Potter B J, Elias E, Thomas H C, Sherlock S
Gastroenterology. 1980 May;78(5 Pt 1):1034-40.
The fractional catabolic rate of C1q was increased markedly in primary biliary cirrhosis, and in HBsAg-positive chronic liver disease. In 3 out of 4 patients with HBSAg-negative chronic active liver disease C1q catabolism was normal. The rate of synthesis of the protein was increased in primary biliary cirrhosis, but it was normal in patients with chronic active liver disease. The fractional catabolic rate and synthetic rate of albumin were normal in these subjects. These data provide further evidence for the activation of the classical pathway of complement in primary biliary cirrhosis and HBsAg-positive chronic active liver disease. In HBsAg-negative chronic active liver disease, the presence of C1q binding macromolecules was not associated with increased C1q catabolism.
在原发性胆汁性肝硬化和乙肝表面抗原(HBsAg)阳性的慢性肝病中,C1q的分解代谢率显著升高。在4例HBsAg阴性的慢性活动性肝病患者中,有3例C1q分解代谢正常。原发性胆汁性肝硬化患者中该蛋白的合成率升高,但慢性活动性肝病患者中合成率正常。这些受试者中白蛋白的分解代谢率和合成率均正常。这些数据为原发性胆汁性肝硬化和HBsAg阳性的慢性活动性肝病中补体经典途径的激活提供了进一步证据。在HBsAg阴性的慢性活动性肝病中,C1q结合大分子的存在与C1q分解代谢增加无关。