Tuberc Respir Dis.  2000 Aug;49(2):149-161. 10.4046/trd.2000.49.2.149.

TNF-alpha, TGF-beta, and fibrinolytic parameters in tuberculous and malignant pleural effusions


Residual pleural thickening(RPT) develops in about 50% of tuberculous pleurisy(PLTB). Some reports have suggested that elevated TNF-α and impaired fibrinolysis could be the cause of RPT, but until now, the mechanism and predictors of RPT have not been well known. TGF-β has been known to promote fibrogenesis and is increased in tuberculous pleural fluid(PF). PLTB and malignant pleurisy(PLMAL) manifest lymphocyte-dominant exudative pleural effusion, and it has clinical implications in the differentiation of the two diseases, based on the findings of pleural effusion. We performed this study to compare pleural fluid TNF-α, TGF-β, and fibrinolytic parameters between PLTB and PLMAL, and to find the predictors of RPT in PLTB.
Thirty-five PLTB and 14 PLMAL patients who were admitted to the Asan Medical Center from February 1997 to August 1999 were enrolled. All PLTB patients were prescribed a primary, short-course, anti-tuberculosis regimen. TNF-α, tissue plasminogen activator (tPA), plasminogen activator inhibitor 1 (PAI-1), plasminogen, α2-antiplasmin, and D-dimer were measured in both PF and PB, TGF-β was measured only in PF. Clinical characteristics, TNF-α, TGF-β, and fibrinolytic parameters were compared between patients with RPT less than 2 mm and patients with more than 2 mm of the thirty patients who completed the anti-tuberculosis treatment.
The levels of TNF-α, tPA, PAI-1, plasminogen, α2-antiplasmin, and D-dimer in PF were higher than those in peripheral blood (PB) in PLTB, whereas only plasminogen, α2-antiplasmin, and D-dimer were higher in PF than in PB in PLMAL. Pleural fluid TNF-α, TGF-β, PAI-1, plasminogen, α2-antiplasmin were increased in PLTB compared with PLMAL, but these factors did not show any further advantages over ADA in differentiation between PLTB and PLMAL. TNF-α, TGF-β, and fibrinolytic parameters did not show any differences between patients with RPT less than 2 mm and patients with RPT more than 2 mm.
Our data suggest that TNF-α, TGF-β, and fibrinolytic parameters may play some role for the development of RPT in PLTB, but they failed to predict the occurrence of RPT in PLTB. Also these parameters did not seem to have any advantages over ADA in differentiating between two diseases.


Fibrinolysis; Malignant pleurisy; Residual pleural thickening; TGF-β; TNF-α; Tuberculous pleurisy
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