• 1 January 1978
    • journal article
    • research article
    • Vol. 92 (3), 671-679
Abstract
Many reports demonstrated an elevation of circulating carcinoembryonic antigen (CEA) in patients with alcoholic liver disease and, less frequently, in patients with nonalcoholic liver disease. Several explanations for this finding were proposed, e.g., increased production or release of CEA by the damaged liver, decreased hepatic metabolism or diminished excretion of CEA of extrahepatic origin. To clarify the mechanism of CEA elevation in liver disease, the CEA plasma level as measured by radioimmunoassay was compared with CEA demonstrable in liver tissue by the indirect fluorescent antibody technique in 7 patients without significant changes in the liver biopsy specimen, 23 patients with alcoholic liver disease and 16 patients with miscellaneous liver diseases such as acute or chronic nonalcoholic hepatitis or extrahepatic biliary obstruction. The mean CEA plasma level in patients with alcoholic liver disease was significantly higher than in patients with nonalcoholic liver disease (8.8 .+-. 9.5 vs. 2.7 .+-. 2.5 ng/ml; P < 0.02). In normal liver tissue, CEA was observed in the apical cytoplasm and along the luminal surface of bile duct epithelial cells, suggesting that under normal conditions CEA accumulates in and is excreted by bile ducts. In patients with alcoholic hepatitis and/or cirrhosis there was marked bile ductular proliferation and prominent cytoplasmic CEA-specific staining and both were associated with elevated CEA plasma levels in more than 80% of cases. In the group of miscellaneous liver diseases, bile ductule counts and CEA-specific staining did not correlate with CEA plasma levels. Proliferating bile ductules may contribute to elevated plasma CEA in alcoholic patients.