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Angioedema attacks are common causes of emergency care, and due to the potential for severity, it is important that professionals who work in these services know their causes and management. The mechanisms involved in angioedema without urticaria may be histamine- or bradykinin-mediated. The most common causes of histamine-mediated angioedema are foods, medications, insect sting and idiopathic. When the mediator is bradykinin, the triggers are angiotensin-converting enzyme inhibitors and factors related to acquired angioedema with deficiency of C1-inhibitor or hereditary angioedema, which are less common, but very important because of the possibility of fatal outcome. Hereditary angioedema is a rare disease characterized by attacks of edema that affect the subcutaneous tissue and mucous membranes of various organs, manifesting mainly by angioedema and abdominal pain. This type of angioedema does not respond to the usual treatment with epinephrine, antihistamines and corticosteroids. Thus, if not identified and treated appropriately, these patients have an estimated risk of mortality from laryngeal edema of 25% to 40%. Hereditary angioedema treatment has changed dramatically in recent years with the development of new and efficient drugs for attack management: plasma-derived C1 inhibitor, recombinant human C1-inhibitor, bradykinin B2 receptor antagonist (icatibant), and the kallikrein inhibitor (ecallantide). In Brazil, plasma-derived C1 inhibitor and icatibant have already been approved for use. Proper management of these patients in the emergency department avoids unnecessary surgery and, especially, fatal outcomes.

Objective To evaluate the positivity of challenge tests of patients suspected of chronic inducible urticaria and the response to treatment. Methods A retrospective study of electronic medical records of patients suspected of chronic inducible urticaria. All patients were submitted to challenge tests with triggering stimuli, according to the clinical history and, subsequently, the response to drug treatment was evaluated. Results A total of 191 patients with suspected chronic inducible urticaria were included. It was confirmed in 118 patients and 122 positive tests (4 patients with 2 different positive tests). Most had dermographic urticaria (70.3%), followed by cholinergic urticaria (17.8%). Regarding treatment, 28% responded to antihistamine in licensed doses, 34.7% with increased doses, 9.3% responded to the addition of another medication. The concomitance of chronic inducible urticaria and chronic spontaneous urticaria was found in 35.3% of patients, being more frequent in females, with longer time to control symptoms and higher frequency of cholinergic urticaria. Conclusion The confirmation of chronic inducible urticaria in patients with this suspicion, after challenge tests, was high. There was a good response to antihistamine. In the concomitance of chronic spontaneous urticaria, longer time to control symptoms and higher frequency of cholinergic urticaria were observed.

The fixed drug eruption is a non-immediate hypersensitivity reaction to drug, characterized by recurrent erythematous or violaceous, rounded, well-defined border plaques, which always appear in the same location every time the culprit drug is administered. The usual practice is to avoid the drug involved and to use a structurally different drug. However, there are situations in which there is no safe and effective therapy. In such situations, desensitization is the only option. We describe the case of a patient who presented fixed eruption due to sulfamethoxazole-trimethoprim, who underwent successful desensitization, but required a repeat procedure twice due to relapse after inadvertent full-dose reintroduction. In non-immediate hypersensitivity reaction to drug, the indication is controversial and there is no technical standardization. Furthermore, the time at which such tolerance is lost after discontinuing the drug involved is unknown. In severe non-immediate reactions of types II and III, desensitization is contraindicated. The patient underwent desensitisation to sulfamethoxazole-trimethoprim three times - the first with recurrence of lesions and the second and third without manifestations, all concluded successfully and with no premedication.