Diagnostic Accuracy of Urinary LTE4 Measurement to Predict Aspirin-Exacerbated Respiratory Disease in Patients with Asthma

Bochenek, Grażyna; Stachura, Tomasz; Szafraniec, Krystyna; Plutecka, Hanna; Sanak, Marek; Niżankowska‐Mogilnicka, Ewa; Sładek, Krzysztof

doi:10.1016/j.jaip.2017.07.001

Cited by 41 publications

(35 citation statements)

References 32 publications

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“…We have not found statistically significant differences between any of the four groups considered at the basal state. These results highlight an important difference between NIUA and NERD, for which high baseline LTE4 levels have been repeatedly reported which may be a reflection of the underlying respiratory disease . This is the first time such information has been made available for NIUA; however, contrasting results exist for NECD.…”

Section: Discussionmentioning

confidence: 96%

Eicosanoid mediator profiles in different phenotypes of nonsteroidal anti‐inflammatory drug‐induced urticaria

Doña

Jurado‐Escobar

Perkins

et al. 2019

Allergy

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Background:The role of arachidonic acid metabolites in NSAID-induced hypersensitivity has been studied in depth for NSAID-exacerbated respiratory disease (NERD) and NSAID-exacerbated cutaneous disease (NECD). However, no information is available for NSAID-induced urticarial/angioedema (NIUA), despite it being the most frequent clinical entity induced by NSAID hypersensitivity. We evaluated changes in leukotriene and prostaglandin metabolites for NIUA patients, using patients with NECD and single-NSAID-induced urticaria/angioedema or anaphylaxis (SNIUAA) for comparison.Methods: Urine samples were taken from patients with confirmed NSAID-induced urticaria and healthy controls, at baseline and at various time intervals after ASA administration. Eicosanoid measurement was performed using high-performance liquid chromatography-tandem mass spectrometry and gas chromatography-mass spectrometry.Results: No differences were found between groups at baseline. Following ASA administration, LTE4 and 9α,11β-PGF2 levels were increased in both NIUA and NECD patients compared to baseline, rising initially, before decreasing toward initial levels. In addition, the levels of these metabolites were higher in NIUA and NECD when compared with the SNIUAA and control groups after ASA administration. No changes were found with respect to baseline values for SNIUAA and control groups. Conclusions:We present for the first time data regarding the role of COX-1 inhibition in NIUA. Patients with this entity show a similar pattern eicosanoid levels following ASA challenge to those with NECD. Further studies will help ascertain the cell populations involved and the underlying molecular mechanisms.Abbreviatons: ASA, acetyl salicylic acid; COX-1, cyclooxygenase 1; LTE4, leukotriene E4; NECD, NSAID-exacerbated cutaneous disease; NIUA, NSAID-induced urticaria/angioedema; NSAIDs, nonsteroidal anti-inflammatory drugs; PGE2, prostaglandin E2; 9a,11b-PGF2, 9α,11β-prostaglandin F2.Inmaculada Doña and Raquel Jurado-Escobar contributed equally to this work.

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Section: Discussionmentioning

confidence: 96%

Eicosanoid mediator profiles in different phenotypes of nonsteroidal anti‐inflammatory drug‐induced urticaria

Doña

Jurado‐Escobar

Perkins

et al. 2019

Allergy

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“…Urinary leukotriene E 4 has been associated with a high negative predictive value for identifying asthmatic patients with aspirin-exacerbated respiratory disease, such that compared with clinical parameters alone, the determination of urinary leukotriene E 4 levels combined with clinical parameters enhances the accuracy of the aspirin-exacerbated respiratory disease diagnosis. 26…”

Section: Acute Phasementioning

confidence: 99%

“…17,19 Histamine determination 61% to 92% 20,22 d This variability could be related to the type of reaction. 17,19 IDHRs at the resolution phase identifying the relevant drug sIgE by using immunoassay 38% to 85% for BLs [21][22][23][24][25] 44% to 92% for NMBAs [26][27][28][29][30][31][32] 26% to 68% for biological agents 39,40 59% to 75% for platins 41 d sIgE to penicillins can produce falsepositive results in patients with penicillin V allergy 120 and in those with high levels of total serum IgE. 121 BAT 44% to 63% for BLs 42,[47][48][49][50][51][52] 36% to 92% for NMBAs 35,36,[53][54][55][56][57][58] 42% to 65% for dipyrone [59][60][61] 57% to 77% for quinolones [62][63][64][65] 46% to 63% for RCM 66,...…”

