Fatal anaphylactoid reaction following ioversol administration

Jansman, Frank G A; Kieft, Hans; Harting, J. W.

doi:10.1007/s11096-007-9126-y

Cited by 12 publications

(3 citation statements)

References 5 publications

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“…Although the introduction of low-osmolar non-anionic contrast materials has diminished the side effects significantly to 2.1% , some symptoms still encountered and include fever, purpura, skin reactions, convulsions, dyspnea, renal damage, and hypersensitivity reactions including Kounis syndrome [3,14]. Non-ionic and dimeric contrast molecules bind to circulating proteins to a lesser extend than ionic and monomeric contrast molecules making them less toxic.…”

Section: Discussionmentioning

confidence: 99%

Kounis syndrome: A manifestation of drug-eluting stent thrombosis associated with allergic reaction to contrast material

Kogias¹,

Papadakis²,

Tsatiris³

et al. 2010

International Journal of Cardiology

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Section: Discussionmentioning

confidence: 99%

Kounis syndrome: A manifestation of drug-eluting stent thrombosis associated with allergic reaction to contrast material

Kogias¹,

Papadakis²,

Tsatiris³

et al. 2010

International Journal of Cardiology

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“…The low-osmolarity non-anionic contrast materials demonstrate lower side effects, at approximately 2.1%, compared to the anionic ones. However, mild symptoms that include fever, purpura, skin reactions, convulsions, dyspnea, renal damage, and the severe reactions such as hypersensitivity reactions including Kounis syndrome (72) and death (73) can be encountered during their use. Nonionic and dimeric contrast molecules bind to circulating proteins and create allergenic haptens to a lesser extent than the ionic and monomeric contrast materials.…”

Section: Radiology and Kounis Syndromementioning

confidence: 99%

Kounis Syndrome—not a Single-organ Arterial Disorder but a Multisystem and Multidisciplinary Disease

Kounis¹,

Koniari²,

Velissaris³

et al. 2019

Balkan Med J

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Coronary symptoms associated with conditions related to mast cell activation and inflammatory cell interactions, such as those involving T-lymphocytes and macrophages, further inducing allergic, hypersensitivity, anaphylactic, or anaphylactic insults, are currently referred to as the Kounis syndrome. Kounis syndrome is caused by inflammatory mediators released during allergic insults, postinflammatory cell activation, and interactions via multidirectional stimuli. A platelet subset of 20% with high-and low-affinity IgE surface receptors is also involved in this process. Kounis syndrome is not just a single-organ but also a complex multisystem and multiorgan arterial clinical condition; it affects the coronary, mesenteric, and cerebral arteries and is accompanied by allergy-hypersensitivityanaphylaxis involving the skin, respiratory, and vascular systems in the context of anesthesia, surgery, radiology, oncology, or even dental and psychiatric medicine; further, it has significantly influences both morbidity and mortality. Kounis syndrome might be caused by numerous and continuously increasing causes, with broad clinical symptoms and signs, via multi-organ arterial system involvement, in patients of any age, thereby demonstrating predominant anaphylactic features in terms of a wide spectrum of mast cell-association disorders. Cardiac symptoms, such as chest pain, coronary vasospasm, angina pectoris, myocardial infarction, stent thrombosis, acute cardiac failure, and sudden cardiac death associated with subclinical, clinical, acute, or chronic allergic reactions, constitute the clinical manifestations of this syndrome. Since its first description, a common pathway between allergic and non-allergic coronary events has been demonstrated. The hypothesis is based on the existence of a much higher degree of mast cell degranulation at plaque erosion or rupture sites compared with at the adjacent areas or even more distant segments in post-acute myocardial infarction of non-allergic etiology. Although mast cell activation, differentiation, and mediator release takes days or weeks, the mast cell degranulation may occur just before any acute coronary event, further resulting in coronary artery vasoconstriction and atheromatous plaque rupture. It seems that medications and natural molecules stabilizing the mast cell membrane as well as monoclonal antibodies protecting the mast cell surface can emerge as novel therapeutic modalities for acute coronary and cerebrovascular event prevention.

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“…In more severe reactions, the respiratory or cardiovascular systems are involved. Even after application of nonionic RCM, fatal reactions are repeatedly described [16]. A recently described hypersensitivity reaction is the Kounis syndrome, which describes the concurrence of acute coronary syndrome with mast cell activation induced by inflammatory mediators released during an allergic reaction in patients.…”

Section: Clinical Manifestations Of Radiocontrast Media Hypersensitivitymentioning

confidence: 99%

Anaphylaxis to radiographic contrast media

Brockow

Ring

2011

Current Opinion in Allergy &Amp; Clinical Immunology

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There are not enough data yet about the value of skin tests for the selection of a 'well tolerated' RCM. Premedication of previous reactors is common among radiologists. However, breakthrough reactions are a concern and physicians should not rely on the efficacy of pharmacological premedication. Instead, radiologists should be prepared to treat severe RCM-induced allergic reactions in their practice.

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Fatal anaphylactoid reaction following ioversol administration

Cited by 12 publications

References 5 publications

Kounis syndrome: A manifestation of drug-eluting stent thrombosis associated with allergic reaction to contrast material

Kounis syndrome: A manifestation of drug-eluting stent thrombosis associated with allergic reaction to contrast material

Kounis Syndrome—not a Single-organ Arterial Disorder but a Multisystem and Multidisciplinary Disease

Anaphylaxis to radiographic contrast media

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