Tumour necrosis factor-alpha and nitric oxide, determined as nitrite, in malignant pleural effusion.

Pleurodesis treatment is often used to stop chronic pleural effusion in malignant pleurisy. During the treatment a strong intrapleural inflammation is induced leading to the cessation of exudation. In this study the concentrations of tumour necrosis factor (TNF-alpha) and nitric oxide (NO), determined as its immediate metabolite nitrite, were measured in pleural fluid, in order to investigate if they were involved in pleural inflammation and pleural fluid exudation. Determinations were made in pleural fluid from patients with malignant pleural effusion, before and during therapeutic quinacrine-induced pleural inflammation. TNF-alpha concentrations were measured by ELISA-technique and NO/nitrite by chemiluminescence. TNF-alpha increased significantly after quinacrine instillation. NO/nitrite was initially present at the same concentrations as found in normal serum, and increased significantly during treatment. Concentrations of TNF-alpha correlate with the amount of pleural fluid production after quinacrine instillation, in that a higher level of TNF-alpha is associated with more pleural fluid production. No correlation was found between TNF-alpha and NO/nitrite, whereas a weak but significant correlation was found between NO/nitrite and concentrations of another cytokine, interleukin-1 beta (IL-1 beta). The results suggest that TNF-alpha might contribute to pleural fluid exudation and that TNF-alpha and NO are of importance in induced pleural inflammation. IL-1 beta might be one of several stimuli for NO formation in this setting.