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Clinical course of patients with aspirin-exacerbated respiratory disease: can we predict the prognosis?

    Joo-Hee Kim

    Division of Pulmonary, Allergy & Critical Care Medicine, Department of Medicine, Hallym University Sacred Heart Hospital, Hallym University College of Medicine, 896 Pyeongan-dong, Dongan-gu, Anyang, Gyeonggi, 431–796, Republic of Korea

    ,
    Gil-Soon Choi

    Department of Allergy, Kosin University Gaspel Hospital, Pusan, Amnan-dong, Seo-gu, 602–702, Busan, Republic of Korea

    ,
    Jeong-Eun Kim

    Department of Internal Medicine, Samsung Changwon Hospital, Sungkyunkwan University School of Medicine, Palyong-ro, MasanHoiwon-gu, 630–723, Changwon, Republic of Korea

    ,
    Hyun-Jung Jin

    Department of Internal Medicine, Yeungnam University College of Medicine, Daemyeong-5dong, Nam-gu, 705–703, Daegu, Republic of Korea

    ,
    Young-Min Ye

    Department of Allergy & Clinical Immunology, Ajou University School of Medicine, Wonchondong San 5, Youngtongku, 443–721, Suwon, Republic of Korea

    ,
    Seung-Hyun Kim

    Department of Allergy & Clinical Immunology, Ajou University School of Medicine, Wonchondong San 5, Youngtongku, 443–721, Suwon, Republic of Korea

    &
    Hae-Sim Park

    * Author for correspondence

    Department of Allergy & Clinical Immunology, Ajou University School of Medicine, San-5, Wonchon-dong, Yeongtong-gu, Suwon, 442–749, Republic of Korea.

    Published Online:https://doi.org/10.2217/pgs.14.2

    Aim: This study aimed to identify prognostic factors of aspirin-exacerbated respiratory disease by comparing clinical and genetic data with the clinical course. Patients & methods: Patients were classified into two groups according to their response to inhalation rechallenge with lysine-aspirin after at least 1 year of regular treatment with antiasthmatic medications. Results: Forty eight patients (39.3%, group I) had negative responses, whereas 74 patients (60.7%, group II) had positive responses (n = 23) or were not rechallenged owing to persistent symptoms (n = 51). FEV1 at diagnosis and follow-up were significantly lower in group II than in group I. The CCR3 polymorphism at -520T/G differed significantly between the two groups, whereas no difference was found in other SNPs. Conclusion: Baseline FEV1 and lower lung function after treatment were clinical factors indicating a poor prognosis of aspirin-exacerbated respiratory disease. The G allele of CCR3 -520T>G was associated with persistent bronchial hypersensitivity to aspirin.

    Original submitted 17 June 2013; Revision 3 January 2014

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