Drug induced Kounis syndrome: does oxidative stress play a role?

Q2 Medicine

Clinical and Molecular Allergy Pub Date : 2018-10-01 eCollection Date: 2018-01-01 DOI:10.1186/s12948-018-0099-2

Luisa Ricciardi, Fabiana Furci, Marco Casciaro, Eleonora Di Salvo, Mariateresa Cristani, Valeria Tigano, Paola Lucia Minciullo, Sebastiano Gangemi

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引用次数: 3

Abstract

Background: Kounis syndrome (KS) has been described as the coincidental occurrence of acute coronary syndromes during an allergic reaction with cardiac anaphylaxis. It is caused by inflammatory mediators released after exposure to drugs, food, environmental and other triggers. Oxidative stress occurring in various inflammatory disorders causes molecular damage with the production of advanced oxidation products (AOPPs) and advanced glycation end products (AGEs).

Case presentation: Markers of oxidative stress were evaluated in a patient who had experienced KS after antibiotic administration in order to investigate the possible role of these molecules in KS. No data, up to now, are available on biomarkers of oxidative stress in patients with drug-induced KS.

Conclusions: AOPPs, but not AGEs, were significantly increased in the KS affected patient compared to controls as already reported in mastocytosis affected patients.

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药物性库尼斯综合征:氧化应激是否起作用?

背景:Kounis综合征(KS)被描述为急性冠状动脉综合征同时发生在心脏过敏反应的过敏反应。它是由暴露于药物、食物、环境和其他触发因素后释放的炎症介质引起的。氧化应激发生在各种炎症性疾病中，通过产生晚期氧化产物(AOPPs)和晚期糖基化终产物(AGEs)导致分子损伤。病例介绍:为了研究这些分子在KS中的可能作用，我们评估了一位在抗生素治疗后经历过KS的患者的氧化应激标志物。到目前为止，还没有关于药物性KS患者氧化应激生物标志物的数据。结论:在肥大细胞增多症患者中，与对照组相比，KS患者的AOPPs显著增加，而AGEs未显著增加。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Clinical and Molecular Allergy Medicine-Immunology and Allergy

CiteScore

8.20

自引率

0.00%

发文量

审稿时长

13 weeks

期刊介绍： Clinical and Molecular Allergy is an open access, peer-reviewed, online journal that publishes research on human allergic and immunodeficient disease (immune deficiency not related to HIV infection/AIDS). The scope of the journal encompasses all aspects of the clinical, genetic, molecular and inflammatory aspects of allergic-respiratory (Type 1 hypersensitivity) and non-AIDS immunodeficiency disorders. However, studies of allergic/hypersensitive aspects of HIV infection/AIDS or drug desensitization protocols in AIDS are acceptable. At the basic science level, this includes original work and reviews on the genetic and molecular mechanisms underlying the inflammatory response.