Differentiating transudative from exudative pleural effusion: should we measure effusion cholesterol dehydrogenase?

INTRODUCTION: Pleural effusions are often classified into transudates and exudates based on Light's criteria. In this study, the diagnostic properties of Light's criteria were compared to those of several other analytes for the classification of pleural fluids into transudative and exudative. METHODS: A total of 471 patients with pleural effusions were evaluated. In pleural effusions and simultaneously drawn blood samples, lactate dehydrogenase (LDH), total protein, albumin, cholesterol, amylase, glucose, pH and the cell number were measured. Retrospectively, the clinical records were used to establish a clinical diagnosis. The diagnostic properties of the biochemical tests were calculated using the clinical diagnoses as gold standard. RESULTS: By clinical diagnosis, 108 patients had transudative and 300 patients had exudative pleural effusions. In addition to pleural LDH activity (accuracy 89%, sensitivity 86%, specificity 97%) and fluid to serum LDH ratio (accuracy 89%, sensitivity 91%, specificity 85%), pleural cholesterol concentration readily identified exudates (accuracy 82%, sensitivity 76%, specificity 98%). Combination of these three parameters achieved a higher overall accuracy (accuracy 95%, sensitivity 93%, specificity 100%) than the Light's criteria (accuracy 93%, sensitivity 100%, specificity 73%). Combination of effusion cholesterol concentration and effusion LDH activity had the highest discriminatory potential (accuracy 98%, sensitivity 98%, specificity 95%). CONCLUSIONS: Including effusion cholesterol, concentration in the routine biochemical work-up of pleural fluid allows for correct classification of more pleural effusions than achieved by use of Light's criteria. Combination of cholesterol and LDH had the highest discriminatory potential and the added advantage that no patient plasma is needed for correct classification.     

Classification tree analysis for the discrimination of pleural exudates and transudates.

BACKGROUND: Classification and regression tree (CART) analysis is a non-parametric technique suitable for the generation of clinical decision rules. We have studied the performance of CART analysis in the separation of pleural exudates and transudates. METHODS: Basic demographic, radiologic and laboratory data were retrospectively evaluated in 1257 pleural effusions (204 transudates and 1053 exudates, according to standard clinical criteria) and submitted for CART analysis. The model's discriminative ability was compared with that of Light's criteria, in both the original formulation and an abbreviated version, i.e., deleting the pleural fluid (PF)/serum lactate dehydrogenase (LDH) ratio from the triad. RESULTS: A first CART model built starting from all available data identified PF/serum protein ratio and PF LDH ratios as the two best discriminatory parameters. This algorithm achieved a sensitivity of 96.8%, slightly lower than that of classical Light's criteria (98.5%) and comparable to that of the abbreviated Light's criteria (97.0%), and significantly better specificity (85.3%) compared to both classical (74.0%) and abbreviated (79.4%) Light's criteria. A second CART model developed after excluding serum measurements selected PF protein and PF LDH as the most discriminatory variables, and correctly classified 97.2% of exudates and 77.0% of transudates. CONCLUSIONS: CART-based algorithms can efficiently discriminate between pleural exudates and transudates.     

Pleural adenosine deaminase in the separation of transudative and exudative pleural effusions

OBJECTIVE: The purpose of this study was to evaluate the usefulness of a new parameter, pleural adenosine deaminase (PADA), for separating transudative pleural effusion from exudative pleural effusion, and to compare the results with other tests (albumin gradient and protein gradient). METHODS: From November 2001 to January 2003, 359 consecutive patients with pleural effusion who underwent a diagnostic thoracentesis were included in the study. Effusions were individually classified as transudates or exudates after the careful evaluation of all clinical data and biochemical parameters of pleural fluid and serum of patients on the basis of Light's criteria. The means and standard deviations of PADA, pleural/serum ADA (P/S ADA) ratio, albumin gradient and protein gradient were evaluated for transudative and exudative effusions. The best cut-off values for each test were identified by using the receiver operating characteristic (ROC) curve. The optimum cut-off level was determined by selecting points of test values that provided the greatest sum of sensitivity and specificity. RESULTS: There were 113 transudates and 246 exudates. For each test, differences in mean value between the transudate group and the exudate group were statistically significant (t test, P<0.001). The optimum cut-off levels for PADA and P/S ADA were 15.3 U/L and 0.66 U/L, respectively. ROC analysis confirmed previous recommendations for albumin gradient (12 g/L) and protein gradient (31 g/L). For detecting exudates, the PADA test yielded a sensitivity and specificity of 85.8% and 82.3%, respectively. Sensitivity and specificity of the albumin gradient were found to be 88.5% and 79.3%, and of the protein gradient 85% and 83.2%, respectively. The areas under the curve (AUC) data and accuracy demonstrated similar discriminative properties in the examined tests. CONCLUSIONS: The measurement of PADA is suggested as a reliable test in the separation of pleural exudates from transudates with accuracy similar to that of the albumin gradient and protein gradient.     

