Levels of YKL-40 in pleural effusions and blood from patients with pulmonary or pleural disease.

BACKGROUND: YKL-40 (a chitinase-like protein) is an inflammatory biomarker that is associated with lung injury pathogenesis. We aimed to identify the diagnostic values of YKL-40 in pleural effusions and to evaluate circulating YKL-40 levels during multiple etiological pulmonary/pleural diseases and the role of YKL-40 as a monitoring marker of inflammatory pulmonary disease. METHODS: Pleural YKL-40 (n=197), YKL-39 (the most homologous chitinase-like protein to human YKL-40), and conventional pleural marker levels were measured in patients with pulmonary/pleural disease. Additionally, serum YKL-40 and YKL-39 levels were analyzed in both patients and controls (n=432) and serially monitored in patients with asthma (n=27) or pneumonia (n=22). RESULTS: Pleural YKL-40 levels were higher than those in the serum and highest in tuberculous pleural effusions (TPEs; 1181 ng/mL), followed by parapneumonic, malignant, and cardiogenic effusions (560 ng/mL). The diagnostic accuracy of pleural YKL-40 (0.78) for discriminating between tuberculous and malignant effusion was comparable to or greater than those of YKL-39, total protein, C-reactive protein and CYFRA 21-1, and lower than those of adenosine deaminase (p<0.05) and carcinoembriogenic antigen (p=0.05). Serum YKL-40 levels were higher in the pneumonia group than in the cancer, asthma, or control groups. Following treatment, serum YKL-40 levels were more greatly reduced in pneumonia patients than in asthma patients. Serum YKL-39 levels did not differ between patients and controls. CONCLUSIONS: Pleural YKL-40 levels are elevated in TPEs and have fairly good diagnostic efficacy for detecting TPEs. However, adenosine deaminase is more efficient for detecting TPEs than pleural YKL-40. Serum YKL-40 levels are highest during pneumonia compared to common pulmonary/pleural diseases and are more useful for monitoring pneumonia than asthma.

Association between elevated pleural interleukin-33 levels and tuberculous pleurisy.

BACKGROUND: Interferon-γ (IFN-γ) plays a crucial role in Mycobacterium tuberculosis induced pleural responses. Interleukin (IL)-33 up-regulates the production of IFN-γ. We aimed to identify whether an association between pleural IL-33 levels and tuberculous pleurisy exists and determine its diagnostic value. METHODS: Pleural IL-33, ST2 (a receptor of IL-33), adenosine deaminase (ADA), and IFN-γ, as well as serum IL-33 and ST2 were measured in 220 patients with pleural effusions (PEs). Patients with malignant (MPEs), parapneumonic (PPEs), tuberculous (TPEs), and cardiogenic (CPEs) pleural effusions were included. RESULTS: Pleural and serum IL-33 levels were highest or tended to be higher in patients with TPEs than in those with other types of PEs. The median pleural fluid-to-serum IL-33 ratio was higher in TPE cases (≥ 0.91) than in other PE cases (≤ 0.56). Pleural IL-33 levels correlated with those of pleural ADA and IFN-γ. However, the diagnostic accuracies of pleural IL-33 (0.74) and pleural fluid-to-serum IL-33 ratio (0.75) were lower than that of ADA (0.95) or IFN-γ (0.97). Pleural ST2 levels in patients with MPEs were higher than in patients with TPEs. Serum ST2 levels did not differ among the groups. CONCLUSIONS: We identified an association between elevated pleural IL-33 levels and tuberculous pleurisy. However, we recommend conventional pleural markers (ADA or IFN-γ) as diagnostic markers of TPE.