COMPARISON BETWEEN ASSAYS FOR COMPLEMENT FRAGMENTS AND TOTAL HEMOLYTIC COMPLEMENT IN THE ROUTINE ASSESSMENT OF COMPLEMENT ACTIVATION

Citation
B. Goldberg et al., COMPARISON BETWEEN ASSAYS FOR COMPLEMENT FRAGMENTS AND TOTAL HEMOLYTIC COMPLEMENT IN THE ROUTINE ASSESSMENT OF COMPLEMENT ACTIVATION, Journal of clinical ligand assay, 20(2), 1997, pp. 212-215
Citations number
16
Categorie Soggetti
Immunology
ISSN journal
10811672
Volume
20
Issue
2
Year of publication
1997
Pages
212 - 215
Database
ISI
SICI code
1081-1672(1997)20:2<212:CBAFCF>2.0.ZU;2-D
Abstract
Several studies have suggested that assays for complement activation f ragments may more accurately predict clinical activity in a variety of diseases (such as systemic lupus erythematosus) than standard assays for complement activation, including total hemolytic complement (CH50) (1-7). In this study, we compared assays for iC3b, C4d, and Bb with CH 50, C3, and C4 in a group of 41 patients referred for evaluation of co mplement activity by CH50 and in 41 age and sex-matched normal blood d onors. Complement activation fragments were determined by enzyme-linke d immunosorbent assay (ELISA). CH50 was determined by a single dilutio n hemolytic method and C3 and C4 were determined by radial immunodiffu sion. The mean level of iC3b was 24.1 mu g/mL for the patient populati on and 8.0 mu g/mL for the control population (P<0.001). No difference in the mean levels for C4d, Bb, CH50, C3, or C4 was observed between the patient and control groups. Of the 41 subjects, 32 had elevated iC 3b. Nine individuals demonstrated one or more abnormalities of CH50, C 3, and C4. Only four of these nine subjects had elevated iC3b. Our res ults demonstrate that iC3b is frequently elevated in a variety of infl ammatory disorders when compared with standard methods for determinati on of complement activation such as CH50, C3, and C4. The absence of a similar elevation of C4d and Bb between patients and controls, as wel l as a lack of correlation between abnormal results for standard compl ement assays, suggest that iC3b elevation in our patient group may hav e been due to decreased iC3b clearance, increased C3 synthesis, or enh anced C3 cleavage by non-immune mechanisms.