Hamlyn A N, Berg P A
Gut. 1980 Apr;21(4):311-7. doi: 10.1136/gut.21.4.311.
Anti-actin antibody was measured by the passive haemagglutination test in the serum of 118 patients with various forms of chronic cholestatic and non-cholestatic liver disease, and of 23 patients with acute hepatitis B or non-A, non-B. Tanned sheep erythrocytes and electrophoretically pure actin prepared from rabbit skeletal muscle were employed; absorption tests confirmed the specificity of positive reactions, defined from healthy controls as a titre of greater than 1/80. The presence of anti-actin activity in chronic liver disease corresponded generally to the immunofluorescent demonstration of smooth muscle antibody (P<0.01). However, in acute hepatitis, with one exception (later progressing to subacute disease) raised anti-actin titres were not found. Thus, the weak smooth muscle antibody occasionally demonstrable in this condition may be neither IgM in class, nor directed against actin. Anti-actin antibody was present in significantly high titre in 54% of 37 active chronic hepatitis patients and 79% of 24 ;mixed-form' cholestatic active chronic hepatitis, as compared with only 21% of 29 primary biliary cirrhosis patients, and 11% of alcoholic liver disease. Anti-actin antibody is therefore associated with chronic autoimmune parenchymal liver damage and its appearance may mark the transition from acute hepatitis. No raised anti-actin titres were seen in 10 primary biliary cirrhosis patients positive for mitochondrial antibody by indirect immunofluorescence, but negative by the complement fixation test. This result suggests that the cytoplasmic fluorescence observed is due to low titre mitochondrial antibody rather than cytoplasmic actin and that these patients do not represent a different disease entity. The generation of anti-actin antibody in chronic parenchymal liver disease, perhaps due to unmasking or schlepping of intracellular or SIg/HLA-associated actin, may characterise autoimmune events at hepatocyte level, point to prognosis, and aid in the differential diagnosis of individual patients.
采用被动血凝试验检测了118例各种类型慢性胆汁淤积性和非胆汁淤积性肝病患者以及23例急性乙型肝炎或非甲非乙型肝炎患者血清中的抗肌动蛋白抗体。使用鞣酸处理的绵羊红细胞和从兔骨骼肌制备的电泳纯肌动蛋白;吸收试验证实了阳性反应的特异性,以健康对照者的滴度大于1/80来定义。慢性肝病中抗肌动蛋白活性的存在通常与平滑肌抗体的免疫荧光显示相符(P<0.01)。然而,在急性肝炎中,除了1例(后来进展为亚急性疾病)外,未发现抗肌动蛋白滴度升高。因此,在这种情况下偶尔可检测到的弱平滑肌抗体可能既不是IgM类,也不是针对肌动蛋白的。37例活动性慢性肝炎患者中有54%以及24例“混合型”胆汁淤积性活动性慢性肝炎患者中有79%的抗肌动蛋白抗体呈显著高滴度,相比之下,29例原发性胆汁性肝硬化患者中只有21%,酒精性肝病患者中只有11%。因此,抗肌动蛋白抗体与慢性自身免疫性实质性肝损伤相关,其出现可能标志着从急性肝炎的转变。10例通过间接免疫荧光法检测线粒体抗体呈阳性但补体结合试验呈阴性的原发性胆汁性肝硬化患者中未发现抗肌动蛋白滴度升高。这一结果表明,观察到的细胞质荧光是由于低滴度线粒体抗体而非细胞质肌动蛋白所致,且这些患者并不代表不同的疾病实体。慢性实质性肝病中抗肌动蛋白抗体的产生,可能是由于细胞内或SIg/HLA相关肌动蛋白的暴露或携带,可能是肝细胞水平自身免疫事件的特征,提示预后,并有助于个别患者的鉴别诊断。