant contact dermatitis, irritant (or nonim-munologic) contact urticaria may be triggered by a wide variety of substances. Well-known triggers of nonallergic contact urticaria include chemicals naturally found in certain foods, fragrances, flavorings, colorings, and preservatives, as well as additives in soaps, shampoos, toothpastes, and so forth. Specific troublemakers include benzoic acid, sodium benzoate, sorbic acid, cinnamic aldehyde, balsam of Peru, acetic acid, butyric acid, and various alcohols.
While the eruption of allergic contact urticaria looks very much like its nonallergic counterpart, a number of clues help your doctor distinguish between the two. For one thing, individuals with the allergic variety demonstrate an allergy to a particular substance that affects only a small percentage of the population at large. Irritants, by contrast, tend to provoke symptoms in the majority of people. In addition, truly allergic persons generally give a history of previous exposure to the presumed allergen sometime in the past that was not followed by the onset of any symptoms. Those with nonallergic rashes usually recall the onset of the problem the very first time they came in contact with the particular substance. And finally, allergic individuals typically report a pattern of worsening symptoms after each episode of contact, while those with irritant urticaria do not.
The list of potential contact urticaria allergens is very long. Some of the more important ones that have been associated with the reaction include bacitracin, benzoyl peroxide, lindane, menthol, neomycin, nickel, parabens, sunscreens, plastic additives, henna, hair sprays, nail polish, perfumes, birch and teak woods, milk, spices, eggs, meats, flour, and even seminal fluid.
The diagnosis of either variety of contact urticaria rests mostly on the history. Blood testing is rarely helpful, but open patch tests have proven useful in some cases related to cosmetics. In these tests a tiny amount of each test material is applied with a glass rod to a half-inch-square area of skin on the hairless part of the forearm. After thirty minutes the sites are checked for the onset of tingling, itching, redness, and hiving. Prick tests, in which small amounts of suspected materials are injected into the skin, are rarely used nowadays because of the potential risk of provoking severe and even life-threatening reactions.
Naturally, avoiding the offending substance is the best form of treatment for all forms of contact urticaria. Acute attacks are usually treated with topical corticosteroid creams and oral antihistamines. More severe attacks may require a short course of an oral corticosteroid, such as prednisone, Medrol, or Decadron.
