Pharmacogenomics · 2014
Clinical course of patients with aspirin-exacerbated respiratory disease: can we predict the prognosis?
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Kim Joo-Hee, Choi Gil-Soon, Kim Jeong-Eun, Jin Hyun-Jung, Ye Young-Min, Kim Seung-Hyun, Park Hae-Sim
Аннотация
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.
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.