[Remission state and five-year survival after transcatheter arterial embolization therapy in patients with hepatocellular carcinoma].

Repeated transcatheter arterial embolization (TAE) therapy was done for 138 cases with hepatocellular carcinoma. Relationship was investigated between long term survival more than 3 years and tumor necrosis rate estimated on radiological images (superselective angiogram and/or computerized tomography) after therapy. Excellent tumor necrosis (radiological disappearance of viable tumor) was attained in 35 out of 138 cases through repeated TAE. When "remission" is defined as excellent tumor necrosis and normal alphafetoprotein value lasting for more than one year, remission state was attained in 17 cases (12.3%). Cumulative three-year survival rate was 37.0%, and 5-year survival was 26.5%. Out of 37 three-year-survivors, only 12 cases (32.4%) experienced remission state in their clinical course. On the other hand, 7 cases (77.7%) of 9 five-year-survivors experienced remission at least one time. Though good tumor necrosis and 3-year survival were achieved by only performing repeated TAE therapy, "remission" state was important and necessary to get 5-year survival.

Hepatic squamous cell carcinoma with hypercalcemia in liver cirrhosis.

Primary squamous cell carcinoma of the liver is exceedingly rare and has previously been reported in association with hepatic teratoma, hepatic cyst or hepatolithiasis. This paper describes an autopsy case of squamous cell carcinoma which developed with hypercalcemia in a cirrhotic liver. This cancer was characterized histologically, immunohistologically and ultrastructurally, and was found to exhibit immunofluorescence positivity for anti-epidermal keratin monoclonal antibody, together with the presence of tonofilaments scattered sparsely in the cytoplasm of the cancer cells.

Seroconversion from HBs-Ag to anti-HBs in a case of liver cirrhosis associated with hepatocellular carcinoma.

This paper reports a case of liver cirrhosis associated with hepatocellular carcinoma (HCC) of a woman who was converted from hepatitis B surface antigen (HBs-Ag) positive to antibody against HBs-Ag (anti-HBs) positive in the serum through an immunoregulatory steroid rebound phenomenon. The histology of the biopsy specimen taken before the seroconversion showed an early stage of liver cirrhosis with moderate infiltration of mononuclear cells. At autopsy about 3 years after the seroconversion, the liver tissue free of the tumor was in an early stage of liver cirrhosis. Fibrosis did not advance as compared with the biopsy specimen. In addition, mononuclear cell infiltration decreased remarkably and piecemeal necrosis disappeared after the seroconversion. The immunohistologic examination of hepatocytes demonstrated that positive stainings for HBs-Ag and for hepatitis B core antigen (HBc-Ag) in the biopsy specimen turned to be negative in the autopsy specimen. These facts indicate that the steroid rebound phenomenon eliminated free hepatitis B virus (HBV) in the hepatocytes in the absence of massive necrosis of hepatocytes. HBV-DNA integration was proved in the genome of HCC by molecular hybridization method.

Primary hepatocellular carcinoma and IgG heavy chain allotypes.

We studied Gm typing of serum samples from 838 donors; 177 had chronic hepatitis, 166 liver cirrhosis, 113 primary hepatocellular carcinoma, 21 alcoholic hepatitis, 18 fatty liver and 343 were unrelated normal blood donors. The distribution of Gm phenotypes and haplotypes in sera from patients with primary hepatocellular carcinoma differed from that in the normal controls; the Gm phenotype (1,2,21,13,15,16) and the haplotype Gm1,2,21 were significantly more common in this patient group (X2 = 18.56, corrected P less than 0.01, relative risk = 3.12; X2 = 25.52, corrected P less than 0.005, respectively). Overall, in the other liver diseases, we observed no significant Gm phenotype or haplotype association. The commitment to progression to primary liver carcinoma seems to be ascribable to a gene or polygenes close to the IgG heavy chain loci.