Tsuge Mitsuru, Ikeda Masanori, Tsukahara Hirokazu
Department of Pediatric Acute Diseases, Okayama University Academic Field of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama 700-8558, Japan.
Okayama University School of Medicine, Okayama 700-8558, Japan.
Children (Basel). 2022 Aug 19;9(8):1253. doi: 10.3390/children9081253.
Anti-inflammatory therapy, centered on inhaled steroids, suppresses airway inflammation in asthma, reduces asthma mortality and hospitalization rates, and achieves clinical remission in many pediatric patients. However, the spontaneous remission rate of childhood asthma in adulthood is not high, and airway inflammation and airway remodeling persist after remission of asthma symptoms. Childhood asthma impairs normal lung maturation, interferes with peak lung function in adolescence, reduces lung function in adulthood, and increases the risk of developing chronic obstructive pulmonary disease (COPD). Early suppression of airway inflammation in childhood and prevention of asthma exacerbations may improve lung maturation, leading to good lung function and prevention of adult COPD. Biological drugs that target T-helper 2 (Th2) cytokines are used in patients with severe pediatric asthma to reduce exacerbations and airway inflammation and improve respiratory function. They may also suppress airway remodeling in childhood and prevent respiratory deterioration in adulthood, reducing the risk of COPD and improving long-term prognosis. No studies have demonstrated a suppressive effect on airway remodeling in childhood severe asthma, and further clinical trials using airway imaging analysis are needed to ascertain the inhibitory effect of biological drugs on airway remodeling in severe childhood asthma. In this review, we describe the natural prognosis of lung function in childhood asthma and the risk of developing adult COPD, the pathophysiology of allergic airway inflammation and airway remodeling via Th2 cytokines, and the inhibitory effect of biological drugs on airway remodeling in childhood asthma.
以吸入性糖皮质激素为核心的抗炎治疗可抑制哮喘患者的气道炎症,降低哮喘死亡率和住院率,并使许多儿科患者实现临床缓解。然而,儿童哮喘在成年期的自然缓解率并不高,且哮喘症状缓解后气道炎症和气道重塑仍会持续。儿童哮喘会损害肺的正常发育,干扰青少年的肺功能峰值,降低成年后的肺功能,并增加患慢性阻塞性肺疾病(COPD)的风险。儿童期早期抑制气道炎症并预防哮喘发作可能会改善肺发育,从而带来良好的肺功能并预防成年期COPD。针对辅助性T细胞2(Th2)细胞因子的生物药物用于治疗重度儿科哮喘患者,以减少发作和气道炎症并改善呼吸功能。它们还可能抑制儿童期的气道重塑并预防成年期的呼吸功能恶化,降低患COPD的风险并改善长期预后。尚无研究证明对儿童重度哮喘的气道重塑有抑制作用,需要进一步开展使用气道成像分析的临床试验,以确定生物药物对儿童重度哮喘气道重塑的抑制作用。在本综述中,我们描述了儿童哮喘肺功能的自然预后以及成年期患COPD的风险、通过Th2细胞因子发生的过敏性气道炎症和气道重塑的病理生理学,以及生物药物对儿童哮喘气道重塑的抑制作用。