Changes of serum 7S fragment of type IV collagen and N-terminal propeptide of type III procollagen after transcatheter arterial embolization as a model of acute liver injury

✍ Scribed by Dr. Takeaki Suou; Sadako Yamada; Junko Kobayashi; Ushio Hoshino; Eiji Nishimuki; Hironaka Kawasaki

• Publisher: John Wiley and Sons
• Year: 1993
• Tongue: English
• Weight: 658 KB
• Volume: 18
• Category: Article
• ISSN: 0270-9139
• DOI: 10.1002/hep.1840180410

✦ Synopsis

To evaluate the mechanism of increased serum concentrations of theN-terminal propeptide of type I11 procollagen and the 75 fragment of type IV collagen in acute liver injury, we serially measured serum levels of these substances after transcatheter arterial embolization in patients with hepatocellular carcinoma. The results demonstrated marked increases in serum levels of the 75 fragment of type IV collagen in accordance with increased serum levels of transaminase after transcatheter arterial embolization. In contrast, a transient decrease in serum levels of the N-terminal propeptide of type I11 procollagen was found after transcatheter arterial embolization and transcatheter arterial infusion, although no significant changes in serum levels of the N-terminal propeptide and 75 fragment were seen after hepatic arteriography alone. The absolute change in serum levels of the 75 fragment after treatment showed positive correlation with serum transaminase levels and negative correlation with the decrease in serum levels of a-fetoprotein, although serum levels of N-termind peptide did not demonstrate such a correlation. The results suggest that in acute liver injury induced by transcatheter arterial embolization, at least in part, increased in serum levels of the 7s fragment of type IV collagen reflect accelerated liberation of type IV collagen from the destroyed surrounding nontumorous tissues and that decreased serum N-terminal propeptide of type I11 procollagen reflects diminished synthesis of type I11 collagen caused by anticancer drugs. (HEPATOLOGY 1993;18:809-815.) Biochemical and immunohistochemical studies have demonstrated increased extracellular deposition of interstitial and basement membrane collagens in the course of liver fibrosis (1-4) as a result of accelerated synthesis or degradation of collagen (5,61. The increased metabolism in hepatic collagens can cause increased