No abstract
Summary Group O donor cells recovered from the circulation of group A or B recipients are agglutinable by a proportion of group O sera, and sometimes by a smaller proportion of group B or A sera, showing that they have taken up A or B substance. The uptake of antigen takes about a fortnight to reach a maximum level and no uptake of antigen could be shown following incubation of group O cells with group A1 blood or plasma for 41 hrs. at 37° C in vitro. Résumé Les érythrocytes de donneurs de groupe O récupéré de la circulation de receveurs de groupe A ou B sont agglutinables par certains sérums de groupe O et, parfois, par un petit nombre de sérum de groupe A ou B; ceci démontre que ces érythrocytes récupérés ont accaparé de la substance A ou B. La prise de l'antigène atteint un maximum en quinze jours; on n'observe pas de prise de l'antigène après incubation d'érythrocytes O dans des sérums ou plasma A1 pendant 41 heures à 37° C. Zusammenfassung O‐Spendererythrozyten, die aus dem Kreislauf von A oder B‐Empfängern stammen, werden durch zahlreiche O‐Seren sowie, wenn auch seltener, durch B‐ bzw. A‐Seren agglutiniert. Dies beruht darauf, daß sie im Empfängerkreislauf A‐ oder B‐Blutgruppensubstanz aufgenommen haben. Die Antigenaufnahme erfolgt langsam und erreicht ungefähr nach 14 Tagen das Maximum. Anläßlich der in‐vitro‐Inkubation bei 37° C von O‐Zellen in A1‐Blut oder Plasma während 41 Stunden konnte keine Antigenaufnahme festgestellt werden.
srNopsis Thirty-four healthy blood donors, found to be persistent HBAg carriers, have been investigated by means of serial liver function tests, bromsulphthalein (BSP) retention, and liver biopsy. Thirty-one of the donors had histological abnormalities including one with cirrhosis, three with chronic aggressive hepatitis, and 11 with chronic persistent hepatitis. In 13 biopsies there were focal areas of necrosis in the liver parenchyma. Serial liver function tests revealed abnormalities in each ofthe donors with cirrhosis orwith chronic aggressive hepatitis, in seven of the 11 donors with chronic persistent hepatitis, and in seven of the 13 with focal parenchymal necrosis. The degree of BSP retention was greatest (>11 %) in the donors with chronic aggressive hepatitis. The severity of the histological changes was related neither to the titre of the antigen in the serum nor to the presence of autoantibodies.The association of the hepatitis B antigen (HBAg, Australia antigen, HAA) with serum hepatitis is now well established. It is also being increasingly implicated in chronic liver disease (Krohn, Finlayson, Jokelainen, Anderson, and Prince, 1970;Hadziyannis, Merikas, and Afroudakis, 1970;Dudley, Fox, and Sherlock, 1971).The routine screening of donor blood by blood transfusion serviceshas identifiedsubstantialnumbers of asymptomatic HBAg carriers (Kliman, Reid, Lilly, and Morrison, 1971;Wallace, Milne, and Barr, 1972) although the full implications of this carrier state remain to be determined. Several reports from other countries have recorded a varying incidence of liver abnormalities (Singleton, Fitch, Merrill, Kohler, and Rettberg, 1971;Bolin, Davis, and Liddelow, 1973). This report records our findings in a group of healthy asymptomatic volunteer blood donors in the north west of England.Patients and Methods Screening of donor blood for the presence of HBAg was begun in March 1970 using immunoelectroosmophoresis (Stratton, 1972 (Public Health Laboratory Service, Manchester) using similar methodology. The results of positive tests were reported to the family practitioners, with whose consent arrangements were subsequently made for these donors to be reviewed in the Liver Clinic at the University Hospital of South Manchester.Thirty-four donors who had persistent antigenaemia were investigated for evidence of liver disease. In each donor an attempt was made by careful questioning to elicit a possible source of infection. The investigations performed included a serum bilirubin, alkaline phosphatase, aspartate and alanine aminotransferases (SGOT/SGPT), albumin and globulin levels, protein electrophoresis, and prothrombin time. These tests were performed at three monthly intervals over a period of one to two years. Using standard indirect immunofluorescence technique the sera were screened for smooth muscle antibody (Johnson, Holborow, and Glynn, 1965), antinuclear factor (Beck, 1961), and antimitochondrial antibody (Goudie, MacSween, and Goldberg, 1966
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