Systemic expression of inflammatory mediators in patients with chronic rhinosinusitis and nasal polyps with and without Aspirin Exacerbated Respiratory Disease

Pezato, Rogério; Świerczyńska-Krępa, Monika; Niżankowska‐Mogilnicka, Ewa; Holtappels, Gabriële; Ruyck, Natalie De; Sanak, Marek; Derycke, Lara; Crombruggen, Koen Van; Bachert, Claus; Pérez-Novo, Claudina

doi:10.1016/j.cyto.2015.10.011

Cited by 21 publications

(16 citation statements)

References 41 publications

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“…Several studies propose alcohol could cause eosinophilic inflammation or induce IgE supporting the first possibility . The latter hypothesis is analogous to reports in NERD, suggesting respiratory mucosal inflammatory disease could be the underlying mechanism in aspirin hypersensitivity . Our results show that many CRSwNP experienced alcohol HR before the diagnosis of CRSwNP was made.…”

Section: Discussionsupporting

confidence: 86%

Alcohol hyper‐responsiveness in chronic rhinosinusitis with nasal polyps

Schryver

Derycke

Campo

et al. 2016

Clin Experimental Allergy

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Section: Discussionsupporting

confidence: 86%

Alcohol hyper‐responsiveness in chronic rhinosinusitis with nasal polyps

Schryver

Derycke

Campo

et al. 2016

Clin Experimental Allergy

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“…Recently, novel mechanisms have been proposed, such as systemic inflammation, aberrant functions of platelets and overexpressed platelet activation242526. Aspirin challenge, for instance the ASA-BPT, is the gold standard for confirming aspirin hypersensitivity, however, there are still risks for bronchospasm as well as various contraindications27.…”

Section: Discussionmentioning

confidence: 99%

Exploration of the Sphingolipid Metabolite, Sphingosine-1-phosphate and Sphingosine, as Novel Biomarkers for Aspirin-exacerbated Respiratory Disease

Trinh

Kim

Cho

et al. 2016

Sci Rep

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Sphingolipid (SL) metabolites have been suggested to be important inflammatory mediators in airway inflammation and asthma. However, little is known about SL metabolites in aspirin-exacerbated respiratory disease (AERD). We aimed to explore the potential AERD biomarkers by conducting lipidomics targeting SL metabolites. The levels of SL metabolites in serum and urine samples from 45 AERD patients and 45 aspirin-tolerant asthma (ATA) patients were quantified through mass spectrometry. During the lysine-aspirin bronchoprovocation test (ASA-BPT), the levels of serum sphingomyelin (SM) were significantly decreased in AERD (P < 0.05) but not in ATA. The serum SM levels were positively correlated with airway responsiveness to methacholine. At the basal status before the ASA-BPT, the levels of serum sphingosine-1-phosphate (S1P) and urine sphingosine were significantly higher in the AERD patients compared with that of ATA patients (P < 0.001) and were positively correlated with a greater decrease in FEV1 (%) values following the ASA-BPT test (P < 0.001 for each), and with serum periostin level (P < 0.05 for each). This study is the first to evaluate serum S1P and urine sphingosine as potential biomarkers of AERD as well as to examine the metabolic disturbance of SL in AERD patients.

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“…The significance of CysLT in the pathophysiology of AERD and possibly other CRSwNP patients, highlights its use as a biomarker for a distict CRS endotype . Because CysLT is metabolized and excreted through the urine, the 24‐hour urinary measurement of LTC 4 has been suggested as a means to identify CRSwNP patients who have the AERD variant .…”

Section: Introductionmentioning

confidence: 99%

A Review of Classification Schemes for Chronic Rhinosinusitis with Nasal Polyposis Endotypes

Dennis¹,

Lam²,

Luong³

2016

Laryngoscope Investigative Otolaryngology

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ObjectiveThe recent development of endotypes to categorize disease variants of chronic rhinosinusitis (CRS) reflects an evolving understanding of the various pathophysiologic and pathogenetic mechanisms that contribute to the clinical heterogeneity of CRS manifestations. This review highlights popular endotype‐based criteria used to define different CRS with nasal polyposis (CRSwNP) subtypes and further discusses the emerging therapeutic advances for each classificatory approach.Data SourcesPubMed literature review.MethodsA review of the current literature was conducted to determine present‐day uses of immunologic and molecular profiles in the CRSwNP disease spectrum to identify specific endotypes.ResultsFour distinct but overlapping classification schemes have emerged to define endotypes within the CRSwNP phenotype: 1) type 2 cytokine‐based approach, 2) eosinophil‐based approach, 3) immunoglobulin (Ig)E‐based approach, and 4) cysteinyl based approach. The identification of key inflammatory biomarkers related to these CRSwNP endotypes has broadened the classification of CRS beyond common phenotypic expressions. Furthermore, CRSwNP endotypes may improve the selection of CRSwNP patients who are suitable candidates for biomarker‐specific treatment options, such as anti‐interleukin‐5; anti‐IgE; and platelet‐directed therapies.ConclusionChronic rhinosinusitis endotyping with key biomarker patterns of inflammation allows for improved diagnostic and potentially therapeutic classifications of CRSwNP variants.

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Systemic expression of inflammatory mediators in patients with chronic rhinosinusitis and nasal polyps with and without Aspirin Exacerbated Respiratory Disease

Cited by 21 publications

References 41 publications

Alcohol hyper‐responsiveness in chronic rhinosinusitis with nasal polyps

Alcohol hyper‐responsiveness in chronic rhinosinusitis with nasal polyps

Exploration of the Sphingolipid Metabolite, Sphingosine-1-phosphate and Sphingosine, as Novel Biomarkers for Aspirin-exacerbated Respiratory Disease

A Review of Classification Schemes for Chronic Rhinosinusitis with Nasal Polyposis Endotypes

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