Allergic reactions to nonsteroidal anti-inflammatory drugs: Is newer better?

Berges-Gimeno, M P; Martín-Lázaro, J

doi:10.1007/s11882-007-0028-9

Cited by 14 publications

(11 citation statements)

References 36 publications

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“…Antibiotics, especially b-lactam antibiotics, and nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, ibuprofen, and other agents, are often implicated, as are chemotherapeutic agents. 24,25,[34][35][36][37][38][39][40] Newly recognized medication triggers include loperamide 37 ; contaminants in medications, such as oversulfated chondroitin sulfate (OSCS)-contaminated heparin 38 ; seemingly innocuous substances, such as vitamins and supplements containing folic acid 39 ; and herbal treatments. 40 Perioperative medications, 41 iodinated contrast media 42 and medical dyes are becoming increasingly relevant triggers in community settings.…”

Section: Pathogenesis Triggers Of Anaphylaxismentioning

confidence: 99%

Anaphylaxis

Simons

2010

Journal of Allergy and Clinical Immunology

396

380

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Anaphylaxis occurs commonly in community settings. The rate of occurrence is increasing, especially in young people. Understanding potential triggers, mechanisms, and patient-specific risk factors for severity and fatality is the key to performing appropriate risk assessment in those who have previously experienced an acute anaphylactic episode. The diagnosis of anaphylaxis is based primarily on clinical criteria and is valid even if the results of laboratory tests, such as serum total tryptase levels, are within normal limits. Positive skin test results or increased serum specific IgE levels to potential triggering allergens confirm sensitization but do not confirm the diagnosis of anaphylaxis because asymptomatic sensitization is common in the general population. Important patient-related risk factors for severity and fatality include age, concomitant diseases, and concurrent medications, as well as other less well-defined factors, such as defects in mediator degradation pathways, fever, acute infection, menses, emotional stress, and disruption of routine. Prevention of anaphylaxis depends primarily on optimal management of patient-related risk factors, strict avoidance of confirmed relevant allergen or other triggers, and, where indicated, immunomodulation (eg, subcutaneous venom immunotherapy to prevent Hymenoptera sting-triggered anaphylaxis, an underused, potentially curative treatment). The benefits and risks of immunomodulation to prevent food-triggered anaphylaxis are still being defined. Epinephrine (adrenaline) is the medication of first choice in the treatment of anaphylaxis. All patients at risk for recurrence in the community should be equipped with 1 or more epinephrine autoinjectors; a written, personalized anaphylaxis emergency action plan; and up-to-date medical identification. Improvements in the design of epinephrine autoinjectors will help to optimize ease of use and safety. Randomized controlled trials of pharmacologic agents, such as antihistamines and glucocorticoids, are needed to strengthen the evidence base for treatment of acute anaphylactic episodes.

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Section: Pathogenesis Triggers Of Anaphylaxismentioning

confidence: 99%

Anaphylaxis

Simons

2010

Journal of Allergy and Clinical Immunology

396

380

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“…NSAIDs commonly trigger anaphylaxis that is medication-specific within this pharmacologic class and is not related to other NSAID-associated diseases such as asthma, rhinitis, nasal polyposis, and chronic urticaria. 74 Anaphylaxis can also be triggered by chemotherapeutic agents such as carboplatin and doxorubicin, and biologic agents such as the monoclonal antibodies cetuximab, rituximab, infliximab, and rarely, omalizumab. 72,[75][76][77] In addition, it can be triggered by contaminants in medications, for example, oversulfated chondroitin sulfate in heparin, 78 and by herbal formulations.…”

Section: Triggers Of Anaphylaxismentioning

confidence: 99%

“…2,24,32,[72][73][74] A written list containing the name of the medication that triggered the anaphylaxis and the names of related and cross-reacting medications should be provided. 2,24,32,[72][73][74] Those who require a drug for which no safe and effective substitute is available should undergo desensitization, defined as induction of a temporary state of tolerance to the relevant medication for one uninterrupted course of treatment. It should be conducted in a healthcare setting, according to an established protocol, by healthcare professionals trained and experienced in such procedures and in management of anaphylaxis if it occurs during the desensitization procedure.…”

Section: Prevention Of Anaphylaxis Recurrencesmentioning

confidence: 99%

World Allergy Organization anaphylaxis guidelines: Summary

Simons

Ardusso

Bilò

et al. 2011

Journal of Allergy and Clinical Immunology

512

591

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“…NSAIDs are reported to induce pseudo-allergic reactions, which are commonly described as intolerant in the medical literature (90). Pseudo-allergic reactions to NSAIDs account for 21% to 25% of all adverse drug reactions (91).…”

Section: Pseudo-allergic Reaction Caused By Nonsteroidal Anti-infl Ammentioning

confidence: 99%

Agents that induce pseudo-allergic reaction

Wang

Hs²,

Zp³

2011

Drug Discov Ther

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Pseudo-allergic reactions may result from the activation of inflammatory or anaphylactic mechanisms independent of antigen-specific immune responses. Recent statistics show that pseudo-allergic reactions may represent as high as two thirds of all immediate hypersensitivity reactions, implying a great amount of morbidity and numerous health care costs. In this review, we concentrate on agents mediating pseudo-allergic reactions and evaluate accurately the available information on their modes of action. The agents discussed here are divided into three types: (i) Direct mast cell activators, which may activate mast cells in an IgE-independent manner, such as opioid drugs, basic secretagogues and calcium ionophore A23187; (ii) Complement activators, including liposomes, radiocontrast media and Cremophor EL, which may activate the complement system by different pathways: the classical pathway, the mannose-binding lectin pathway or the alternative pathway; (iii) Nonsteroidal anti-inflammatory drugs, which may inhibit the function of cyclooxygenase-1, resulting in the occurrence of adverse reactions. In addition, nonclinical detection methods of pseudoallergic reactions are also reviewed in order to supply valuable information for clinical diagnosis.

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Allergic reactions to nonsteroidal anti-inflammatory drugs: Is newer better?

Cited by 14 publications

References 36 publications

Anaphylaxis

Anaphylaxis

World Allergy Organization anaphylaxis guidelines: Summary

Agents that induce pseudo-allergic reaction

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