At least three FEV1 blows are required at each time point during the assessment of bronchial hyperresponsiveness.

pleural effusions, as Dr. Kiropoulos mentioned. Momi et al2 and Hamed et al3 measured VEGF levels both in the serum and pleural fluid of tuberculous pleurisy patients. They found elevated VEGF levels both in the serum and pleural fluid of tuberculous pleurisy patients compared with congestive heart failure patients. In congestive heart failure patients, both of the studies reported higher VEGF levels in serum than in pleural fluid, as expected. Second, pleural fluid VEGF levels in tuberculous pleurisy patients were lower than the respective serum levels found in the study by Kiropoulos. However, in the studies by Momi et al2 and Hamed et al,3 VEGF levels in pleural fluid were higher than those in the serum of tuberculous pleurisy patients. This is an important discrepancy since the proposed mechanism for the increase in VEGF levels in the pleural fluid may be strictly different. The proposed mechanisms for the increase of VEGF in pleural fluid are increased vascular permeability, and local production by mesothelial cells and/or pleural macrophages. Another important issue is the standardization of tuberculous patients. A tuberculous pleurisy patient may also have a tuberculous lesion in the lung parenchyma. In this situation, VEGF may be secreted from active tuberculosis lesions beside those in the pleura. In conclusion, while we agree with Dr. Kiropoulos on the possible role of VEGF as a mediator of pleural fluid formation, we think that well-standardized studies with more tuberculous patients are needed in order to clarify the underlying mechanisms. We appreciate the contributions by Dr. Kiropoulos.