近年已经认识到,无论外源性或内源性哮喘,由于速发型(Ⅰ型)或免疫复合物型(Ⅲ型)变态反应,以及植物神经功能紊乱,导致β受体功能低下,或者支气管壁细胞与其他靶细胞花生四烯酸的代谢障碍的后果,造成支气管敏感性增加,发生哮喘,在某种程度上,均与遗传因素有关。哮喘发病具有过敏性的家族聚集现象,早在1952年,Schwartz综合4611例的文献报告,其中有过敏性家族史者占23～83%,平均为48%。裴德恺(1964)报告140例在四代内患哮喘者占57.1%,对照者家属 In recent years, it has been recognized that both the exacerbated (type I) or immunocomplex (type III) allergy and autonomic dysfunction, either exogenous or endogenous asthma, result in impaired beta receptor function or bronchial wall The consequences of a metabolic disorder of arachidonic acid in cells and other target cells, resulting in increased bronchial sensitivity and asthma, are to some extent related to genetic factors. As early as in 1952 Schwartz’s literature on 4611 patients reported, of whom 23 to 83% had an atopic family history of 48% with an average of 48%. Of the 140 cases Pei Takai (1964) reported asthma in the fourth generation accounted for 57.1% of the families of controls