Urticaria, or hives, is a cutaneous IgE-mediated reaction marked by the development of pruritic, erythemic wheals of varying size that generally disappear quickly. Erythema multiforme is a more pronounced urticarial variant, characterized by typical target lesions. Angioedema is believed to be an IgE-mediated reaction characterized by edema formation in the dermis, most generally involving the face and neck. These manifestations may accompany many allergic reactions. As with all allergic manifestations, a detailed history of exposures, ingestions, medications, and infections and a family history should be obtained. If an etiologic agent can be identified, future reactions may be avoided. Treatment of these reactions is generally supportive and symptomatic, with attempts to identify and remove the offending agent. Epinephrine, antihistamines, and steroids are most often tried. Oral antihistamines and steroids for several days may be beneficial. The addition of an H 2 receptor blocker, such as ranitidine, may also be useful in more severe cases. Cold compresses may be soothing to affected areas. Referral to an allergy specialist is indicated.13
Angioedema of the tongue, lips, and face occurs in 0.1 to 0.2 percent of patients taking angiotensin-converting enzyme (ACE) inhibitor antihypertensives. Fortunately, most cases are mild and transient. Management is supportive, with special attention to the airway, which can become occluded rapidly and unpredictably. One must anticipate and be prepared for airway problems in any patient who presents with angioedema. Typical allergic-reaction drugs, such as antihistamines and steroids, are not proven to be beneficial due to the pathophysiology of ACE-inhibitor angioedema. Normally, ACE inactivates bradykinin, a potent vasodilator, and converts angiotensin I to angiotensin II, a potent vasoconstrictor. ACE inhibitors therefore allow accumulation of bradykinin and angiotensin I, which leads to vasodilation, hypotension, and angioedema. Also, ACE inhibitor angioedema is not associated with an increase in IgE. For this reason, angioedema is usually refractory to standard medical therapy. Epinephrine, antihistamines, and steroids are still used; however, their benefits have not been clearly demonstrated in the literature. Immediate withdrawal from the ACE inhibitor is indicated, and another antihypertensive should be prescribed as needed. Patients with mild swelling and no evidence of airway obstruction can be observed in the emergency department and discharged if swelling diminishes. Rebound or recurrent swelling will not occur unless the patient takes an ACE inhibitor again. Patients with moderate-to-severe swelling, dysphagia, or respiratory distress are best admitted for close observation. 1 J.5
Hereditary angioedema is an autosomal dominant disorder with a characteristic complement pathway deficiency: low levels of C1 esterase inhibitor or elevated levels of dysfunctional C1 esterase inhibitor with low levels of C4 between acute attacks. Reactions often involve the upper respiratory tract and gastrointestinal tract. Attacks can last from a few hours to 1 to 2 days. Minor trauma often precipitates a reaction. Many of the typical treatments of allergic problems, such as epinephrine, steroids, and antihistamines, have been tried, but their effectiveness is not clearly demonstrated. 13 Prophylaxis of acute attacks is possible with attenuated adrogens, such as stanozolol 2 mg/d or danazol 200 mg/d.16 Acute attacks can be shortened by C1 esterase inhibitor replacement, either by a concentrate or fresh-frozen plasma infusion.17 Treatment of patients is complex and best done in coordination with the appropriate specialist.
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