Complement metabolism in chronic liver disease: catabolism of C1q in chronic active liver disease and primary biliary cirrhosis.
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.
D000328:Adult; D002908:Chronic Disease; D003172:Complement C1 / Q000378:metabolism* / Q000494:pharmacology; D003165:Complement System Proteins / Q000378:metabolism*; D005260:Female; D006509:Hepatitis B / Q000276:immunology / Q000378:metabolism; D006514:Hepatitis B Surface Antigens; D006801:Humans; D008105:Liver Cirrhosis, Biliary / Q000276:immunology / Q000378:metabolism*; D008107:Liver Diseases / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D012709:Serum Albumin / Q000378:metabolism / Q000494:pharmacology
D003172:Complement C1; D006514:Hepatitis B Surface Antigens; D012709:Serum Albumin; D003165:Complement System Proteins