Section: Expert Consensusmentioning

confidence: 99%

Controversies in drug allergy: In vitro testing

Mayorga

Ebo

Lang

et al. 2019

Journal of Allergy and Clinical Immunology

101

106

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Despite their low frequency, drug hypersensitivity reactions (DHRs) can be serious and result in lifelong sequelae. The diagnosis is critical to avert future reactions and should identify the culprit drug or drugs and safe alternatives. However, making the diagnosis can be complex and challenging. Reliable in vitro tests can offer the potential to improve a diagnosis of DHR and influence medical decision making. Importantly, in vitro testing is frequently not performed as a test in isolation but rather as a component of a diagnostic algorithm along with additional tests. There are several in vitro approaches for the different endotypes of DHRs. However, only few are available for routine diagnosis, and many are restricted to research laboratories. In vitro tests exhibit varying sensitivity and specificity depending on the drug involved and the clinical phenotype. In vitro tests can complement skin tests, especially in patients with negative or equivocal skin test responses inconsistent with the clinical presentation and in severe reactions in which drug provocation tests are contraindicated. The main unmet need for many in vitro tests for the diagnosis of DHRs is validation in larger studies with standardized controls that could harmonize diagnostic management between the United States, European Union, and other regions of the world.

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“…The gold standard for diagnosing AERD is aspirin challenge, but challenge testing carries the risk of severe bronchospasm. Urinary leukotriene E4, the end‐product of arachidonic acid metabolism, is raised in AERD and may have a role in diagnosing AERD . Treatment options include avoidance of aspirin and NSAIDs, desensitization, and leukotriene receptor antagonists.…”

Section: Exogenous Cofactorsmentioning

confidence: 99%

Precision medicine in united airways disease: A “treatable traits” approach

Yii

Tay

Choo

et al. 2018

Allergy

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United airways disease (UAD) is the concept that the upper and lower airways, which are anatomically and immunologically related, form a single organ. According to this concept, upper and lower airway diseases are frequently comorbid because they reflect manifestations of a single underlying disease at different sites of the respiratory tract. Allergic asthma-allergic rhinitis is the archetypal UAD, but emerging data indicate that UAD is a heterogeneous condition and consists of multiple phenotypes (observable clinical characteristics) and endotypes (pathobiologic mechanisms). The UAD paradigm also extends to myriad sinonasal diseases (eg, chronic rhinosinusitis with or without nasal polyps) and lower airway diseases (eg, bronchiectasis, chronic obstructive pulmonary disease). Here, we review currently known phenoendotypes of UAD and propose a "treatable traits" approach for the classification and management of UAD, wherein pathophysiological mechanisms and factors contributing to disease are identified and targeted for treatment. Treatable traits in UAD can be analyzed according to a framework comprising airway inflammation (eosinophilic, neutrophilic), impaired airway mucosal defense (impaired mucociliary clearance, antibody deficiency), and exogenous cofactors (allergic sensitizers, tobacco smoke, microbes). Appreciation of treatable traits is necessary in advancing the effort to deliver precise treatments and achieve better outcomes in patients with UAD.

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Diagnostic Accuracy of Urinary LTE4 Measurement to Predict Aspirin-Exacerbated Respiratory Disease in Patients with Asthma

Cited by 41 publications

References 32 publications

Eicosanoid mediator profiles in different phenotypes of nonsteroidal anti‐inflammatory drug‐induced urticaria

Eicosanoid mediator profiles in different phenotypes of nonsteroidal anti‐inflammatory drug‐induced urticaria

Controversies in drug allergy: In vitro testing

Precision medicine in united airways disease: A “treatable traits” approach

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