Godfrey S
Institute of Pulmonology, Hadassha University Hospital, Jerusalem.
Agents Actions Suppl. 1993;40:109-43. doi: 10.1007/978-3-0348-7385-7_10.
Asthma is a common disease of children the basis of which is a state of chronic immunological inflammation which causes bronchial hyperreactivity and renders the patient liable to develop widespread airways obstruction in response to a variety of stimuli. In many instances it is likely that the immunological inflammation results from ongoing antigenic stimuli with the release of chemical mediators responsible for short term bronchospasm and cytokines responsible for the ongoing inflammatory process. Other insults can apparently result in very similar immunological events in asthmatics, particularly viral infections and a similar process can be initiated in children without asthma, including those with chronic bacterial infections of the lungs. There are differences in the bronchial hyperreactivity of asthma and other diseases which suggest that in the asthmatic the mast cell is either different structurally or functionally and this renders the patient susceptible to exercise induced asthma in addition to the bronchial hyperreactivity to chemical mediators common to a number of diseases with hyperreactivity. There is good evidence of direct genetic control of atopy and the large majority of children with asthma are atopic but there is no direct genetic link between atopy and asthma and twin studies strongly suggest the existence of a 'permissive' asthma gene which will allow the disease to develop if there is an appropriate external trigger. The only drugs which have been shown to significantly reduce bronchial reactivity are the corticosteroids with a lesser effect noted for sodium cromoglycate and nedocromil. Inhaled corticosteroids can reverse the immunologic inflammatory process and reduce bronchial reactivity, sometimes to normal levels, but on stopping treatment the patient reverts back to the asthmatic state. At the present time it appears that controlled longterm inhaled corticosteroid therapy is the most rational treatment for significant perennial childhood asthma.
哮喘是儿童的常见疾病，其基础是慢性免疫炎症状态，这种状态会导致支气管高反应性，并使患者易于因各种刺激而出现广泛的气道阻塞。在许多情况下，免疫炎症可能源于持续的抗原刺激，导致负责短期支气管痉挛的化学介质以及负责持续炎症过程的细胞因子释放。其他损伤显然也可在哮喘患者中引发非常相似的免疫反应，尤其是病毒感染，并且在无哮喘的儿童中，包括患有慢性肺部细菌感染的儿童中，也可启动类似过程。哮喘与其他疾病在支气管高反应性方面存在差异，这表明哮喘患者的肥大细胞在结构或功能上有所不同，这使得患者除了对多种具有高反应性的疾病所共有的化学介质产生支气管高反应性外，还易患运动诱发性哮喘。有充分证据表明特应性受直接遗传控制，大多数哮喘儿童患有特应性，但特应性与哮喘之间没有直接的遗传联系，双胞胎研究强烈提示存在一种“许可性”哮喘基因，如果有适当的外部触发因素，该基因会使疾病得以发展。已证明能显著降低支气管反应性的唯一药物是皮质类固醇，色甘酸钠和奈多罗米的效果稍差。吸入皮质类固醇可逆转免疫炎症过程并降低支气管反应性，有时可降至正常水平，但停止治疗后患者会恢复到哮喘状态。目前，对于严重的常年性儿童哮喘，似乎控制性长期吸入皮质类固醇疗法是最合理的治疗方法。
