Geddes D M, Webley M, Brewerton D A, Turton C W, Turner-Warwick M, Murphy A H, Ward A M
Lancet. 1977 Nov 19;2(8047):1049-51. doi: 10.1016/s0140-6736(77)91883-9.
alpha 1-antitrypsin (alpha 1-A.T.) phenotypes were determined in 55 patients with rheumatoid arthritis (R.A.), 33 patients with R.A. and either obstructive airways disease or recurrent chest infections, 49 patients with fibrosing alveolitis (F.A.), 22 patients with R.A. and F.A., and 200 healthy controls. A highly significant increase in the frequency of MZ phenotype was found among patients with F.A., both with and without R.A. Patients with R.A. alone had a normal distribution of phenotypes. Inherited modification of immune function may predispose to F.A. Alternatively, lowered levels of alpha 1-A.T. associated with non-M phenotypes may predispose to tissue damage with subsequent fibrosis.
在55例类风湿性关节炎（R.A.）患者、33例患有R.A.且伴有阻塞性气道疾病或反复胸部感染的患者、49例肺纤维化（F.A.）患者、22例患有R.A.和F.A.的患者以及200名健康对照者中，测定了α1 -抗胰蛋白酶（α1 - A.T.）表型。在患有F.A.的患者中，无论是否患有R.A.，均发现MZ表型的频率显著增加。仅患有R.A.的患者表型分布正常。免疫功能的遗传修饰可能易患F.A.。或者，与非M表型相关的α1 - A.T.水平降低可能易导致组织损伤并随后发生纤维化。
