[Hepatocyte receptors for polymerized albumin. Experimental study on isolated hepatocytes and in vivo animals]. / Recettori epatocitari per albumina polimerica. Studio sperimentale su epatociti isolati ed animali in vivo.

In the present work receptors for polymerized rat serum albumin (P-RSA) were studied by incubation of radiolabelled polymers with rat hepatocytes isolated with mechanical techniques. Isolated rat hepatocytes showed a receptor activity for polymerized albumin and such a membrane receptor seems to be controlled by the cellular cytoskeleton. During rat total body scintigraphy receptor expression was detected exclusively in the liver. These observations support the hypothesis of a selective receptor activity of the liver cells for polymerized albumin. To confirm our results, further studies were performed on rat bile, after 125I-P-RSA infusion in vivo.

Cryptogenic chronic liver disease and serum or liver hepatitis B virus markers. Their possible correlations and etiologic significance.

In an attempt to evaluate a possible correlation between cryptogenic chronic liver disease and a present or past hepatitis B virus (HBV) infection, we studied 17 patients with hepatitis B surface antigen (HBsAg)-negative, nonalcoholic chronic liver disease; 9 of them were positive for serum HBsAg detected by a solid-phase enzyme immunoassay with monoclonal antibody (M-EIA) and 8 were negative for the same marker. Liver hepatitis B core antigen (HBcAg), studied by an indirect immunofluorescence technique, was present in 55.5% of the patients positive for serum HBsAg by M-EIA. In the same group of patients, liver HBV-DNA was found in 66.6% of the patients. On the other hand, only 1 patient without serum positivity for HBsAg by M-EIA was positive for liver HBcAg and HBV-DNA. None of our patients showed serum positivity for HBV-DNA sequences. We conclude that HBV infection may be a possible cause of cryptogenic chronic liver disease; this HBV-related, HBsAg-negative chronic liver disease seems to have no viral replication or undetectable levels of HBV-DNA in serum. HBsAg, detected by a monoclonal assay, seems to be a suitable marker to identify this subgroup of patients with HBsAg-negative chronic liver disease.

HBV-DNA sequences are rarely detected in the liver of patients with HBsAg-negative chronic active liver disease and with hepatocellular carcinoma in Italy.

Hepatitis B virus sequences were studied by molecular hybridization in liver biopsies from patients with HBsAg-negative chronic liver disease or hepatocellular carcinoma, collected in Italy. Among the 42 patients with chronic liver disease who had no history of drug addiction, alcohol abuse nor evidence of metabolic and autoimmune disorders, only two (5%) had HBV-DNA sequences in the liver, although 23 of them (57%) were positive for antibodies to HBV in serum. HBV-DNA was also demonstrated in integrated form in the tumorous tissue of one out of eight cases with HBsAg-negative hepatocellular carcinoma. These incidences of HBV-DNA positivity in the liver are lower than those reported from other Mediterranean areas and similar to those of North Europe, United States and Japan, suggesting that etiologic factors other than HBV are responsible for the majority of HBsAg-negative chronic liver diseases in our region.

Influence of hepatitis delta virus infection on progression to cirrhosis in chronic hepatitis type B.

Serological markers of hepatitis delta virus (HDV) infection were found in 18 (12%) of 146 consecutive patients with chronic hepatitis B, and the characteristics of patients who had antibody to HDV (anti-HDV-positive) were analyzed. During one to 15 years of follow-up, histological deterioration was documented in 77% of anti-HDV-positive patients; however, in hepatitis B surface antigen (HBsAg) carriers without HDV infection, histology deteriorated in 30% but improved or remained unchanged in the majority of patients (P less than .01). In seven (70%) of the 10 anti-HDV-positive patients who showed transition from chronic active hepatitis to cirrhosis, this event was observed within the first two years of follow-up. The probability of evolution to cirrhosis was significantly higher in anti-HDV-positive patients than in patients without antibody to HDV (P less than .001). These findings indicate that HDV infection in patients with chronic hepatitis B is associated with a more-rapid progression to cirrhosis compared with HBsAg carriers with chronic hepatitis and no evidence of HDV infection.

Detection of hepatitis B virus DNA sequences in bone marrow of children with leukemia.

To investigate the possibility that hemopoietic cells may become infected with hepatitis B virus (HBV), viral DNA was studied by molecular hybridization in bone marrow aspirates of 51 children with leukemia. HBV-DNA was found in the bone marrow of eight children (15%) and Southern blot analysis revealed the presence of free, monomeric viral sequences. Only one of the eight children with HBV-DNA in bone marrow cells was HBsAg-positive in serum, whereas two additional patients were transiently HBsAg-positive in serum during follow-up, but were negative at the time HBV-DNA was found in bone marrow. Four other cases developed antibodies to HBV. Cases of myeloid leukemia were more frequently positive for HBV-DNA in bone marrow (55%), compared with cases of lymphoid leukemia (7%). These results indicate that hemopoietic cells are susceptible to infection with hepatitis B virus and stimulate new interest into the relation of HBV infection to the development of some forms of leukemia, as four of eight cases of myeloid leukemia were HBV-DNA positive in bone marrow aspirates at diagnosis, prior to receiving any transfusion therapy.