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.
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