Pleural effusion is a common complication of various diseases. Conventional methods are not always capable of establishing the cause of pleural effusion, so alternative tests are needed. The aim of this study was to explore means of discriminating between different pleural effusion groups, malignant, parapneumonic and tuberculous, based on the combined function of seven biological markers.Adenosine deaminase (ADA), interferon-c, C-reactive protein (CRP), carcinoembryonic antigen, interleukin-6, tumour necrosis factor-a and vascular endothelial growth factor concentration levels were measured in pleural fluid from 45 patients with malignant, 15 with parapneumonic and 12 with tuberculous pleural effusion. Receiver operating characteristic curve analysis, multinomial logit modelling and canonical variate analysis were applied to discriminate the pleural effusion groups.The three groups could be discriminated successfully using the measured markers. The most important parameters for discrimination were ADA and CRP concentration levels. An individual with an ADA concentration level of .45 U?L -1 and a CRP concentration of ,4 mg?dL -1 was more likely to belong to the tuberculous pleural effusion group, whereas one with an ADA concentration level of ,40 U?L -1 and a CRP concentration of .6 mg?dL -1 was more likely to belong to the parapneumonic pleural effusion group, and one with a CRP concentration of ,4 mg?dL -1 to the malignant pleural effusion group. The combination of adenosine deaminase and C-reactive protein levels might be sufficient for discriminating between the three different groups of exudative pleural effusion: malignant, tuberculous and parapneumonic.

Rationale: The acute effect of secondhand smoke (SHS) on lung function and the duration of system disruption remain unknown. Objectives: To assess the SHS effects and their duration on lung function and inflammatory markers. Methods: In a randomized single-blind crossover experiment data were obtained from 16 (8 women) nonsmoking adults at baseline and at 0, 1, and 3 hours after a 1-hour SHS exposure set at bar/ restaurant SHS levels. Measurements and Main Results: Serum and urine cotinine, lung function, and cytokines IL-4, IL-5, IL-6, tumor necrosis factor (TNF)-a, and IFN-g. At 0 hours most lung function parameters were significantly reduced (indicative: FEV 1 , 4.3 6 0.4 vs. 3.8 6 0.3 L; FEV 1 /FVC, 0.9 6 0.1 vs. 0.8 6 0.1; P , 0.05) but at 3 hours they were at baseline levels. In contrast, cotinine (serum, 8.9 6 3.2 vs. 35.5 6 10.2 ngÁml 21 ), IL-4 (41.3 6 5.8 vs. 44.2 6 4.5 pgÁml 21 ), IL-5 (36.1 6 3.2 vs. 60.1 6 7.0 pgÁml 21 ), IL-6 (2.5 6 0.3 vs. 7.6 6 1.4 pgÁml 21 ) and IFN-g (0.3 6 0.2 vs. 0.6 6 0.2 IUÁml 21 ) at 3 hours were higher than at baseline (P , 0.05). IL-4 and TNF-a increased only in men, whereas IL-5, IL-6, and IFN-g were different between sexes after exposure (P , 0.05). Regression analyses revealed inverse associations of FEV 1 and FEV 1 /FVC ratio with IL-5 (P , 0.05) in men and with IL-5 (P 5 0.01), IL-6 (P , 0.001), IFN-g (P 5 0.034) and serum cotinine (P , 0.001) in women. Conclusions: We conclude that 1 hour of SHS exposure at bar/ restaurant levels is accompanied by significant decrements on lung function and marked increases in inflammatory cytokines, particularly in men. More importantly, whereas most smoke-induced effects on lung function appear to recede within 60 minutes, inflammatory cytokines remain elevated for at least 3 hours after exposure to SHS. Keywords: passive smoking; cotinine; respiration; inflammatory markersIn the 10 minutes you will spend reading this article, 111 people will die somewhere in the world from tobacco-induced illnesses.* Fourteen of them have never smoked. † An overwhelming amount of evidence has emerged over the past decades on the adverse health effects of secondhand smoke (SHS) (1-5). Nevertheless, more than 126 million American and 130 million Chinese adult nonsmokers suffer daily SHS exposure, whereas global estimates include 700 million children and 50 million pregnant women (1). Latest reports show that, despite current measures, the prevalence rates of smoking are increasing (2, 3), while the tobacco industry predicts a global expansion of the tobacco epidemic in the near future (3). Moreover, arguments are being expressed that only chronic exposures to SHS represent a health risk and that there is no scientific basis for claims that brief, acute, transient SHS exposures represent a significant acute health hazard in nonsmokers (6). This is, in part, because our knowledge on the effects of SHS is based predominantly on longitudinal epidemiological studies, whereas experimental studies assessing the acute and short-term effects of SHS are sca...

No abstract

No abstract