In children, pleural empyema is a recognized complication of severe pneumonia and is characterized by loculated effusions with fibrin septations. The aim of this study was to evaluate the relationship between proinflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6], intrapleural fibrinolytic system enzymes [tissue-type plasminogen activator (tPA) and plasminogen activator inhibitor type 1 (PAI-1)], and common biochemical indices during pleural infection.
Children with pneumonia complicated by para-pneumonic effusions were enrolled into our study and underwent real-time chest sonography. The patients were divided into 3 groups by ultrasound using a recognized staging system of pleural effusions. Staging of progressive pleural infection was used to correlate with the characteristics of pleural effusions. The correlation of various pleural variables with the formation of complicated para-pneumonic effusions (CPE) was performed and pleural variables for predicting subsequent intervention procedures were also analyzed.
A total of 57 patients were enrolled in the present study. Univariate analysis revealed that the amounts of biochemical indices (pH, glucose, lactate dehydrogenase), proinflammatory cytokines (TNF-α, IL-1β, IL-6), and fibrinolytic system enzymes (tPA, PAI-1) were significantly different with the progressive stages of para-pneumonic effusions (P trend < 0.05). For all proinflammatory cytokines, a positive correlation was found with lactate dehydrogenase and PAI-1, whereas a negative correlation was found with pH, glucose, and tPA. Moreover, these cytokines were also significantly correlated with PAI-1 in both non-CPE and CPE. The pleural fluid findings of IL-1β (≥50 pg/mL), PAI-1 (≥1252 ng/mL), and pH (≤7.30) were the most significant predictive factors for subsequent intervention procedures (P < 0.001).
The increased release of proinflammatory cytokines in pleural fluid caused by bacteria may result in an imbalance of the fibrinolytic system, which can subsequently lead to fibrin deposition and intervention procedures.
From the *Graduate Institute of Clinical Medical Sciences, Chang Gung University; the Departments of †Pulmonology, ‡Allergy, Asthma and Rheumatology, and §Infectious Diseases, Chang Gung Children's Hospital; and the ∥Department of Clinical Proteomics Center, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan.
Accepted for publication February 26, 2008.
Address for correspondence: Kin-Sun Wong, MD, or Jing-Long Huang, MD, Department of Pediatrics, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, 5, Fu-Hsin Street, Kueishan, Taoyuan, Taiwan. E-mail: firstname.lastname@example.org or email@example.com.