Air travel is a risk factor for PTE, and the incidence of PTE increases with the duration of the air travel. However, the low incidence of PTE among long-distance passengers, similar to that observed in other international airports, does not justify social alarm.

The bacillary population described in tuberculous pleuritis is small, and its most likely pathogenetic mechanism is essentially immunologic. This explains why, until now, the diagnostic identification of tuberculous pleuritis (TP) has been based on the presence of granulomas in pleural biopsy. Correcting this diagnostic deficiency through other parameters related to the specific pathogenetic mechanism has been widely studied. The determination of the levels of adenosine deaminase (ADA) in pleural fluid offers high performance in its discriminating capacity to identify TP (sensitivity 87 to 100%, specificity 81 to 97%). Adenosine deaminase expresses the sum of two isoenzymes (ADA1 and ADA2). ADA1 is ubiquitous in all cells, including lymphocytes and monocytes, whereas ADA2 is found only in monocytes. Analysis and determination of these isoenzymes have shown that ADA in TP increases particularly at the expense of ADA2 and that the ADA1 /ADAp activity ratio improves performance in terms of sensitivity, specificity, and efficacy (100%, 92 to 97%, and 98%, respectively) in correcting all false-negative and false-positive results except 1 to 9% of nonlymphoproliferative malignancies. Only the high performance of ADA in the identification of TP allows it to be assumed that pleural biopsy can be obviated, especially in patients aged less than 35 years of age or having a lymphocyte-to-neutrophil proportion of more than 0.75 in regions of high prevalence. Quick determination and low cost justify its routine use in exudates. The ADA1 /ADAp activity ratio improves performance even more and could be used in cases with uncertain diagnoses or in regions with low prevalence of tuberculosis.

It has been stated that malignancy is the most common aetiology of massive pleural effusions. To determine the most frequent causes of massive pleural effusions and to assess the diagnostic yield of different diagnostic procedures and survival, we prospectively studied 1084 patients with pleural effusion. Massive pleural effusions were identified in 121 of 1084 patients (11.2%). Compared with non-massive pleural effusions, massive pleural effusions were significantly more likely to be malignant (53.7% vs. 38.3%, P=0.03) or secondary to cirrhosis (9.9% vs. 2.6%, P=0.0000). On the other hand, massive pleural effusions were significantly less likely to be secondary to infection (10.7% vs. 19.2%, P=0.003) or congestive heart failure (0.8% vs. 6.7%, P=0.03). There was a significant increase in the yield of diagnostic studies in patients with massive malignant pleural effusions (56.9% for cytological studies and 36.9% for biopsies). On the other hand, there was no difference in the diagnostic yield of microbiological and histological studies in the group of tuberculous pleural effusions. In our study population, patients with non-massive malignant pleural effusions had a significantly better survival than those with massive malignant pleural effusions, with a median survival of 8 months (95% confidence interval, 7-9) compared with 5 months (95% confidence interval, 4-6) (P=0.0009). We conclude that malignancy is the most common cause of a massive exudative effusion. Massive malignant pleural effusions are associated with worse survival, independent of age and histologic subgroup, than are non-massive malignant pleural effusions.

Adenosine deaminase (ADA) can aid in the diagnosis of tuberculous pleural effusions, but false-positive findings from lymphocytic effusions have been reported. The purpose of this study is to assess the ADA levels in nontuberculous lymphocytic pleural effusions (lymphocyte count w50%) of different aetiologies.Altogether, 410 nontuberculous lymphocytic pleural fluid samples were consecutively selected. These included malignant effusions (n=221), idiopathic effusions (n=76), parapneumonic effusions (n=35), postcoronary artery bypass graft surgery effusions (n=6), miscellaneous exudative effusions (n=21) and transudative effusions (n=51).The ADA level reached the diagnostic cut-off for tuberculosis (40 U?L -1 ) in seven of the 410 cases (1.71%). The negative predictive value of ADA for the diagnosis of pleural tuberculosis was 99% (403 of 407 cases) in the group of lymphocytic pleural effusions. In five of these seven patients ADA 1 and ADA 2 were measured, and in all these cases (100%) ADA 1 /ADA p correctly classified these lymphocytic effusions as nontuberculous (ratio v0.42).This prospective study provides additional evidence that adenosine deaminase levels in nontuberculous lymphocytic pleural effusions seldom exceed the cut-off set for tuberculous effusions. The pleural fluid adenosine deaminase levels were significantly higher in different types of exudative effusions than in transudates. An adenosine deaminase level v40 IU?L -1 virtually excluded a diagnosis of tuberculosis in lymphocytic pleural effusions. Adenosine deaminase 1 /adenosine deaminase p correctly classified all nontuberculous lymphocytic pleural effusions with high adenosine deaminase levels. Eur Respir J 2003; 21: 220-224.

We analysed the efficacy of pleural adenosine deaminase (ADAp) and the ADA1/ADAp ratio in the diagnosis of pleural tuberculosis in 103 pleural effusions, 27 of which were tuberculosis (TB) and 76 other diagnoses (non-TB). Smears, cultures and pleural biopsies were carried out in all cases, and were used for final diagnosis. The diagnostic yield of the parameters under study were as follows: smears/cultures of mycobacteria in fluid 11.1%/33.3%; biopsy 33.3%/51.8% and tuberculosis granulomas 85.1%. The levels of ADAp and ADA1/ADAp ratio in TB and non-TB groups showed very significant differences (P < 0.00001); in the TB group: ADAp 54.7 +/- 23.5 IU and ADA1/ADAp 0.27 +/- 0.08; in the non-TB group: ADAp 18.3 +/- 43.2 IU and ADA1/ADAp 0.64 +/- 0.14. The assay established ADA levels in pleural fluid > or = 40 IU and an ADA1/ADAp ratio < or = 0.42 as cut-off levels to identify individuals in the TB group, with a sensitivity of 88.8%/100%, a specificity of 92%/98.6%, a positive predictive value (PPV) of 80%/96.4%, a negative predictive value (NPV) of 95.8%/100% and an accuracy of 91.2%/99.02%. The ADAp levels in 27 patients with TB, showed close correlation with the number of monocyte macrophages (P = 0.001), but not with the number of lymphocytes (P = n.s.). The ADA1/ADAp ratio overcomes the limitations of ADAp (false positives and negatives), and is the most useful parameter for diagnosis on account of a high diagnostic yield, low cost and speed of the assay for identifying a pleural tuberculosis diagnosis, when compared with traditional methods.