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Updated: Jun 12, 2026

Basophil Activation Test for Investigation of IgE-Mediated Mechanisms in Drug Hypersensitivity
Published on: September 16, 2011
Nonsteroidal anti-inflammatory drug hypersensitivity in preschool children
Mona Iancovici Kidon1, Liew Woei Kang, Chiang Wen Chin
1Rheumatology, Immunology and Allergy Service, Department of Paediatric Medicine, KK Children's Hospital, Singapore. Mona.Kidon@kkh.com.sg.
Insights
Nonsteroidal anti-inflammatory drug (NSAID) hypersensitivity is poorly understood in young children. This review examines NSAID reactions, including acetaminophen
Area of Science:
- Pediatric Allergy and Immunology
- Pharmacology
- Clinical Medicine
Background:
- Nonsteroidal anti-inflammatory drug (NSAID) hypersensitivity is extensively studied in adults but poorly defined in children, particularly young ones.
- While pediatricians rarely encounter severe issues, epidemiological data on NSAID hypersensitivity in children is conflicting.
- Some asthmatic children exhibit acetylsalicylic acid (ASA)-sensitive asthma with bronchoconstriction, and ibuprofen can cause respiratory issues in a small subset.
Purpose of the Study:
- To review current data on nonsteroidal anti-inflammatory drug (NSAID) hypersensitivity in preschool children.
- To explore the potential role of acetaminophen's mechanism of action in NSAID hypersensitivity.
- To discuss the genetic and atopic factors associated with NSAID hypersensitivity in early childhood.
Main Methods:
- Literature review of published data on NSAID hypersensitivity in preschool children.
- Analysis of existing epidemiological studies and clinical observations.
- Examination of the pharmacological mechanisms, including cyclooxygenase (COX) enzyme inhibition.
Main Results:
- Bronchoconstriction after acetylsalicylic acid (ASA) challenge occurs in 0-22% of challenged asthmatic children.
- Ibuprofen at antipyretic doses can trigger acute respiratory problems in a small percentage of mild to moderate asthmatics.
- Acetaminophen's inhibition of cyclooxygenase (COX)-3 may explain adverse reactions in patients with cross-reactive NSAID hypersensitivity.
Conclusions:
- NSAID hypersensitivity in preschool children requires further definition and research.
- Genetic predisposition and atopy are strongly associated with NSAID hypersensitivity, even in very young children.
- Understanding the role of COX-3 inhibition by acetaminophen may offer insights into managing NSAID hypersensitivity in pediatric populations.
Abstract:
: Although extensively studied in adults, nonsteroidal anti-inflammatory drug (NSAID) hypersensitivity in children, especially in young children, remains poorly defined. Pediatricians, prescribing antipyretics for children, rarely encounter significant problems, but the few epidemiologic studies performed show conflicting results. Although it is clear that some patients with acetylsalicylic acid (ASA)-sensitive asthma have their clinical onset of disease in childhood and bronchoconstriction after ASA challenge is seen in 0 to 22% of asthmatic children so challenged, ibuprofen at antipyretic doses may cause acute respiratory problems only in a very small number of mild to moderate asthmatics. The recently elucidated mechanism of action of acetaminophen may explain some occurrences of adverse reactions in patients with cross-reactive NSAID hypersensitivity on the basis of its inhibitory activity on the newly described enzyme, cyclooxygenase (COX)-3. This nonspecific sensitivity to inhibition of COX is most likely genetically determined and shows a remarkable association with atopic disease even in the very young age group and possibly an increased predilection in specific ethnic groups. This review summarizes state-of-the-art published data on NSAID hypersensitivity in preschool children.
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