胸水胆固醇和尿酸在鉴别渗出液和漏出液中的价值

目的　探讨胸水胆固醇(Pch)浓度、胸水与血清胆固醇(Sch)浓度的比值(P/Sch)、胸水尿酸(Pua)浓 度对胸腔积液渗漏性的鉴别诊断价值。方法　对85例胸腔积液患者检测Pch和65例患者检测Pua,并计算出 P/Sch,分别研究Pch、P/Sch、Pua、胸水总蛋白(Ptpr)对胸水渗漏性诊断的受试者工作特征曲线(ROC)、灵敏度、 特异性与诊断效率。结果　Pch、P/Sch、Pua、Ptpr对胸水渗出液诊断的灵敏度分别为96.2%、90.4%、79.5%和 90.6%,特异性分别为100.0%、89.7%、61.9%和80.6%。Pch鉴别渗出液和尿酸鉴别漏出液的ROC曲线下面 积分别是0.986和0.655。结论　Pch、P/Sch、Ptpr对胸水渗出液具有较高的鉴别诊断价值,ROC亦证明Pch鉴 别渗出液和Pua监测漏出液是可行的,Pch的诊断效率最高(P<0.05)。Pua对胸水监测漏出液有一定价值,尿 酸增加表示机体抗氧化状态佳,提示预后较好。     

Lipoproteins and apolipoproteins in human pleural effusions.

We investigated the lipoproteins and apoproteins in human serum and pleural effusions of different origin: transudates, inflammatory exudates, and malignant exudates. Transudates had a low cholesterol content of 35 +/- 12 mg/dl (mean +/- SD) because of low levels of low-density lipoprotein (LDL) cholesterol--representing 16% of serum levels--whereas inflammatory exudates (cholesterol 92 +/- 26 mg/dl) and malignant exudates (cholesterol 86 +/- 6 mg/dl) exhibited high levels of LDL, with 67% and 69% of serum levels. Apolipoprotein (apo) B level corresponded with LDL and presented with multiple split-products in sodium dodecyl sulfate-polyacrylamide gel electrophoresis in exudative effusions. LDL levels in effusions correlated with serum levels in exudates but did not correlate with those in transudates. In contrast, lipoprotein(a) appeared in all effusions from patients with detectable serum levels. The isoforms were similar as demonstrated by immunoblotting. Differences were found in the composition of the high-density lipoprotein (HDL) fraction: transudates had cholesterol-rich HDL when compared with serum. HDL particles of malignant exudates were poor in cholesterol, and isoelectric focusing demonstrated more sialized apolipoprotein E. A strongly abnormal HDL level with accumulation of cholesterol was found in a long-standing tuberculous effusion. In conclusion, cholesterol in acute effusions is bound to lipoproteins and derived from the blood. The difference in total cholesterol levels between transudates and exudates is based on the lack of LDL in transudates. Transudates show the lipoprotein characteristics of interstitial fluid. Alterations of lipoproteins occur in chronic inflammation and in malignancy with possible de novo synthesis of apolipoprotein E by tumor cells. Lipoprotein(a) accumulates independently from LDL in the pleural space, a finding that supports the view that the physiologic function of lipoprotein(a) is located in the interstitial space.     

Clinical value of CYFRA21-1, NSE, CA15-3, CA19-9 and CA125 assay in the elderly patients with pleural effusions

