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Canadian Journal of Cardiology

Recurrent Type III Kounis Syndrome: Will Anti–Immunoglobulin E Drug Be Another Option?

Published:December 09, 2019DOI:https://doi.org/10.1016/j.cjca.2019.12.007

      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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      Linked Article

      • Humanized Monoclonal Antibodies Against IgE Antibodies as Therapy for IgE-Mediated Coronary Syndromes: Are We There Yet?
        Canadian Journal of CardiologyVol. 36Issue 6
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          Immunoglobulin 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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