Suou T, Yamada S, Hosho K, Yoshikawa N, Kawasaki H
Second Department of Internal Medicine, Tottori University Faculty of Medicine, Yonago, Japan.
Hepatology. 1996 May;23(5):1154-8. doi: 10.1053/jhep.1996.v23.pm0008621148.
We evaluated the mechanism of increased serum concentrations of the 7S fragment of the N-terminal domain of type IV collagen (7S collagen) in chronic liver disease. We measured the concentrations of hepatic-free and deposited 7S collagens after extraction with Tris-HCl buffer and bacterial collagenase, then compared them with the serum levels in 8 normal controls and 48 patients with chronic liver disease. The hepatic 7S collagen levels extracted with Tris-HCl buffer and collagenase accounted for 7% and 93%, respectively, of the total 7S collagen levels in normal controls. Both hepatic 7S collagen levels as well as serum levels increased in accordance with the progress of liver disease. Serum levels of 7S collagen showed a closer correlation with the hepatic 7S collagen levels extracted with Tris-HCl buffer (r = .822), compared with those extracted with collagenase (r = .382). On the other hand, the histological degrees of liver fibrosis were highly correlated with the hepatic collagenase-extracted 7S collagen levels (r = .822), compared with serum and the hepatic Tris-HCl buffer-extracted levels (r = .478 and r = .537, respectively). Although there was no difference in serum and hepatic 7S collagen levels between B and C viral patients, the serum and hepatic Tris-HCl buffer-extracted 7S collagen levels were higher in patients with alcoholic cirrhosis than patients with viral cirrhosis. However, the hepatic collagenase-extracted levels were similar in both groups. Gel filtration demonstrated that the serum and hepatic Tris-HCl buffer-extracted 7S collagens were mainly eluted in the macromolecular 7S collagen-reactive fraction in cirrhosis, whereas the hepatic collagenase-extracted 7S collagen was eluted in the authentic 7S collagen-reactive fraction. The results suggest that serum 7S collagen levels are not a particularly reliable measure of hepatic fibrosis but reflect the enhanced metabolism, especially synthesis of type IV collagen in the liver.
我们评估了慢性肝病患者血清中IV型胶原N端结构域7S片段（7S胶原）浓度升高的机制。在用Tris-HCl缓冲液和细菌胶原酶提取后，我们测量了肝内游离和沉积的7S胶原浓度，然后将其与8名正常对照者和48例慢性肝病患者的血清水平进行比较。在正常对照者中，用Tris-HCl缓冲液和胶原酶提取的肝7S胶原水平分别占总7S胶原水平的7%和93%。肝7S胶原水平和血清水平均随肝病进展而升高。与用胶原酶提取的肝7S胶原水平（r = 0.382）相比，血清7S胶原水平与用Tris-HCl缓冲液提取的肝7S胶原水平相关性更强（r = 0.822）。另一方面，与血清及用Tris-HCl缓冲液提取的肝7S胶原水平（分别为r = 0.478和r = 0.537）相比，肝纤维化的组织学程度与用胶原酶提取的肝7S胶原水平高度相关（r = 0.822）。虽然B型和C型病毒性肝炎患者的血清和肝7S胶原水平无差异，但酒精性肝硬化患者血清及用Tris-HCl缓冲液提取的肝7S胶原水平高于病毒性肝硬化患者。然而，两组患者用胶原酶提取的肝7S胶原水平相似。凝胶过滤显示，血清及用Tris-HCl缓冲液提取的肝7S胶原在肝硬化患者中主要在大分子7S胶原反应性组分中洗脱，而用胶原酶提取的肝7S胶原在真正的7S胶原反应性组分中洗脱。结果表明，血清7S胶原水平并非肝纤维化的特别可靠指标，但反映了肝脏中IV型胶原代谢增强，尤其是合成增加。
