Urticaria (Hives) and Angioedema
Mitchell R. Lester
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Treatment of Urticaria and Angioedema
The mainstay of therapy of urticaria/angioedema is H1 receptor blockade. Second generation antihistamines are preferred because they are longer-acting and far less frequently sedating than the first generation antihistamines. There is no antihistamine that is consistently better than another, so patients should the one that is most effective. A trial of several products might be necessary. A brief course of oral corticosteroids may shorten the duration and lessen the severity of severe cases and sometimes will abort an acute case. However, frequent or prolonged courses of oral steroids carries risk greater than the condition itself. Whenever possible (however impractical), cofactors to onset and triggers of physical urticaria should be avoided.

Treatment of CU is analogous to that of allergic airway disease in that a step-wise approach is taken with gradual steps down after consistent control is achieved. If monotherapy with a second generation antihistamine (step 1) is only partially effective, higher/more frequent doses may provide further benefit. If higher doses are more effective, current studies indicate that second generation antihistamines doses can be increased to as much as four times the usual recommended dose. Of course, if higher doses do not provide additional relief, they need not be continued. The addition of another second generation antihistamine and/or a first generation antihistamine at bed time should also be considered. This “mix and match” approach often identifies a combination of antihistamines that provides the best relief.

Some patients with CU benefit from the addition of H2 blockers or leukotriene receptor antagonists (LTRAs). Only a small proportion of cutaneous histamine receptors are H2 receptors. It is possible their utility stems from competition for metabolic pathways, increasing serum H1-blocker levels. There are conflicting data regarding the effectiveness of LTRAs in CU. In poorly controlled CU, a trial of an LTRA might be considered. If there is no response in a short time, the LTRA can be discontinued.

Step 3 treatment recommends daytime use of hydroxyzine or doxepin. On a molar basis, the tricyclic antidepressants (TCAs) have more potent antihistaminic effect than the antihistamines themselves. However, their high risk of sedation can limit their use. Gradually increasing daytime doses of first generation antihistamines and TCAs allows some patients to accommodate to their soporific effects.

Step 4 therapy with alternative agents is reserved for patients with CU refractory to maximally tolerated antihistamine therapy. Omalizumab 150-300 mg SC q4weeks has been approved for patients 12 or older with CIU unresponsive to antihistamines and TCAs. Other alternative therapies including cyclosporine, dapsone, sulfasalazine, mycophenolate, and methotrexate have limited data supporting their utility. They appear to have moderate effects in some patients but there are not enough data to recommend their use until other treatments have failed.

Urticaria and angioedema are common in pediatrics. A thorough history will usually identify if there is a potential preceding and avoidable trigger, especially in acute cases. The majority of CU are idiopathic or have a physical trigger. Without a supportive history of an IgE-mediated trigger or underlying systemic disease, testing is rarely indicated in acute or chronic cases.

Antihistamines are usually adequate to treat urticaria and angioedema, but finding the best antihistamine combination and dose can take some time.

Parents and patients should be instructed on trigger avoidance in acute urticaria and reassured about the benign nature and treatability of almost all CU.


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