Metabolism of the third component of complement in acute type B hepatitis, HBs antigen positive glomerulonephritis, polyarteritis nodosum, and HBs antigen positive and negative chronic active liver disease
Thomas, H.C.; Potter, B.J.; Elias, E.; Sherlock, S.
Gastroenterology 76(4): 673-679
1979
ISSN/ISBN: 0016-5085 PMID: 33867 Document Number: 142167
The contribution of complement [C] consuming immune mechanisms to the various syndromes which follow HBV [hepatitis B virus] infection was studied by measuring the catabolism of radioiodinated, purified, hemolytically active C3. Albumin catabolism was studied in parallel to determine whether changes in C3 catabolism are specific and consistent with C activation, or merely a result of a generalized state of hypercatabolism of all plasma proteins. Two patients studied during the 1st wk of acute type B hepatitis showed increased fractional catabolic rates (FCR) of C3 and albumin; the ratio of the FCR C3/FCR albumin was normal. Six patients with HBsAg [HBV surface antigen]-positive chronic active liver disease (CALD) showed increased FCR of C3 but normal FCR albumin; the ratio of FCR C3/albumin was significantly increased. Six patients with HBsAg-negative CALD showed normal FCR of C3. Three patients with chronic persistent hepatitis (CPH) 1 with membranous glomerulonephritis and 1 with polyarteritis nodosum, showed increased catabolism of C3 but normal albumin catabolism. The ratio of FCR C3/FCR of albumin was greater than in patients with HBsAg-positive CALD. C3 catabolism is specifically increased in HBsAg-positive CPH and CALD but is normal in HBsAg-negative CALD. C-fixing immune mechanism are probably recruited in the HBV-related chronic disease states. In early acute type B hepatitis and in HBs-negative CALD there is no evidence of increased immune catabolism of C3.