哮喘联盟

    背景：可逆性的气流受阻和气道的高反应性（AHR）是哮喘的特征表现，但非哮喘型嗜酸粒细胞性支气管炎（EB）的患者则缺少上述表现。两种疾病都有气道重塑，这表明重塑和气道功能异常是相互分离的，但两种疾病的气道几何构型是否有差异尚不清楚。
    方法：通过CT成像研究哮喘和EB患者气道的几何构型。共有12名轻-中度哮喘患者，14名难治性哮喘患者，10名EB患者及11名健康志愿者入选本研究。采用细准直器（0.75 mm）CT扫描主动脉弓至隆凸，记录右上肺尖支气管（RB1）的影像。哮喘和EB患者在泼尼松龙（0.5 mg/kg）治疗前和治疗2周后分别进行CT扫描。
    结果：轻-中度和难治性哮喘与RB1壁增厚有关，相反，非哮喘性EB维持RB1构型而无增厚[平均(SD) % 壁面积和腔面积在轻至中度哮喘患者为67.7 (7.3)% 和6.6 (2.8) mm2/m2, 难治性哮喘患者为 67.3 (5.6)%和6.7 (3.4) mm2/m2, 健康对照组为59.7 (6.3)% 和8.7 (3.8) mm2/m2, EB患者为61.4 (7.8)%和11.1 (4.6) mm2/m2 P < 0.05]。
    结论：EB患者保持气道构型能预防发展成AHR，而哮喘患者气道增厚可能加速AHR发生。

（苏楠 审校）
Siddiqui S, et al. Allergy. 2009 Feb 10. [Epub ahead of print]

Airway wall geometry in asthma and nonasthmatic eosinophilic bronchitis.

Background: Variable airflow obstruction and airway hyperresponsiveness (AHR) are features of asthma, which are absent in nonasthmatic eosinophilic bronchitis (EB). Airway remodelling is characteristic of both conditions suggesting that remodelling and airway dysfunction are disassociated, but whether the airway geometry differs between asthma and nonasthmatic EB is uncertain.
Methods: We assessed airway geometry by computed tomography (CT) imaging in asthma vs EB. A total of 12 subjects with mild-moderate asthma, 14 subjects with refractory asthma, 10 subjects with EB and 11 healthy volunteers were recruited. Subjects had a narrow collimation (0.75 mm) CT scan from the aortic arch to the carina to capture the right upper lobe apical segmental bronchus (RB1). In subjects with asthma and EB, CT scans were performed before and after a 2-week course of oral prednisolone (0.5 mg/kg).
Results: Mild-moderate and refractory asthma were associated with RB1 wall thickening in contrast to subjects with nonasthmatic EB who had maintained RB1 patency without wall thickening [mean (SD) % wall area and luminal area mild-t0-moderate asthma 67.7 (7.3)% and 6.6 (2.8) mm(2)/m(2), refractory asthma 67.3 (5.6)% and 6.7 (3.4) mm(2)/m(2), healthy control group 59.7 (6.3)% and 8.7 (3.8) mm(2)/m(2), EB 61.4 (7.8)% and 11.1 (4.6) mm(2)/m(2) respectively; P < 0.05]. Airway wall thickening of non-RB1 airways generation three to six was a feature of asthma only. There was no change in airway geometry of RB1 after prednisolone. Proximal airway wall thickening was associated with AHR in asthma (r = -0.56; P = 0.02).
Conclusions: Maintained airway patency in EB may protect against the development of AHR, whereas airway wall thickening may promote AHR in asthma.