Airway wall geometry in asthma and nonasthmatic eosinophilic bronchitis.

Airway wall geometry in asthma and nonasthmatic eosinophilic bronchitis.
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DOI:
10.1111/j.1398-9995.2009.01951.x
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发表时间:
2009-06
期刊:
影响因子:
12.4
通讯作者:
Brightling C
Brightling C
中科院分区:
医学1区
文献类型:
--
作者:
Siddiqui S;Gupta S;Cruse G;Haldar P;Entwisle J;Mcdonald S;Whithers PJ;Hainsworth SV;Coxson HO;Brightling C

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可变气流阻塞和气道高反应性 (AHR) 是哮喘的特征,而非哮喘性嗜酸性支气管炎 (EB) 则不存在这些特征。气道重塑是这两种疾病的特征,表明重塑和气道功能障碍无关,但哮喘和非哮喘 EB 之间的气道几何形状是否不同尚不确定。我们通过计算机断层扫描 (CT) 成像评估哮喘与 EB 的气道几何形状。总共招募了 12 名轻中度哮喘受试者、14 名难治性哮喘受试者、10 名 EB 受试者和 11 名健康志愿者。受试者从主动脉弓到隆突进行窄准直 (0.75 mm) CT 扫描,以捕获右上叶心尖段支气管 (RB1)。在患有哮喘和 EB 的受试者中,在口服泼尼松龙(0.5 mg/kg)两周疗程之前和之后进行 CT 扫描。轻度至中度和难治性哮喘与 RB1 壁增厚相关,而非哮喘 EB 受试者则保持 RB1 通畅而无壁增厚 [平均 (SD) % 壁面积和管腔面积轻度至中度哮喘 67.7 (7.3)% 和 6.6 (2.8) mm2/m2,难治性哮喘 67.3 (5.6)% 和 6.7 (3.4)mm2/m2,健康对照组分别为59.7(6.3)%和8.7(3.8)mm2/m2,EB分别为61.4(7.8)%和11.1(4.6)mm2/m2; P<0.05]。第三代至第六代非 RB1 气道的气道壁增厚仅是哮喘的一个特征。泼尼松龙治疗后 RB1 的气道几何形状没有变化。近端气道壁增厚与哮喘的 AHR 相关(r = -0.56;P = 0.02)。 EB 患者保持气道通畅可以防止 AHR 的发生,而气道壁增厚可能会促进哮喘患者发生 AHR。
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. 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). 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) mm2/m2, refractory asthma 67.3 (5.6)% and 6.7 (3.4) mm2/m2, healthy control group 59.7 (6.3)% and 8.7 (3.8) mm2/m2, EB 61.4 (7.8)% and 11.1 (4.6) mm2/m2 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). Maintained airway patency in EB may protect against the development of AHR, whereas airway wall thickening may promote AHR in asthma.
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