“…One obvious disadvantage of measuring the static profile of the complement components is that an increased rate of synthesis can mask hypercatabolism. Moreover, normal variation of the components, especially C3, is multifactorial [19], The normal levels of Clq, C3, C4, factor B and Ba have been established in this laboratory, and these data were compared with those in the lepromatous patients without or with ENL [4,15,18], More recently, direct quantitation of the breakdown products of C3 and properdin factor B have facilitated a dynamic estimation of the involvement of the complement system [2,5,9,12,13,19], Perrin et al [12,13] demonstrated elevated serum levels of C3d and Ba fragments in patients with systemic lupus erythematosus and membranoproliferative glomerulonephritis, Fn contrast, the serum levels of factor B and complemetit component C3 were near normal, suggesting the coexistence of increased synthesis of C3 and factor B and their hypercatabolism. Similar observations were made by Hunder et al during the study of complement cativation in synovial fluids [9].…”