2013
DOI: 10.1111/all.12187
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Mediator release after nasal aspirin provocation supports different phenotypes in subjects with hypersensitivity reactions to NSAIDs

Abstract: Data support the observation that MNSAID-UA, although sharing a common response with AERD to COX inhibitors, seems to have a distinctive phenotype, based on the response to nasal challenge and the release of inflammatory mediators.

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Cited by 34 publications
(38 citation statements)
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“…This classification system supports clinicians in diagnosing cases of suspected NSAID-H. Furthermore, categorization of these clinical phenotypes is an initial requirement in pharmacokinetic studies [6,11] .…”
Section: Introductionmentioning
confidence: 76%
See 1 more Smart Citation
“…This classification system supports clinicians in diagnosing cases of suspected NSAID-H. Furthermore, categorization of these clinical phenotypes is an initial requirement in pharmacokinetic studies [6,11] .…”
Section: Introductionmentioning
confidence: 76%
“…To date, the clinical phenotypes of NSAID-H have been investigated and classified in detail with a focus on adults [7,9,11,15,16] ; however, the classifications may not be the same for paediatric patients. Therefore, we aimed to define the clinical characteristics of and risk factors for NSAID-H during childhood.…”
Section: Introductionmentioning
confidence: 99%
“…NERD and NECD are considered to be caused by a nonspecific immunological mechanism whereby NSAIDs inhibit COX enzymes, leading to a dysregulation of leukotriene homeostasis [7]. Since Szczeklik associated the capacity of NSAIDs to block the COX-1 enzyme with asthma exacerbations [10], many studies on the basis of this hypothesis have been published [11][12][13][14][15][16][17][18][19][20]. However, despite considerable study, there is a lack of evidence to support this hypothesis for NIUA [7].…”
Section: Introductionmentioning
confidence: 99%
“…In addition to the cyclooxygenase pathway, dysregulation of the lipooxygenase pathway has also been studied extensively in CI patients. For example, it has been shown that these patients have higher basal LTs levels that are augmented after drug intake [13][14][15]20] and related to the severity of symptoms [25]. This dysregulation is not only found for NERD patients; in fact, NECD patients also show high levels of LTs [17,19].…”
Section: Introductionmentioning
confidence: 99%
“…Symptoms are induced by at least two chemically unrelated NSAIDs [4,5]. Alterations of arachidonic acid metabolism through cyclooxygenase (COX)-1 inhibition are thought to have a central role [7]; however, current data suggest the participation of additional mechanisms [8,9].…”
Section: Introductionmentioning
confidence: 99%