The reports of measurement of VEGF levels in tuberculous pleural effusions are scarce.3 The elevated levels of VEGF in the tuberculous effusions of our patients confirm the previously available data. Additionally, the elevated levels in the serum of these patients compared with the CHF control subjects suggest that serum VEGF may be a marker of disease activity in patients with tuberculous pleural effusions, as it is in patients with active parenchymal tuberculosis.1 However, the origin of the VEGF in tuberculous effusions is not clear. In a study by Kraft et al,3 the VEGF levels in malignant pleural effusions were several-fold higher compared to matched serum samples, being suggestive of a significant local release of this cytokine from the tumor within the pleural cavity. Additionally, VEGF has been reported as a major regulator of angiogenesis with an important role in the development of granulomas.5 However, VEGF is a potent inducer of vascular permeability, and may thus represent a significant mediator in pleural fluid formation.6 The significantly higher levels of VEGF in the serum compared to the pleural fluid of our patients are suggestive of the latter role of VEGF, being responsible, at least in part, for the increased vascular permeability that leads to the formation of tuberculous pleural effusions. This is the first study to our knowledge that examines the levels of VEGF both in the pleural fluid and serum of patients with tuberculous pleural effusions, suggesting a possible role of this mediator in the formation of such effusions.