The flow‐cytometric determination of basophil activation induced by aspirin and other non‐steroidal anti‐inflammatory drugs (NSAIDs) is useful for <i>in vitro</i> diagnosis of the NSAID hypersensitivity syndrome

Gamboa, P. M.; Sánz, M L; Caballero, M. Rosario; Urrutia, I.; Antépara, I.; Esparza, Rogelio; Weck, A.L. de

doi:10.1111/j.1365-2222.2004.02050.x

Cited by 125 publications

(116 citation statements)

References 42 publications

(68 reference statements)

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“…Mast cells are the key cell model for urticaria and release histamine and other chemical mediators, which produce urticarial symptoms, 20 and mast cell activation has been reported in ASA-intolerant urticaria patients. 21 Besides, PGE2 could suppress excessive anti-IgE-induced cysteinyl leukotriene production in mast cells in patients with AERD. 12 Our result confirmed that the functional study of PTGER4 promoter polymorphism in HMC-1 cell line showed differential transcriptional regulation by dual-luciferase activity.…”

Section: Discussionmentioning

confidence: 99%

Genetic variability of prostaglandin E2 receptor subtype EP4 gene in aspirin-intolerant chronic urticaria

et al. 2012

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Prostaglandin E2 receptor subtype EP4 (PTGER4) is one of the four subtypes of receptors for prostaglandin E2 (PGE2). Overproduction of cysteinyl leukotriene in mast cells may be related with suppression of PGE2 in patients with aspirin hypersensitivity. Considering the association of PTGER4 in mast cells, urticaria-and aspirin-related disease, we hypothesized the genetic variability of PTGER4 may be associated with aspirin-intolerant chronic urticaria (AICU). The case-control study was performed in 141 with AICU, 153 with aspirin-tolerant chronic urticaria (ATCU) and 174 with normal controls (NCs). PTGER4 promoter single-nucleotide polymorphism was genotyped using a primer extension method with the SNAPshot ddNTP primer extension kit. The functional variability of PTGER4 promoter polymorphism was carried out by dual-luciferase system and electrophoretic mobility shift assay (EMSA) in human mast cells (HMC-1). Furthermore, the effect of aspirin was performed for PTGER4 mRNA expression using real-time PCR, and PGE2 production was checked in HMC-1 cells using ELISA. AICU patients carrying GG genotype at À1254 G4A showed significantly higher frequency compared with NC (P ¼ 0.032). Similarly, the minor allele frequency, G allele was significantly higher in AICU compared with NC (P ¼ 0.031). In vitro functional study demonstrated that the À1254 G allele had lower luciferase activity (Po0.001) in HMC-1 cells. EMSA finding showed that PTGER4 À1254 G produced a specific band. Significantly decreased PTGER4 expression (P ¼ 0.008) and PGE2 production by aspirin exposure was confirmed in in vitro HMC cell line model (P ¼ 0.001). The PTGER4 À1254 G allele demonstrated a higher frequency in AICU patients and lower promoter activity with decreased expression of PTGER4 and contributes to the development of AICU.

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Section: Discussionmentioning

confidence: 99%

Genetic variability of prostaglandin E2 receptor subtype EP4 gene in aspirin-intolerant chronic urticaria

et al. 2012

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“…Measurement of cell surface molecule CD63 expression upon in vitro challenge has been proposed for in vitro diagnosis of AERD (35). However, reported specificity and sensitivity were variable, and no firm conclusion could be proposed for the reliability of this test in the routine setting (36).…”

Section: Basophil Activation Test (Bat)mentioning

confidence: 99%

Hypersensitivity to nonsteroidal anti-inflammatory drugs (NSAIDs) - classification, diagnosis and management: review of the EAACI/ENDA# and GA2LEN/HANNA*

Kowalski

Makowska

Blanca³

et al. 2011

Allergy

383

366

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Following the first description of hypersensitivity reaction to aspirin (ASA) by Hirschberg in 1902, several types of hypersensitivity reactions to nonsteroidal anti-inflammatory drugs (NSAIDs) have been described. The NSAIDs-induced hypersensitivity reactions involve different mechanisms and present a wide range of clinical manifestations from anaphylaxis AbstractNonsteroidal anti-inflammatory drugs (NSAIDs) are responsible for 21-25% of reported adverse drug events which include immunological and nonimmunological hypersensitivity reactions. This study presents up-to-date information on pathomechanisms, clinical spectrum, diagnostic tools and management of hypersensitivity reactions to NSAIDs. Clinically, NSAID hypersensitivity is particularly manifested by bronchial asthma, rhinosinusitis, anaphylaxis or urticaria and variety of late cutaneous and organ-specific reactions. Diagnosis of hypersensitivity to a NSAID includes understanding of the underlying mechanism and is necessary for prevention and management. A stepwise approach to the diagnosis of hypersensitivity to NSAIDs is proposed, including clinical history, in vitro testing and/ or provocation test with a culprit or alternative drug depending on the type of the reaction. The diagnostic process should result in providing the patient with written information both on forbidden and on alternative drugs.

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“…37 There is no reliable in vitro diagnostic test for AERD, and, as such, in the absence of a history of aspirin or NSAID use or an ambiguous history of symptoms after exposure, the patient should be referred for aspirin challenge to receive a definitive diagnosis. 1,10,38,39 Diagnostic challenges must be performed without LT modifiers (in contrast to desensitization [as described below]) because these agents can completely mask the symptoms and signs of a reaction. 17,[40][41][42] As such, this diagnostic tool must be used with caution because the expected reaction to aspirin in a patient who is allergic has the potential to induce severe bronchospasm.…”

Section: Diagnosismentioning

confidence: 99%

Aspirin-Exacerbated Respiratory Disease: Prevalence, Diagnosis, Treatment, and Considerations for the Future

Kennedy

Stoner

Borish

2016

Am J Rhinol�Allergy

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The flow‐cytometric determination of basophil activation induced by aspirin and other non‐steroidal anti‐inflammatory drugs (NSAIDs) is useful for in vitro diagnosis of the NSAID hypersensitivity syndrome

Abstract: Flowcytometric determinations of basophil activation following stimulation with NSAIDs show a high sensitivity (60-70%) with specificity above 90%. So this test may help avoiding some cumbersome and dangerous provocation challenges.

Cited by 125 publications

References 42 publications

Genetic variability of prostaglandin E2 receptor subtype EP4 gene in aspirin-intolerant chronic urticaria

Genetic variability of prostaglandin E2 receptor subtype EP4 gene in aspirin-intolerant chronic urticaria

Hypersensitivity to nonsteroidal anti-inflammatory drugs (NSAIDs) - classification, diagnosis and management: review of the EAACI/ENDA# and GA2LEN/HANNA*

Aspirin-Exacerbated Respiratory Disease: Prevalence, Diagnosis, Treatment, and Considerations for the Future

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