Abstract
Kounis syndrome was recognized as the concurrence of acute cardiovascular events with
hypersensitivity reactions. We report a case of Kounis syndrome type III (coronary
thrombosis) variant in a 48-year-old man who had experienced recurrent acute myocardial
infarctions after scallion-induced hypersensitivity reactions. After appropriate antithrombotic,
antihistamine, and reperfusion strategies, the patient was found to have elevated
levels of immunoglobulin E and chronic urticaria. Upon administration of omalizumab,
there was an improvement of chronic urticaria, a decrease in immunoglobulin E levels,
and resolution of the ischemic attacks.
Résumé
Il est reconnu que le syndrome de Kounis est caractérisé par la survenue concomitante
d’événements cardiovasculaires aigus et de réactions d’hypersensibilité. Nous rapportons
un cas de syndrome de Kounis de type III (thrombose coronaire) chez un homme de 48
ans qui avait subi des infarctus aigus du myocarde récurrents après des réactions
d’hypersensibilité induites par l’oignon vert. Après des stratégies de traitement
antithrombotique, de traitement antihistaminique et de reperfusion, on s’est aperçu
que le patient avait des concentrations élevées d’immunoglobuline E et une urticaire
chronique. À l’administration d’omalizumab, on a noté une amélioration de l’urticaire
chronique, une diminution des concentrations d’immunoglobuline E et la fin des accidents
ischémiques.
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References
- Kounis syndrome: new classification.Int J Cardiol. 2018; 256: 11
- Thrombotic responses to coronary stents, bioresorbable scaffolds and the Kounis hypersensitivity-associated acute thrombotic syndrome.J Thorac Dis. 2017; 9: 1155-1164
- Platelet activation and stent thrombosis.Hellenic J Cardiol. 2017; 58: 49-50
- Metal allergy to everolimus-eluting cobalt chromium stents confirmed by positive skin testing as a cause of recurrent multivessel in-stent restenosis.Catheter Cardiovasc Interv. 2016; 87: 137-142
Article info
Publication history
Published online: December 09, 2019
Accepted:
December 1,
2019
Received:
October 26,
2019
Footnotes
See editorial by Kounis et al., pages 816-819 of this issue.
See page 966.e6 for disclosure information.
Identification
Copyright
© 2019 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.
ScienceDirect
Access this article on ScienceDirectLinked Article
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- PreviewImmunoglobulin E (IgE) antibodies are synthesized and released by B lymphocytes as a result of a complex interplay between genes, cytokines, and environmental antigen exposure. IgE antibodies participate in atopic diseases and systemic anaphylaxis, constituting components of a protein network implicated in signalling response to antigens and allergens.1 IgEs are very short lived in plasma (∼ 1 day), but receptor-bound IgE can remain fixed to cells in tissues for weeks or months. Their biologic activity is mainly dependent on binding to specific fragment crystallisable region (FcR) receptors high-affinity FCεRI and FCγRI and low-affinity FCεRII and FCγRII situated on the surface, mainly of mast cells, but also of basophils, eosinophils, monocytes, and epithelial and dendritic cells.
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