The in vivo metabolism of C3 in hepatobiliary disease associated with ulcerative colitis.
To study possible pathogenetic mechanisms in hepatobiliary disease associated with ulcerative colitis (UC), we performed a metabolic investigation of component C3 of the most important effector of humoral immunity, the complement system. Purified and biologically active C3 was labelled with 125I and injected together with 131I-albumin into seven patients. All had hepatobiliary disease, and total colectomy had previously been performed for severe UC in all patients. The results were compared with those for 16 normal individuals. The fractional catabolic rates (FCR) were calculated by the metabolic clearance method and by analysis of the plasma radioactivity disappearance curve. An increase in the FCR of C3 was found in the patient group, indicating that humoral immune mechanisms may be of pathogenetic importance in hepatobiliary disease associated with UC. The increased FCR was compensated for by and increased synthesis rate of the protein.
D000328:Adult; D001660:Biliary Tract Diseases / Q000150:complications / Q000175:diagnosis / Q000276:immunology*; D002761:Cholangitis / Q000150:complications / Q000175:diagnosis / Q000276:immunology; D003093:Colitis, Ulcerative / Q000150:complications*; D003176:Complement C3 / Q000378:metabolism*; D005260:Female; D006801:Humans; D008107:Liver Diseases / Q000150:complications / Q000175:diagnosis / Q000276:immunology*; D008297:Male; D012598:Sclerosis; D012711:Serum Albumin, Radio-Iodinated / Q000378:metabolism
D003176:Complement C3; D012711:Serum Albumin, Radio-Iodinated