Study objectives: The aim of this study was to determine the role of c
omplement components in pleural effusion measured with novel markers o
f complement activation, to assess which pathway of activation is pred
ominant in different diseases, and to find out whether the analysis df
complement components and their activation products could help in dia
gnostic procedure differentiating the etiologies of pleural effusion.
Patients: The study population consisted of 71 patients who had pleura
l effusion secondary to tuberculosis (n=23), rheumatic disease (n=10),
or malignancy (n=38). Measurements: Complement components and their a
ctivation products, including the soluble terminal complex SC5b-9, wer
e measured in plasma and pleural fluid.Results: In all patients with r
heumatic pleurisy, pleural fluid SC5b-9 was higher than 2 AU/mL and in
all patients with malignant pleural fluid it was lower than 2 AU/mL.
The mean level of SC5b-9 in rheumatic pleural effusion was also signif
icantly higher than in tuberculosis. In addition, the concentrations o
f pleural fluid C3 and C4 were significantly lower and the ratio C4d/C
4 was significantly higher in rheumatic compared with tuberculous or m
alignant pleurisy. In plasma, both SC5b-9 and Cls-Clr-C lINH-complexes
were significantly higher in rheumatic subjects than in other patient
s. In stepwise multinominal logistic regression analyses, the most sig
nificant predictors for rheumatic pleural fluid were high pleural flui
d SC5b-9 and low C4. Conclusions: These observations indicate that the
complement cascade is activated through both the classic and the alte
rnative pathways in rheumatic pleurisy. Determinations of SC5b-9 and C
4d/C4 in pleural fluid were the best variables differentiating rheumat
ic, tuberculous, and malignant effusions.