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윤정은 ( Jeong-eun Yun ),정지웅 ( Jiung Jeong ),강혜련 ( Hye-ryun Kang ) 대한천식알레르기학회 2023 Allergy Asthma & Respiratory Disease Vol.11 No.2
Drug desensitization is a treatment strategy for patients with hypersensitivity to essential drugs without alternatives. The gradual increase in the drug dosage from low doses to therapeutic levels induces a transient immune tolerance to the culprit drug. Although desensitization has traditionally been recommended for IgE-mediated immediate hypersensitivity, this indication has recently been expanded to include non-IgE-mediated immediate responses, nonimmunological responses, and T-cell-mediated delayed hypersensitivity reactions. Although the exact mechanism behind desensitization remains unclear, the process is thought to attenuate various intracellular signals in target cells through Fcε receptor 1 internalization, alteration in signaling pathways in mast cells and basophils, reduction in Ca<sup>2+</sup> influx, and production of anti-drug IgG4 blocking antibody. Desensitization can be used for the safe administration of anti-neoplastic agents, antibiotics, aspirin, and nonsteroidal anti-inflammatory drugs. Various desensitization protocols have been proposed for each drug. The optimization of drug concentration, target dosage, administration interval, and route of administration is key to successful desensitization. In addition, the desensitization protocol should be individualized for each patient with consideration of the severity of the initial hypersensitivity response, the characteristics of the culprit drug, and the nature of the breakthrough reactions. (Allergy Asthma Respir Dis 2023;11:63-71)
유지은 ( Ji Eun Yu ),최영환 ( Young Hwan Choi ),정지웅 ( Jiung Jeong ),조규만 ( Kyu Man Cho ),고영일 ( Young Il Koh ) 대한천식알레르기학회(구 대한알레르기학회) 2015 Allergy Asthma & Respiratory Disease Vol.3 No.6
Stevens-Johnson syndrome (SJS) manifests with severe cutaneous reactions, most commonly triggered by medications, which are characterized by fever and mucocutaneous lesions leading to necrosis and sloughing of the epidermis. To our knowledge, pravastatin- induced SJS has not yet been reported. Here, we describe a case of SJS due to pravastatin, which was diagnosed by a patch test. A 70-year-old woman presented with maculopapular skin rashes, which developed 2 weeks after medication of bisoprolol, amlodipine, pravastatin, spironolactone, and indobufene for cardiac problems. Various bullous-erosive mucocutaneous lesions occupied less than 10% of the total body surface area. Painful oropharyngeal mucous membrane lesions were observed. The vermilion border of the lips became denuded and developed serosanguinous crusts. With the drug withdrawal and the use of systemic corticosteroids, her manifestations resolved. Drug patch tests with bisoprolol, amlodipine, pravastatin, spironolactone, and indobufene were performed, resulting in a positive reaction to pravastatin, but not to the other drugs. To the best of our knowledge, this is the first case of pravastatin-induced SJS. (Allergy Asthma Respir Dis 2015;3:446-448)