Pleural fluid interferon-γ and tumour necrosis factor-α in tuberculous and rheumatoid pleurisy

Abstract

Tuberculous and rheumatoid pleural effusions show features suggesting a strong local cellular immune response. Pleural fluid (Pf) from patients with tuberculosis, rheumatoid arthritis (RA) and other diseases were compared with respect to interferon-γ (IFN-γ) and tumour necrosis factor-α (TNF-α). Immunoassays were used to determine Pf-IFN-γ and Pf-TNF-α in 102 patients, including 11 with RA, 31 with verified tuberculosis, 23 with suspected tuberculosis 11 with pneumonia, 14 with lung cancer and 12 with congestive heart failure. Measurable Pf-IFN-γ occurred exclusively in patients with verified (median 1.8 ng·mL-1; 95% confidence interval (95% CI) 0.63-4.0 ng·mL-1) or suspected (0.37 ng·mL-1; 95% CI 0-0.7 ng·mL-1) tuberculosis. The highest median Pf-IFN-γ was observed in those patients who showed a positive pleural fluid culture for Mycobacterium tuberculosis. In pleural effusions due to other diseases, including RA, IFN-γ was undetectable. The highest Pf-TNF-α occurred in verified tuberculosis (median 198 ng·L-1; 95% CI 169-222 ng·L-1 and RA (210 ng·L-1; 95% CI 147-231 ng·L-1). Pleural fluid interferon-γ is a highly useful marker for diagnosing tuberculous pleurisy. Although tuberculous and rheumatoid pleural effusions share several biochemical features, they are strikingly different with respect to interferon-γ.