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자료유형
학술저널
저자정보
Kim, Seong Han (Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine) Yang, Seo Yeon (Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine) You, Jihong (Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine) Lee, Sang Bae (Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine) You, Jin (Department of Internal Medicine, Kunkuk University School of Medicine) Chang, Yoon Soo (Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine) Kim, Hyung Jung (Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine) Ahn, Chul Min (Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine) Byun, Min Kwang (Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine) Park, Hye Jung (Department of Internal Medicine, Gangnam Severance Hospital, Yonsei University College of Medicine) Park, Jung-Won (Division of Allergy)
저널정보
대한결핵 및 호흡기학회 Tuberculosis and Respiratory Diseases 결핵 및 호흡기 질환 제79권 제4호
발행연도
2016.1
수록면
295 - 301 (7page)

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Background: Specific immunoglobulin E (IgE) sensitization to staphylococcal enterotoxin (SE) has been recently considered to be related to allergic disease, including asthma. Despite studies on specific IgE (sIgE) to SE and its relationship to asthma diagnosis and severity, the association of sIgE to SE with airway hyperresponsiveness (AHR) remains unclear. Methods: We enrolled 81 asthma patients admitted to the Severance Hospital in Korea from March 1, 2013, to February 28, 2015 and retrospectively reviewed the electronic medical records of the enrolled subjects. The serum levels of sIgE to SE (A/B) of all subjects was measured using the ImmunoCAP 250 (Phadia) system with SE-sIgE positive defined as >0.10 kU/mL. Results: The SE-sIgE level was not significantly correlated with asthma severity (forced expiratory volume in 1 second [$FEV_1$], $FEV_1$/forced vital capacity, sputum eosinophils, and serum eosinophils), whereas the SE-sIgE level in patients with positive AHR ($mean{\pm}standard$ error of the mean, $0.606{\pm}0.273kU/mL$) was significantly higher than that in patients with negative AHR ($0.062{\pm}0.015kU/mL$, p=0.034). In regression analysis, SE sensitization (sIgE to SE ${\geq}0.010kU/mL$) was a significant risk factor for AHR, after adjustment for age, sex, $FEV_1$, and sputum eosinophils (odds ratio, 7.090; 95% confidence interval, 1.180-42.600; p=0.032). Prevalence of SE sensitization was higher in patients with allergic rhinitis and non-atopic asthma patients, as compared to patients without allergic rhinitis and atopic asthma patients, respectively, but without statistical significance. Conclusion: SE sensitization is significantly associated with AHR.

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