Mochizuki H, Shigeta M, Arakawa H, Kato M, Tokuyama K, Morikawa A
Department of Pediatrics, Gunma University School of Medicine, Maebashi, Gunma, Japan.
Pediatrics. 2000 Dec;106(6):1442-6. doi: 10.1542/peds.106.6.1442.
To assess at what age bronchial hyperresponsiveness (BHR) is acquired in children with asthma.
A relationship between BHR and infantile wheezing diseases has been reported. Infants with a genetic predisposition to atopy are more likely to wheeze with respiratory viral infection or bronchiolitis, and it is suspected that the continued BHR after the first attack of asthma may be induced or triggered by some viral infections. Also, recent studies have reported the existence of atopic and BHR-related genes. However, whether BHR is congenital or acquired after asthma attacks, and when BHR in children with asthma is established or acquired remain unclear.
We performed methacholine inhalation challenge using a transcutaneous oxygen pressure (tcPO(2)) monitoring system in 205 children without asthma from 6 months to 6 years of age. During follow-up, 18 of these participants were diagnosed with asthma (group N-A). This group and 15 age-matched children without asthma (group N-N) were tested twice using methacholine inhalation challenge. For comparison, 39 age-matched atopic-type asthmatic children (group A-A) were also given the inhalation challenge twice. Methacholine inhalation challenge using a tcPO(2) monitoring system was performed while the participants were asleep in the supine position. Sequential doses of inhaled methacholine delivered by oxygen mask were doubled until a 10% decrease in tcPO(2) from the baseline was reached. The cumulative dose of methacholine at the inflection point of tcPO(2) (minimal dose of methacholine [Dmin]-PO(2)) was considered to represent BHR.
In groups N-N and A-A, there was no difference in Dmin-PO(2) between the first and second challenge. However, the Dmin-PO(2) in group N-A significantly decreased from the first challenge to the second challenge. There was no significant difference between the Dmin-PO(2) in group N-N and the first Dmin-PO(2) in group N-A; or between the Dmin-PO(2) in group A-A and the second Dmin-PO(2) in group N-A.
These data suggest that BHR in many infants with asthma is acquired after several asthma attacks.bronchial hyperresponsiveness, childhood asthma, methacholine inhalation challenge, transcutaneous oxygen pressure.
评估哮喘患儿在何年龄获得支气管高反应性（BHR）。
已有报道称BHR与婴幼儿喘息性疾病之间存在关联。有特应性遗传易感性的婴儿在呼吸道病毒感染或细支气管炎时更易喘息，并且怀疑哮喘首次发作后的持续性BHR可能由某些病毒感染诱发或触发。此外，最近的研究报道了特应性和BHR相关基因的存在。然而，BHR是先天性的还是在哮喘发作后获得的，以及哮喘患儿的BHR何时确立或获得仍不清楚。
我们使用经皮氧分压（tcPO₂）监测系统，对205名6个月至6岁无哮喘的儿童进行了乙酰甲胆碱吸入激发试验。在随访期间，这些参与者中有18人被诊断为哮喘（N-A组）。该组和15名年龄匹配的无哮喘儿童（N-N组）使用乙酰甲胆碱吸入激发试验进行了两次测试。为作比较，39名年龄匹配的特应性哮喘儿童（A-A组）也进行了两次吸入激发试验。使用tcPO₂监测系统的乙酰甲胆碱吸入激发试验在参与者仰卧位睡眠时进行。通过氧气面罩给予的吸入乙酰甲胆碱的连续剂量加倍，直至tcPO₂较基线下降10%。tcPO₂拐点处的乙酰甲胆碱累积剂量（乙酰甲胆碱最小剂量[Dmin]-PO₂）被认为代表BHR。
在N-N组和A-A组中，第一次和第二次激发试验的Dmin-PO₂无差异。然而，N-A组的Dmin-PO₂从第一次激发试验到第二次激发试验显著降低。N-N组的Dmin-PO₂与N-A组的第一次Dmin-PO₂之间；或A-A组的Dmin-PO₂与N-A组的第二次Dmin-PO₂之间均无显著差异。
这些数据表明，许多哮喘婴幼儿的BHR是在多次哮喘发作后获得的。支气管高反应性、儿童哮喘、乙酰甲胆碱吸入激发试验、经皮氧分压
