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H Kumada

Publications and source records attributed to H Kumada.

At least 163 records · Page 9Linked to original sources

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.

Carcinoma, Hepatocellular↗

Short-term prednisolone for inducing seroconversion from hepatitis B e antigen to antibody along with clinical improvement in patients with chronic active hepatitis type B.

Short-term prednisolone therapy was instituted on 27 patients with chronic active hepatitis (CAH) type B, in an attempt to induce seroconversion from hepatitis B e antigen (HBeAg) to the corresponding antibody (anti-HBe). Patients with CAH received a four-week regimen of prednisolone with daily dosage tapering from 40 to 10 mg (total 700 mg). Within one year after the withdrawal of prednisolone, 19 (70%) lost HBeAg and 11 of them (41% of the total) developed anti-HBe, at rates significantly higher than 3 (12%) and 1 (4%) who spontaneously showed respective serological changes among 26 matched controls during one year (p less than 0.001). Within two years after the withdrawal, 21 (78%) lost HBeAg and 19 (70%) developed anti-HBe, in contrast to 6 (23%) and 2 (8%) of controls who showed respective changes during that period (p less than 0.001). Seroconversion to anti-HBe was invariably accompanied by clinical and biochemical improvements along with loss of DNA polymerase from circulation. Elevation in transaminase levels, reflecting the rebound of steroid withdrawal, always heralded and appeared to be required for the seroconversion, but serious aggravation of hepatitis was not encountered in any of the patients.

Adult↗

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.

Carcinoma, Hepatocellular↗