Hypersensitivity Reactions to Nonsteroidal Anti-Inflammatory Drugs
Summary
Nonsteroidal anti-inflammatory drugs (NSAIDs) rank among the most widely used medications worldwide, yet they are also a leading cause of adverse drug reactions. Hypersensitivity to NSAIDs encompasses a spectrum of clinical phenotypes that arise principally through cyclooxygenase‐1 (COX-1) inhibition, leading to an imbalance in the arachidonic acid cascade and overproduction of leukotrienes. These reactions are broadly classified into cross‐reactive forms, in which patients develop symptoms on exposure to chemically diverse NSAIDs, and selective responses, driven by immunological mechanisms to a single agent. Cross‐reactive phenotypes include NSAID-exacerbated respiratory disease (NERD), characterised by bronchoconstriction and nasal polyposis; NSAID-induced urticaria/angioedema (NIUA); and NSAID-exacerbated cutaneous disease (NECD). Selective reactions comprise immediate hypersensitivity (SNIUAA) and delayed responses (SNIDR), in which skin manifestations or systemic symptoms occur days after ingestion. Diagnosis relies on a detailed clinical history, in vitro assays in specialised laboratories, skin testing for delayed forms and, when necessary, controlled provocation challenges. Genetic predisposition plays an increasing role in understanding individual risk, while desensitisation protocols and avoidance strategies inform tailored management. Advances in phenotyping and molecular characterisation are reshaping precision approaches to analgesia in vulnerable populations.
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Hypersensitivity Reactions to Nonsteroidal Anti-Inflammatory Drugs publication trend
The graph below shows the total number of articles in hypersensitivity reactions to nonsteroidal anti-inflammatory drugs across all publications each year (not limited to Nature Index journals).
Technical terms
Cyclooxygenase (COX): An enzyme critical to prostaglandin synthesis; its inhibition by NSAIDs diverts arachidonic acid to leukotriene production.
Arachidonic acid pathway: A lipid‐mediated inflammatory cascade that produces prostaglandins and leukotrienes, central to NSAID hypersensitivity mechanisms.
Cross‐reactive hypersensitivity: A pharmacological reaction pattern in which inhibition of COX-1 by one NSAID precipitates symptoms upon exposure to others.
Selectiv e hypersensitivity: Immune‐mediated reactions directed against a single NSAID, often presenting with immediate urticaria or delayed skin eruptions.
Provocation testing: A controlled oral or nasal challenge to confirm hypersensitivity when in vitro or skin tests are inconclusive.
References
- Genetic Susceptibility of HLA Alleles to Non-Steroidal Anti-Inflammatory Drug Hypersensitivity in the Taiwanese Population. Biomedicines (2023).
- NSAID hypersensitivity – recommendations for diagnostic work up and patient management. Allergo Journal International (2018).
- Pharmacogenomics of Hypersensitivity to Non-steroidal Anti-inflammatory Drugs. Frontiers in Genetics (2021).
- Genetic Variants in Cytosolic Phospholipase A2 Associated With Nonsteroidal Anti-Inflammatory Drug–Induced Acute Urticaria/Angioedema. Frontiers in Pharmacology (2021).
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