Toru Shinohara

A case report of primary hepatic carcinoma with prolonged HV virus infection and monoclonal gammopathy

SummaryA case of alpha-feto protein (AFP) positive hepatic cell carcinoma has been presented in which the appearance of a mono-clonal gammopathy can be explained by persistent infection with HB virus (HBV). The patient, a fifty year old male, developed acute jaundice with hepatitis in July, 1952, and died of an hepatic cell carcinoma in December, 1973. The interest of this case lies in the fact that during the seven months prior to be patient’s demise, a mono-clonal gammopathy of IgG (L type), together with positive titeres for HBs Ag (adr) and AFP, was demonstrated.

Detection of liver igg fc receptors using soluble immune complexes of peroxidaseantiperoxidase I. detection in liver tissue from patients with liver diseases

SummaryThe presence of liver IgG Fc receptor sites was demonstrated in the liver tissue from 23 patients with liver diseases and 2 patients without liver lesions by the localization of soluble immune complexes of peroxidaseantiperoxidase (PAP). Cryostat sections of liver tissues were incubated with the complexes and the peroxidase activity was revealed histochemically. In the normal liver tissue, PAP were localized on the liver cell membrane, the Kupffer cells, and some of the sinusoidal walls. In acute hepatitis, a strongly positive reaction on swollen Kupfifer cells was remarkable but positive reaction on the liver cell membrane was very weak. In chronic aggressive hepatitis, PAP were strongly positive on multiplied Kupffer cells and many PAP-positive infiltrated cells were observed at the area of piecemeal necrosis. However, the positive reaction on the liver cell membrane in patients with chronic aggressive hepatitis was generally fainter than in the normal cases without liver diseases. These results correlated well with the severity of liver cell necrosis. In chronic persistent hepatitis, the number of PAP-positive infiltrated cells in the portal area and positive Kupffer cells were fewer than in chronic aggressive hepatitis. Similar results were obtained with liver cirrhosis, and in particular, the liver cell membrane with regenerative nodules gave a positive reaction. A negative result was obtained by incubation with PAP-F(ab’)2 alone. PAP reaction was significantly inhibited by pretreatment with aggregated human IgG, trypsin, and pronase but not with neuraminidase.

Detection of liver IgG Fc receptors using soluble immune complexes of peroxidase-antiperoxidase II. detection in liver tissue from mice with D-Galactosamine-induced hepatitis

SummaryThe presence of liver IgG Fc receptor sites was demonstrated in the liver tissue from C-57 black mice with D-Galactosamine (GalN)-induced hepatitis by the localization of soluble immune complexes of peroxidaseantiperoxidase (PAP). Cryostat sections of liver tissues were inbubated with the complexes and the peroxidase activity was revealed histochemically. In the normal liver tissue, PAP were localized on the Kupffer cells, some of the sinusoidal walls, and the liver cell membrane mainly at the side of the sinusoid. Twenty-four hours after single administration of GalN (l,500mg/kg body weight), positive PAP reaction was mainly observed on the membrane surface of infiltrating cells in the area of hepatocellular focal necrosis, and faintly observed on the degenerative hepatic cell membrane and the sinusoidal walls. After 48 hours, these features became more remarkable, especially at the sites with severe necrotic lesions. After 72 hours, the positive reaction on the regenerative hepatic cell membranes again became distinct. At the chronic stage 13 weeks after repeated administrations of GalN and Freund’s complete adjuvant, a strong positive reaction was found on swollen and multiplied Kupffer cells, and a faint one found on the liver cell membrane, especially at the periphery of the lobules; moreover, many PAP-positive infiltrated cells were found in the area of piecemeal necrosis. The relationship between liver IgG Fc receptors and the severity of liver cell necrosis is discussed.

Pathological study of chronic d-galactosamine induced hepatitis in mice by administration of adjuvants An animal model of the chronic active hepatitis

SummaryAn animal model for human chronic active hepatitis was created in inbred C-57 Black mice using prolonged (13 weeks) administration of D-Galactosamine (GalN) and adjuvants. Intraperitoneal injections of GalN (l,500 mg/kg) were repeated once a week. Simultaneously, Freund’s complete adjuvant (FCA) was given subcutaneously to limbs. These mice showed a progressive inflammatory response; piecemeal necrosis of the portal area with marked cellular infiltration developed by the 13th week. The figure of severe liver cell degeneration and necrosis as well as lobular distortion and increased fibrous tissue closely resembled those in human chronic active hepatitis. Only a mild inflammatory response occurred in the groups given GalN alone or GalN with Freund’s incomplete adjuvant. All mice given GalN with BCG developed massive hepatic necrosis and died by the 4th week. Indirect immunofluorescent antibody detection technique showed little correlation between the disease activity and the presence of anti-liver cell membrane antibody in any of the group at the 13th week. The importance of the host immune reaction was indicated in the development of chronic hepatitis.