Increased amount of serum type IV collagen peptide in human liver fibrosis as determined by enzyme-immunoassay with monoclonal antibodies.

Chronic liver injury by various toxic agents causes an increase in collagen biosynthetic activity, resulting in deposition of excessive amounts of collagen and rearrangement of the lobular architecture leading to hepatocellular dysfunction and portal hypertension. The authors have developed sandwich enzyme-immunoassay for human serum type IV collagen peptide using monoclonal antibody as a marker of fibrogenesis and examined the relationship between the amount of this collagen peptide and hepatic disorders including chronic active hepatitis and liver cirrhosis. Sera from patients with chronic active hepatitis or liver cirrhosis were used after confirmation of the histopathological diagnosis. Control sera were obtained from healthy subjects without any serological abnormality in liver function tests. Serum type IV collagen peptide levels were significantly higher in patients with chronic hepatic disorders associated with fibrosis than in healthy subjects. This non-invasive enzyme-immunoassay gave reproducible quantitation, and serum type IV collagen peptide was concluded to be a useful, and reproducible marker for the early detection of fibrogenesis in the liver.