Incidence and associated factors of cetuximab-induced hypersensitivity infusion reactions in 1392 cancer patients treated in four French areas: a possible association with Lyme disease?

Dupont, M; Carlier, Claude; Gower‐Rousseau, Corinne; Barbier-Lider, P; Botsen, Damien; Brasseur, Mathilde; Burgevin, Alice; Chourbagi, Christophe; D’Almeida, R; Hautefeuille, V; Hentzien, Maxime; Lambert, Aurélien; Lamuraglia, M; Lavau‐Denès, Sandrine; Lopez, Anthony; Parent, D.; Slimano, Florian; Brügel, Mathias; Bouché, Olivier

doi:10.1186/s12885-022-10192-4

Cited by 5 publications

(5 citation statements)

References 61 publications

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“…6 A second study in France described the incidence of Lyme disease in association with cetuximab infusion reactions and described rechallenge techniques with both increased premedications and no premedication modifications. 2 In the United States, tickborne illnesses are more common in the Southeast. Our practice site is in the Midwest; therefore, neither patient presented had any IgE testing completed, furthermore, the practice is not standard of care at our institution and not recommended by national standards.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…The package insert also recommends reducing the infusion rate by 50% for Grades 1 and 2 infusion-related reactions, but there are only a few case reports on how premedications can be escalated to reduce the risk of infusion-related reactions. 2 Patients should receive a premedication regimen with a histamine-2 antagonist. 1 At UW Health, the current standard premedication strategy includes diphenhydramine 50 mg IV and acetaminophen 650 mg orally given 30 min prior to cetuximab.…”

Section: Introductionmentioning

confidence: 99%

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Premedication strategy in cetuximab rechallenge after Grade 2 hypersensitivity reactions

Lofy,

Jung,

Dow-Hillgartner

2023

J Oncol Pharm Pract

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Introduction Cetuximab, an IgG1 monoclonal antibody, is utilized in the treatment of metastatic colorectal cancer and squamous cell head and neck cancers. Due to the risk of hypersensitivity reactions, standard premedication with a histamine-1 (H-1) antagonist is recommended prior to administration, however, there is less guidance for premedication strategies to assist with rechallenge after infusion reactions. Here, we describe two cases of successful cetuximab treatment after Grade 2 reactions, in addition to risk factors and proposed premedication strategies for successful rechallenge. Case report Two patients who experienced Grade 2 hypersensitivity reactions were both successfully rechallenged with increased premedications 1–2 weeks after initial infusions. The first patient was a 56-year-old male diagnosed with metastatic colorectal cancer receiving cetuximab as part of a clinical trial. The second patient was a 73-year-old male diagnosed with head and neck cancer receiving cetuximab as part of standard of care concurrent with radiation. Management and outcome Each patient was rechallenged with an increased premedication strategy including dexamethasone, famotidine, diphenhydramine, and acetaminophen in addition to reducing the infusion rate. Both patients either continued treatment or successfully completed therapy, without any additional infusion-related reactions. Discussion We aimed to review risk factors related to cetuximab infusion reactions and propose a premedication strategy for rechallenge postreaction. Known risk factors include male sex and the accumulation of cetuximab-specific IgE. These may be mitigated by the addition of increased premedication with dexamethasone and famotidine with concurrent reduced infusion rate.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Premedication strategy in cetuximab rechallenge after Grade 2 hypersensitivity reactions

Lofy,

Jung,

Dow-Hillgartner

2023

J Oncol Pharm Pract

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“…They bind to the epidermal growth factor receptor and block receptor-dependent signal transduction pathways, such as anti-apoptosis, angiogenesis, and tumor metastasis. Both non-anti-TNF-α and anti-TNF-α chimeric monoclonal antibodies have been implicated in the development of immediate or delayed cardiac hypersensitivity reactions [ 40 ]. Chest pain, hypotension, severe anaphylaxis, and the acute hypersensitivity-associated coronary Kounis syndrome are the main adverse clinical manifestations [ 18 , 19 , 41 , 42 ].…”

Section: Hypersensitivity To Monoclonal Antibodiesmentioning

confidence: 99%

Cardio-Oncoimmunology: Cardiac Toxicity, Cardiovascular Hypersensitivity, and Kounis Syndrome

