Drug-induced urticaria and angioedema

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Abstract

Urticaria and angioedema are the most common manifestations of drug hypersensitivity and are caused by drugs that differ in chemical nature and mechanisms of action. The pathogenesis of drug-induced urticaria and angioedema can be based on immunological and non-immunological reactions. Immunological (allergic) urticaria and associated angioedema most often develop due to immunoglobulin E-mediated reactions. Non-immunological hypersensitivity is caused by the direct action of an agonist drug on target cells, followed by the release of a wide range of inflammatory mediators and cytokines, or the effect of drugs on the metabolism of several biologically active substances that stimulate inflammatory cells. Isolated angioedema (not accompanied by urticaria) may be a sign of drug allergy but is more often due to heterogeneous non-immunological reactions that activate mastocytes and basophils in various ways. Another common variant of drug-induced isolated angioedema is not associated with target cell degranulation but develops according to different mechanisms, leading to excessive bradykinin accumulation. Finally, some drugs may exacerbate the pathology of the complement system in patients with hereditary or acquired angioedema.

Here, the etiology, pathogenesis, clinical picture, diagnosis, principles of therapy, and prevention of heterogeneous variants of drug-induced urticaria and angioedema are considered from modern positions.

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About the authors

Irina I. Vorzheva

Irkutsk State Medical Academy of Postgraduate Education, Russian Medical Academy of Continuous Professional Education

Author for correspondence.
Email: vorzheva.irina@gmail.com
ORCID iD: 0000-0002-9405-854X
SPIN-code: 4872-0998

MD, Cand. Sci. (Med.), Associate Professor

Russian Federation, Irkutsk

Boris A. Chernyak

Irkutsk State Medical Academy of Postgraduate Education, Russian Medical Academy of Continuous Professional Education

Email: ba.chernyak@gmail.com
ORCID iD: 0000-0002-5902-6198
SPIN-code: 5928-2586

MD, Dr. Sci. (Med.), Professor

Russian Federation, Irkutsk

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Supplementary files

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2. Fig. 1. Urticaria caused by Tempalgin. Multiple wheals of various sizes on erythematous background. (Photo from authors’ archive).

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3. Fig. 2. Bradykinin angioedema caused by ACE inhibitor. (Photo from authors’ archive).

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4. Fig. 3. Protein allergic contact systemic dermatitis caused by bee venom in medicine “Sofya Balm.” Rubbing was done along the spine in the lower thoracic region and sacrum, which has the most pronounced confluent rashes are observed. The patient has history of contact urticaria when using “Apizartron” ointment, which also contains bee venom. (Photo from authors’ archive).

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5. Fig. 4. Skin tests with levofloxacin. The prick test with whole solution (5 mg/1 ml) is ambiguous. IT at a dilution of 1:100 with a volume of 0.02 ml: after 20 minutes, a giant wheal with pseudopodia appeared, which resolved within 1 hour. There were no late skin reactions or systemic clinical manifestations the day after IT. IT was regarded as a false positive, owing to non-immunological mediator raised from skin mast cells. The intravenous provocation test with levofloxacin the next day was negative. Prior to coaxial arthroplasty surgery, an examination was carried out. The patient had a history of anaphylaxis during penicillin administration and urticaria during treatment with azithromycin. Prior to the skin test, no levofloxacin was administered. Following the examination, the patient given levofloxacin in the postoperative period, and no hypersensitivity was observed. (Photo from authors’ archive).

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