Hypersensitivity Reactions to Nonsteroidal Anti-Inflammatory Drugs: An Update on Pharmacogenetics Studies

Plaza-Serón, María del Carmen; García‐Martín, Elena; Agúndez, José A. G.; Ayuso, Pedro

doi:10.2217/pgs-2018-0079

Cited by 14 publications

(12 citation statements)

References 90 publications

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“…In the clinical description of this group, several entities have been included that clearly represent well-differentiated forms 3. These have been described in detail in a previous section of this review and reported elsewhere 14,17,54,55. The combination of both NERD plus NECD has been reported but much more frequent than NERD are those with mixed reactions.…”

Section: Impactmentioning

confidence: 99%

“…The combination of both NERD plus NECD has been reported but much more frequent than NERD are those with mixed reactions. We prefer this term to blended reactions, though it is still pending a defined nomenclature that is awaiting further discussion and consensus agreements 14,17. Clinical data in children and adolescents point in this direction 22,134.…”

Section: Impactmentioning

confidence: 99%

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<p>NSAID-induced reactions: classification, prevalence, impact, and management strategies</p>

Blanca‐López¹,

Soriano²,

García‐Martín³

et al. 2019

JAA

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Nonsteroidal anti-inflammatory drugs (NSAIDs) are the leading cause of hypersensitivity drug reactions. The different chemical structures, cyclooxygenase 1 (COX-1) and/or COX-2 inhibitors, are taken at all ages and some can be easily obtained over the counter. Vasoactive inflammatory mediators like histamine and leukotriene metabolites can produce local/systemic effects. Responders can be selective (SR), IgE or T-cell mediated, or cross-intolerant (CI). Inhibition of the COX pathway is the common mechanism in CI, with the skin being the most frequent organ involved, followed by the lung and/or the nose. An important number of cases have skin and respiratory involvement, with systemic manifestations ranging from mild to severe anaphylaxis. Among SR, this is the most frequent entity, often being severe. Recent years have seen an increase in reactions involving the skin, with many cases having urticaria and/or angioedema in the absence of chronic urticaria. Aspirin, the classical drug involved, has now been replaced by other NSAIDs, with ibuprofen being the universal culprit. For CI, no in vivo/in vitro diagnostic methods exist and controlled administration is the only option unless the cases evaluated report repetitive and consistent episodes with different NSAIDs. In SR, skin testing (patch and intradermal) with 24–48 reading can be useful, mainly for delayed T-cell responses. Acetyl salicylic acid (ASA) is the test drug to establish the diagnosis and confirm/exclude CI by controlled administration. Desensitization to ASA has been extensively used in respiratory cases though it can also be applied in those cases where it is required.

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Section: Impactmentioning

confidence: 99%

Section: Impactmentioning

confidence: 99%

<p>NSAID-induced reactions: classification, prevalence, impact, and management strategies</p>

Blanca‐López¹,

Soriano²,

García‐Martín³

et al. 2019

JAA

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“…NSAIDs intake brings about an imbalance in the inflammatory mediators' production in individuals who manifest cross-intolerant reactions to these drugs by mechanisms that are not fully understood [53]. Hence, an increasing number of studies support the hypothesis that additional pathways may contribute toward the underlying mechanisms of DHRs to NSAIDs [54,55].…”

Section: Nonspecific Immunological Reactionsmentioning

confidence: 99%

Variability of the Genes Involved in the Cellular Redox Status and Their Implication in Drug Hypersensitivity Reactions

2021

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Adverse drug reactions are a major cause of morbidity and mortality. Of the great diversity of drugs involved in adverse drug reactions, the most frequent are non-steroidal anti-inflammatory drugs followed by -lactam antibiotics. The redox status regulates the level of reactive oxygen and nitrogen species (RONS). RONS interplay and modulate the action of diverse biomolecules, such as inflammatory mediators and drugs. In this review, we address the role of the redox status in the initiation, as well as in the resolution of inflammatory processes involved in drug hypersensitivity reactions. We summarize the association findings between drug hypersensitivity reactions and variants in the genes that encode the enzymes related to the redox system such as enzymes related to glutathione: Glutathione S-transferase (GSTM1, GSTP, GSTT1) and glutathione peroxidase (GPX1), thioredoxin reductase (TXNRD1 and TXNRD2), superoxide dismutase (SOD1, SOD2, and SOD3), catalase (CAT), aldo-keto reductase (AKR), and the peroxiredoxin system (PRDX1, PRDX2, PRDX3, PRDX4, PRDX5, PRDX6). Based on current evidence, the most relevant candidate redox genes related to adverse drug reactions are GSTM1, TXNRD1, SOD1, and SOD2. Increasing the understanding of pharmacogenetics in drug hypersensitivity reactions will contribute to the development of early diagnostic or prognosis tools, and will help to diminish the occurrence and/or the severity of these reactions.

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“…Most of aspirin-induced delayed hypersensitivity reactions are severe, such as DIHS/DRESS (drug-induced hypersensitivity syndrome/drug reaction with eosinophilia and systemic symptoms), AGEP (acute generalized exanthematous pustulosis), and less frequent TEN/SJS (Stevens-Johnson syndrome/toxic epidermal necrolysis). 4 Mechanically, aspirin-induced delayed hypersensitivity is T cell-dependent. 5 Aspirin-induced thrombocytopenia has been rarely reported.…”

Section: Introductionmentioning

confidence: 99%

“…The immunological mechanisms underlying drug-induced thrombocytopenia can be divided into six types according to the types of antigens. 9 In the case, the mechanisms underlying the immune impairment induced by platelet IIb/IIIa and Ia/ IIa antibodies (IgG) was not clear. We speculate that aspirin, a soluble drug, induced the production of plateletspecific antibodies, namely platelet IIb/IIIa and Ia/IIa antibodies, and accelerated the clearance of platelets and thus leading to thrombocytopenia.…”

mentioning

confidence: 96%

Aspirin “Allergy”-Induced Thrombocytopenia: A Case Report

Fu¹,

Xu²,

Qing³

et al. 2021

JAA

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Aspirin is clinically widely used to inhibit platelet aggregation after coronary intervention. Herein we describe a case of aspirin-induced thrombocytopenia that may be related to allergy to aspirin. A 47‐year‐old man developed a delayed hypersensitivity reaction to aspirin, with pruritus, purpura and thrombocytopenia, increased peripheral blood eosinophils and enlarged inguinal lymph node. All the symptoms disappeared in 2 years after stopping aspirin. Aspirin-induced thrombocytopenia related to allergy is rarely reported. Aspirin hypersensitivity should be taken into consideration in case of unexplained thrombocytopenia in patients taking aspirin. Aspirin “allergy”-induced thrombocytopenia may involve both aspirin related IgG and IgE antibodies.

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Hypersensitivity Reactions to Nonsteroidal Anti-Inflammatory Drugs: An Update on Pharmacogenetics Studies

Cited by 14 publications

References 90 publications

<p>NSAID-induced reactions: classification, prevalence, impact, and management strategies</p>

<p>NSAID-induced reactions: classification, prevalence, impact, and management strategies</p>

Variability of the Genes Involved in the Cellular Redox Status and Their Implication in Drug Hypersensitivity Reactions

Aspirin “Allergy”-Induced Thrombocytopenia: A Case Report

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