Presentation: Serum LTE4 metabolite as a biomarker for aspirin exacerbated respiratory disease ( World Allergy Congress)

Friday, 16 October 2015

Hall D1 Foyer (Floor 3) (Coex Convention Center)

Ga Young Ban, MD , Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, South Korea

Kumsun Cho , Department of Pharmacology and Biomeidcal Sciences, Seoul National University College of Medicine, Seoul, South Korea

Seung-Hyun Kim, PhD , Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, South Korea

Yong Eun Kwon, MD , Department of Internal Medicine, Chosun University College of Medicine, Gwangju, South Korea

Moon Gyeong Yoon, M.S , Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, South Korea

Ji Hye Kim, MD , Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, South Korea

Yoo Seob Shin, MD, PhD , Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, South Korea

Young Min Ye, MD, PhD , Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, South Korea

Dong-Ho Nahm, MD, PhD , Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, South Korea

Hae-Sim Park, MD, PhD , Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, South Korea

Background: Provocation tests with aspirin are the most reliable method to confirm the diagnosis of aspirin exacerbated respiratory disease (AERD). To date, there is not an appropriate in vitro test to diagnose AERD.

Objectives: To further understand the pathogenic mechanisms of AERD and investigate the potential biomarkers for AERD using metabolomics.

Subjects and Method: Forty five AERD, 44 aspirin tolerant asthma (ATA) and 28 normal controls were enrolled. Urine and serum samples were collected from all asthma subjects before and after lysine-aspirin bronchoprovocation test (Lys-ASA BPT). The metabolites of LTE₄ and PGF₂α were analyzed using liquid chromatography with mass spectrometry.

Results: Baseline serum and urine LTE₄levels were significantly higher in AERD than ATA (18.14 ± 7.19 pg/ml vs. 14.65 ± 4.39 pg/ml, P = 0.007; 7.36 ±13.19 pmol/mg creatinine vs. 2.69 ±3.62 pmol/mg creatinine, P=0.047, respectively). The ROC curve analysis that discriminates AERD from ATA indicated the cutoff value of the serum LTE₄was 14.5 pg/ml, with 71.1% sensitivity and 52.3% specificity (AUC = 0.651, P = 0.014) which was improved further if combined with serum periostin level (81.4% sensitivity, 63.4% specificity, AUC = 0.761, P < 0.001). However, the ROC curves were not formed using urine LTE₄ level. There were no significant correlations between serum and urine levels of two metabolites. Urine LTE₄ levels were significantly correlated with those of PGF₂α before and after Lys-ASA BPT (r = 0.562, P < 0.001; r = 0.627, P < 0.001). Baseline urine LTE₄and PGF₂α were significantly correlated with fall of FEV₁ % after Lys-ASA BPT (r = 0.463, P = 0.008, and r = 0.610, P <0.001, respectively).

Conclusion: Serum LTE₄ level can be a useful serum biomarker for representing the phenotype of AERD considering serum collection is simpler than any other sample collections. Overproduction of LTE4 and mast cell activation can contribute to induce bronchoconstriction to inhaled aspirin in the pathogenic mechanisms of AERD.

3015 Serum LTE4 metabolite as a biomarker for aspirin exacerbated respiratory disease