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Complement components and their activation products in pleural fluid
E R Salomaa1, M Viander, T Saaresranta
1Department of Pulmonary Diseases and Clinical Allergology, Turku University Hospital, Finland. eirisa@utu.fi
Insights
Complement activation markers, specifically soluble C5b-9, can differentiate rheumatic pleural effusion from malignant or tuberculous causes. Analysis of complement components aids in diagnosing pleural effusion etiologies.
Area of Science:
- Immunology
- Pulmonology
- Biochemistry
Background:
- Pleural effusion diagnosis can be challenging.
- Complement system activation plays a role in inflammatory processes.
- Novel markers of complement activation may improve diagnostic accuracy.
Purpose of the Study:
- To investigate the role of complement components in pleural effusion.
- To identify predominant complement activation pathways in different pleural effusion etiologies.
- To assess the utility of complement markers in differentiating pleural effusion causes.
Main Methods:
- Analyzed complement components and activation products (SC5b-9) in plasma and pleural fluid.
- Studied 71 patients with pleural effusion due to tuberculosis, rheumatic disease, or malignancy.
- Utilized stepwise multinomial logistic regression for predictor analysis.
Main Results:
- Pleural fluid SC5b-9 levels distinguished rheumatic from malignant effusions.
- Rheumatic effusions showed higher SC5b-9 and C1s-C1r-C1INH-complexes, with lower C3/C4 and higher C4d/C4 ratio.
- High pleural fluid SC5b-9 and low C4 were key predictors for rheumatic pleural fluid.
Conclusions:
- Complement cascade is activated via both classic and alternative pathways in rheumatic pleurisy.
- SC5b-9 and C4d/C4 ratio effectively differentiate rheumatic, tuberculous, and malignant effusions.
- Complement analysis offers a valuable tool for diagnosing pleural effusion.
Study Objectives:
The aim of this study was to determine the role of complement components in pleural effusion measured with novel markers of complement activation, to assess which pathway of activation is predominant in different diseases, and to find out whether the analysis of complement components and their activation products could help in diagnostic procedure differentiating the etiologies of pleural effusion.
Patients:
The study population consisted of 71 patients who had pleural effusion secondary to tuberculosis (n=23), rheumatic disease (n=10), or malignancy (n=38).
Measurements:
Complement components and their activation products, including the soluble terminal complex SC5b-9, were measured in plasma and pleural fluid.
Results:
In all patients with rheumatic 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 significantly higher than in tuberculosis. In addition, the concentrations of pleural fluid C3 and C4 were significantly lower and the ratio C4d/C4 was significantly higher in rheumatic compared with tuberculous or malignant pleurisy. In plasma, both SC5b-9 and C1s-C1r-C1INH-complexes were significantly higher in rheumatic subjects than in other patients. In stepwise multinominal logistic regression analyses, the most significant predictors for rheumatic pleural fluid were high pleural fluid SC5b-9 and low C4.
Conclusions:
These observations indicate that the complement cascade is activated through both the classic and the alternative pathways in rheumatic pleurisy. Determinations of SC5b-9 and C4d/C4 in pleural fluid were the best variables differentiating rheumatic, tuberculous, and malignant effusions.