Haemagglutinating anti-actin antibodies in acute and chronic liver disease. Issue 4 (April 1980)

• Record Type: Journal Article
• Authors: Hamlyn, A N; Berg, P A
• Is Part Of: Gut. Volume 21:Issue 4(1980)
• Page Start: 311
• Page End: 317
• Publication Date: 1980-04
• Subjects: Gastroenterology -- Periodicals; 616.33
• DOI: 10.1136/gut.21.4.311
• Languages: English
• ISSNs: 0017-5749

Abstract

Abstract : 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.