We investigated the expression of transforming growth factor-alpha (TGF-alpha) and its receptor during human liver development and maturation, using immunohistochemistry. In the fetal liver, strong immunoreactivity for TGF-alpha and its receptor was noted in intrahepatic bile duct cells of various developmental stages; moderate immunoreactivity for TGF-alpha and mild immunoreactivity for TGF-alpha receptor were found in immature hepatocytes. In the postnatal liver, reactivity for TGF-alpha in hepatocytes decreased gradually and was negative or only weakly positive in the adult liver, while reactivity for TGF-alpha receptor in hepatocytes increased gradually and was strongly positive in the adult liver. In contrast, immunoreactivity of TGF-alpha and its receptor in intrahepatic bile duct cells persisted in the postnatal liver and was positive in the adult liver. These data suggest that the system of TGF-alpha and its receptor has an important role in the proliferation and differentiation of intrahepatic biliary cells and hepatocytes in the fetal liver. The decreasing expression of TGF-alpha in hepatocytes in the postnatal liver may indicate that proliferative activity of hepatocytes gradually decreases with liver maturation. The presence of TGF-alpha and its receptor in intrahepatic bile ducts in the postnatal liver suggests that the system of TGF-alpha and TGF-alpha receptor is operative postnatally.
A multi-center double-blind controlled trial of ursodeoxycholic acid (UDCA) for treatment of primary biliary cirrhosis (PBC) was carried out. Twenty two and 23 patients were treated with 600 mg/day UDCA and placebo, respectively, for 24 weeks. In UDCA-treated patients, fall of serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and gamma-glutamyltranspeptidase activities started within 4 weeks after start of the trial and continued throughout the trial period. The serum IgM level fell in 7 UDCA-treated patients examined but not in 10 placebo-treated patients examined. Serum bilirubin concentration showed no significant change at the end of the study in either of UDCA- and placebo-treated group of patients. There was no significant difference between these two groups with respect to the frequency of improvement of pruritus. In UDCA-treated patients, serum bile acid composition changed markedly, though its concentration showed no significant change. The percentage of total bile acid which ursodeoxycholic acid took up increased, whereas those which cholic acid, chenodeoxycholic acid and deoxycholic acid took up were decreased.
Lipomatous pseudohypertrophy of the pancreas was found at autopsy in a 52-year-old Japanese woman with cirrhosis due to chronic hepatitis B. Clinically, there were no clear symptoms of pancreatic insufficiency during the entire course. Marked atrophy and fat deposition of the pancreas had already been detected by computed tomography (CT) at least 6 years before her death. She died of hepatic failure due to decompensated cirrhosis. Autopsy revealed uniform enlargement of the pancreas due to massive fat replacement (lipomatous pseudohypertrophy): the exocrine glandular elements showed marked atrophy and loss, while the islets of Langerhans were preserved. Although the etiology and pathogenesis of lipomatous pseudohypertrophy is still unclear, this case suggests that this condition is causally related to chronic hepatitis B or other chronic advanced hepatic lesions.
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