In the present study, we investigated the role of the spleen in experimental hepatic ischemia/reperfusion in the rat. After a 90‐min period of ischemia in the left and middle hepatic lobes, the ischemia was released and the liver was reperfused for up to 24 h. Plasma alanine aminotransferase reached a peak 3 h after the onset of reperfusion, and gradually decreased thereafter. A histological examination revealed evidence of hepatocellular necrosis and degeneration, especially 24 h after the onset of reperfusion. In addition, there was a noticeable accumulation of polymorphonuclear cells in the liver following ischemia/reperfusion. A splenectomy performed just prior to ischemia/reperfusion reduced both biochemical and histological hepatocellular injury. The number of polymorphonuclear cells in the liver following ischemia/reperfusion was significantly reduced in rats subjected to splenectomy, suggesting that the increase in polymorphonuclear cells may contribute to liver injury. The number of mononuclear cells also increased in the marginal zones of the spleen following ischemia/reperfusion, and appeared to be derived from the splenic monocyte/macrophage population, based on immunohistochemical studies. The spleen plays an important role in the pathogenesis of hepatic ischemia/reperfusion injury and the splenic monocyte/macrophage population contributes to liver damage.

An immunohistochemical study of HBV‐associated antigen in the liver of 16 Japanese infants with biliary atresia revealed positive findings in 13 of the cases for HBc and/or HBs antigens. The positive cells were mainly small liver cells distributed in the peripheral zone of the lobule, and a few lymphocytes were observed in contact with or around the positive liver cells for HBV‐associated antigen. Again, HBc antigen was demonstrated almost exclusively in the cytoplasm of positive liver cells. As these findings suggest the possibility of destruction and drop‐out of cells constituting the interlobular bile duct in the junctional area by an immunological mechanism, the probability of HBV infection being an important factor in causing and accelerating biliary atresia cannot be denied. Positive findings for HBV‐associated antigen similar to those found in biliary atresia are also seen in neonatal hepatitis and choledochal cysts. These conditions are therefore presumed to belong to the same category.

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This study focused on 32 patients who were diagnosed as having autoimmune hepatitis based upon clinical and histological factors. Fifteen of these patients were positive for HCV‐RNA and for one of the HCV‐related markers tested, including anti‐C100, ELISA II, and RIBA 2 (Group 2). The remaining 17 patients were negative for all HCV‐related markers (Group 1). Clinical factors in the two groups, including the frequency of autoantibodies, serum levels of aminotransferase and gammaglobulin, HLA phenotypes, and the response to corticosteroid treatments, were compared. The titer of serum anti‐nuclear antibodies and the level of serum aminotransferase at initial diagnosis were significantly higher in Group 1 than in Group 2. Furthermore, the genetic background of the two groups, as indicated by HLA phenotypes, differed. All cases in Group 1 were HLA‐DR4‐positive, whereas only 60% of those in Group 2 cases had HLA‐DR4. Also, all cases in Group 1 but only 66.7% of the cases in Group 2 showed good clinical responses to corticosteroid treatment. Finally, no cases of HCV‐related‐marker‐positive autoimmune hepatitis (Group 2) had antibodies for LKM, suggesting that these cases were clinically different from type II autoimmune hepatitis. These data indicated that immunosuppressive treatment might be the preferred initial treatment in patients who either satisfy the criteria for AIH or who are sero‐positive for an HCV‐marker.

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