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Coincidental Australia Antigenemia in Primary Biliary Cirrhosis

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Supported by research grant AM05966 and training grant AM-05180 from the National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Md.; and the Harold C. Strong Liver Research Fund.

Dr. Saito was the recipient of a James Hudson Brown Memorial Fellowship, Yale University, New Haven, Conn.

▸Request for reprints should be addressed to Gerald Klatskin, M.D., Department of Medicine, Yale University, 333 Cedar St., New Haven, Conn. 06510.

New Haven, Connecticut, and Bethesda, Maryland

Ann Intern Med. 1972;76(5):705-709. doi:10.7326/0003-4819-76-5-705
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To investigate the role of the long-incubation hepatitis (SH) virus in the pathogenesis of primary biliary cirrhosis, we have tested for Australia (Au) antigen and antibody in the serums of 97 patients with the disease. Our techniques included immunodiffusion, immunoelectroosmophoresis, complement fixation, hemagglutination, hemagglutination inhibition, and electron microscopy. Australia antigen was detected in five (5%) of the group—by immunoelectroosmophoresis and complement fixation in one, by complement fixation alone in one, and hemagglutination inhibition alone in three. Of the five Au-positive patients, all had undergone laparotomy, and three had received blood transfusions before serum sampling. Australia antibody in low titer was demonstrated by hemagglutination in 12 (12%) of the group, but this was not considered significant, since neither the incidence nor the titer differed from those in 589 healthy controls. All other tests for Au antigen and antibody showed negative results. We suggest that the SH virus is not implicated in the pathogenesis of primary biliary cirrhosis and that the occasional occurrence of Au antigen in the serum of such patients is attributable to coincidental, asymptomatic intercurrent infections with the virus.





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