Kounis,

Hung,

de Gregorio

et al. 2024

Life

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Cancer therapy can result in acute cardiac events, such as coronary artery spasm, acute myocardial infarction, thromboembolism, myocarditis, bradycardia, tachyarrhythmias, atrio-ventricular blocks, QT prolongation, torsades de pointes, pericardial effusion, and hypotension, as well as chronic conditions, such as hypertension, and systolic and diastolic left ventricular dysfunction presenting clinically as heart failure or cardiomyopathy. In cardio-oncology, when referring to cardiac toxicity and cardiovascular hypersensitivity, there is a great deal of misunderstanding. When a dose-related cardiovascular side effect continues even after the causative medication is stopped, it is referred to as a cardiotoxicity. A fibrotic response is the ultimate outcome of cardiac toxicity, which is defined as a dose-related cardiovascular adverse impact that lasts even after the causative treatment is stopped. Cardiotoxicity can occur after a single or brief exposure. On the other hand, the term cardiac or cardiovascular hypersensitivity describes an inflammatory reaction that is not dose-dependent, can occur at any point during therapy, even at very low medication dosages, and can present as Kounis syndrome. It may also be accompanied by anti-drug antibodies and tryptase levels. In this comprehensive review, we present the current views on cardiac toxicity and cardiovascular hypersensitivity, together with the reviewed cardiac literature on the chemotherapeutic agents inducing hypersensitivity reactions. Cardiac hypersensitivity seems to be the pathophysiologic basis of coronary artery spasm, acute coronary syndromes such as Kounis syndrome, and myocarditis caused by cancer therapy.

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“…They bind to the epidermal growth factor receptor and block receptor-dependent signal transduction pathways such as anti-apoptosis, angiogenesis, and tumor metastasis. Both non-anti-TNF-α and anti-TNF-α chimeric monoclonal antibodies have been implicated in the development of immediate or delayed cardiac hypersensitivity reaction [18]. Chest pain, hypotension, severe anaphylaxis and acute hypersensitivity-associated coronary Kounis syndrome are the main adverse clinical manifestation [19][20][21][22].…”

Section: Hypersensitivity To Monoclonal Antibodiesmentioning

confidence: 99%

Cardio-Oncology: Cardiac Toxicity, Cardiovascular Hypersensitivity and Kounis Syndrome

Kounis,

Hung,

De Gregorio

et al. 2024

Preprint

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The most frequent cause of cardiac failure globally is ischemic heart disease, with chemothera-py-related cardiovascular side effects emerging as the second most frequent cause. Cancer therapy can result in acute cardiac events, such as coronary artery spasm, acute myocardial infarction, thromboembolism, myocarditis, bradycardia, tachyarrhythmias, atrio-ventricular blocks, QT pro-longation, torsades de pointes, pericardial effusion and hypotension, as well as chronic conditions, such as hypertension, systolic and diastolic left ventricular dysfunction presenting clinically as heart failure or cardiomyopathy. In cardio-oncology, when referring to cardiac toxicity and cardiovas-cular hypersensitivity, there is a great deal of misunderstanding. When a dose-related cardiovas-cular side effect continues even after the causative medication is stopped, it is referred to as cardi-otoxicity. A fibrotic response is the ultimate outcome of cardiac toxicity, which is defined as a dose-related cardiovascular adverse impact that lasts even after the causative treatment is stopped. Cardiotoxicity can occur after a single or brief exposure. On the other hand, the term cardiac or cardiovascular hypersensitivity describes an inflammatory reaction that is not dose-dependent, can occur at any point during therapy, even with very low medication dosages, and can show up as Kounis syndrome. It may also be accompanied by anti-drug antibodies and tryptase levels. In this comprehensive review, we present the current views on cardiac toxicity and cardiovascular hypersensitivity, together with the reviewed cardiac literature on the chemotherapeutic agents inducing hypersensitivity reactions. Cardiac hypersensitivity seems to be the pathophysiologic basis of coronary artery spasm, acute coronary syndromes such as Kounis syndrome and myocardi-tis caused by cancer therapy.

show abstract

Incidence and associated factors of cetuximab-induced hypersensitivity infusion reactions in 1392 cancer patients treated in four French areas: a possible association with Lyme disease?

Cited by 5 publications

References 61 publications

Premedication strategy in cetuximab rechallenge after Grade 2 hypersensitivity reactions

Premedication strategy in cetuximab rechallenge after Grade 2 hypersensitivity reactions

Cardio-Oncoimmunology: Cardiac Toxicity, Cardiovascular Hypersensitivity, and Kounis Syndrome

Cardio-Oncology: Cardiac Toxicity, Cardiovascular Hypersensitivity and Kounis Syndrome

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