Hypercatabolism of complement in Crohn's disease--assessment of circulating C3c

Split products from the main complement component 3 (C3) were investigated in untreated outpatients, 20 with Crohn's disease and 20 with ulcerative colitis. The median plasma concentration of c split product of C3 (C3c) in normals was 2 mg X 1(-1), in patients with Crohn's disease 20 mg X 1(-1) and in patients with ulcerative colitis 3 mg X 1(-1). This tenfold increase in C3c was significant at the 0.005-level. Plasma C3c exceeded the reference interval in two patients with ulcerative colitis. C3c levels did not correlate to the activity of the disease or to the occurrence of the C3 phenotypes S, FS and F. Substantially elevated plasma C3c in Crohn's disease suggests hypercatabolism of C3, that is, involvement of complement reactions. Further studies are needed to reveal the site of cascade activation and to define the role of complement for the pathogenesis of the disease.