text: Avoidance of triggers\n\nMany patients with urticaria assume that a causative agent can be identified and avoidance of the trigger will cure their ailment. This may be possible in acute urticaria, but unfortunately it is not possible in the majority of chronic urticaria cases because of the idiopathic nature of the condition. General education about urticaria and avoidance of triggers can help patients understand their condition and come to terms with it. \n\nIn general, patients should avoid drugs known to either cause or exacerbate hives, such as aspirin, NSAIDs, opiates, and ACE inhibitors. (Alcohol should also be avoided.) Acetaminophen may be a substitute treatment to control pain. Several studies have shown that COX-2 inhibitors, such as rofecoxib and celecoxib, appear to be safely tolerated in these patients(7,8). The recent withdrawals of rofecoxib (Vioxx) and valdecoxib (Bextra) leave celecoxib (Celebrex) as the currently available COX-2 inhibitor in the United States. ACE inhibitors should be discontinued in anyone experiencing angioedema. Can angiotensin II receptor blockers (ARBs) be used in these patients? A recent study(10) showed that a small percentage of patients with angioedema that was induced by ACE inhibitor use continued to have symptoms when their treatment was switched to an ARB. Therefore, caution should be exercised(16). \n\nPharmacotherapy\n\nPharmacotherapeutic options for urticaria are listed in table 2. What is the first-line treatment? Antihistamines, antihistamines, antihistamines! Newer-generation H1 antihistamines are generally quite effective in controlling the condition and have a side effect profile of minimal or no sedation and dry mucous membranes. First-generation antihistamines, such as hydroxyzine (Atarax, Vistaril), diphenhydramine hydrochloride, and cyproheptadine hydrochloride, may be an add-on therapy. Cyproheptadine is the treatment of choice for both cold urticaria and cholinergic urticaria(3). \n\nTaking antihistamines according to a schedule rather than on an as-needed basis is the key to attaining disease control. Doses may need to be adjusted upward, depending on the severity of the disease. The relative potency of these agents needs to be considered; for example, 10 mg of cetirizine (Zyrtec) is about equivalent to 30 mg of hydroxyzine(3,11). In a study of the central nervous system effects of higher doses of the nonsedating antihistamine fexofenadine, Hindmarch and colleagues(17) found that doses of up to 360 mg did not cause psychomotor or cognitive dysfunction. \n\nIf symptoms are not optimally controlled with H1 antihistamines, addition of an H2 blocker should be considered. Another option is to add doxepin hydrochloride (Sinequan), a tricyclic antidepressant with potent H1 and H2 antihistamine properties and strong antipruritic action. Unfortunately, the severe sedation and dry mouth associated with this medication tend to limit its use. Leukotriene receptor blockers used as add-on therapy to H1 antihistamines have been shown to provide some benefit(18,19). However, as solo therapy, they have not been found to be effective(20). Glucocorticoids are generally not necessary and should be avoided, if possible, because of their associated side effects and the tendency for lesions to recur after discontinuation of these drugs. \n\nWhat are the options for patients with severe, unremitting urticaria who have had poor response to standard therapy? To ensure that the diagnosis is correct, a biopsy and a referral to an allergist should be considered. Nonstandard therapy, such as cyclosporine (Gengraf, Neoral, Sandimmune), has been used with some effectiveness(21). Other nonstandard therapies include intravenous immunoglobulin, plasmapheresis, methotrexate (Rheumatrex, Trexall), colchicine, dapsone, sulfasalazine (Azulfidine), hydroxychloroquine sulfate (Plaquenil), and warfarin sodium (Coumadin)(21). \n\n\nManagement of angioedema\nManagement of angioedema is more difficult than t