The aim of this study was to evaluate the individual and combined diagnostic value of five tumour markers in the elderly patients with pleural effusions. Serum and pleural fluid levels of cytokeratin fragment 19 (CYFRA21-1), neuron-specific enolase (NSE), carbohydrate antigen 15-3 (CA15-3), carbohydrate antigen 19-9 (CA19-9) and carbohydrate antigen 125 (CA125) were assayed in 32 elderly patients with malignant pleural effusions resulting from advanced lung cancer and in 30 elderly patients with benign pleural effusions by ELISA. Serum levels of CYFRA21-1, NSE, CA15-3, CA19-9 and CA125 in patients with malignant pleural effusions were 12.84 +/- 6.48 microg/l, 22.07 +/- 11.25 microg/l, 65.74 +/- 30.26 kU/l, 56.32 +/- 25.6 kU/l and 71.86 +/- 31.45 kU/l, respectively, and were significantly higher than those in patients with benign pleural effusions (p < 0.01). Pleural fluid levels of CYFRA21-1, CA15-3, CA19-9 and CA125 except NSE in patients with malignant pleural effusions were 18.64 +/- 8.15 microg/l, 59.31 +/- 27.35 kU/l, 48.24 +/- 21.56 kU/l and 62.16 +/- 27.79 kU/l, respectively, and were significantly higher than those in patients with benign pleural effusions (p < 0.01). The parallel combined testing of five tumour markers in serum increased the diagnostic sensitivity to 90.6%, and serial combined testing increased the diagnostic specificity to 93.3%. The sensitivity (%) and specificity (%) of these tumour markers in pleural fluid were as follows: CYFRA21-1, 84.4/90; CA15-3, 62.5/73.3; CA19-9, 37.5/66.7; CA125, 56.3/70; for differentiating malignant effusions from benign effusions. When CYFRA21-1 and CA15-3 combined, the sensitivity and specificity were increased (100% and 90% respectively). Serum and pleural fluid levels of the five tumour markers shows certain values in the diagnosis and differentiate diagnosis for malignant pleural effusions in the elderly patients from benign. The combined assay of five tumour markers in serum and the CYFRA21-1 combined with CA15-3 in pleural fluid were helpful and can increase the sensitivity and specificity in diagnosing malignant pleural effusions.     

Sonographic appearances in transudative pleural effusions: not always an anechoic pattern

Pleural effusion patterns in sonographic appearances can be subclassified as anechoic, complex nonseptated, complex septated and homogeneously echogenic. Previous studies have suggested that transudates are usually anechoic; however, in daily practice we find frequently that heterogeneous echogenic material is present in transudative pleural effusions. This clinical study was to re-evaluate the sonographic appearances of transudative pleural effusions. A total of 127 patients with transudative pleural effusion that met Light's criteria ([1] a pleural fluid-serum protein ratio of <0.5, [2] a pleural fluid-serum lactate dehydrogenase [(LDH] ratio of <0.6 and [3] a pleural fluid LDH of less than two thirds of the upper limit of normal for serum LDH) and clinical presentations were enrolled. Results showed that transudative pleural effusions had the following sonographic appearances: an anechoic pattern in 45% (57/127) and a complex nonseptated pattern in 55% (70/127). There was no complex septated or homogenously echogenic pattern. In conclusion, sonographic presentations in transudative pleural effusions are not always in an anechoic pattern. If an afebrile patient without infectious symptoms/signs has bilateral pleural effusion compatible with transudate of Light's criteria, treat the underlying problems and ignore the complex nonseptated sonographic appearance. (E-mail: hsuwh@www.cmuh.org.tw).     

Diagnostic value of the combined determination of carcinoembryonic antigen (CEA) in pleural effusion and serum with an enzyme immunoassay (EIA). Sensitivity, specificity and relation to tumor type

Measurement of carcinoembryonal (CEA) levels in pleural fluid are suggested to improve the unsatisfactory sensitivity of pleural cytology in the differential diagnosis of malignant pleural effusions. We evaluated simultaneously determined pleural and serum CEA levels in 117 patients with pleural effusions of different aetiology (74 malignant, 30 inflammatory exudates and 13 transudates) by use of an enzyme immunoassay (EIA). Despite considerable scatter, pleural levels of CEA in malignant effusions were significantly higher (p less than 0.001) than the values in benign effusions. Using a cut off level of 5 ng/ml, 41% (= sensitivity) of malignant pleural effusions showed elevated concentrations of CEA. Only one out of 43 benign effusions showed a level of 5 ng/ml, which is equivalent to a specificity of 98%. However, malignant effusions due to small cell lung cancer, pleural mesothelioma and metastasising ovarian carcinoma never showed elevated levels of CEA. Highest pleural values of CEA were observed in cases of alveolar cell or adenocarcinoma of the lung or metastasising breast cancer. Although pleural and serum CEA levels correlated significantly (rs = 0.77), the evaluation of serum CEA levels alone yielded a lower sensitivity (36%) and specificity (93%) than pleural levels. 77% of cases with malignant pleural effusions showing elevated pleural CEA levels were characterized by an increased ratio Pleura/Serum greater than 1, particularly in effusions due to lung cancer. The CEA ratio was significantly higher (p less than 0.05) in patients with malignant than with benign effusions. EIA appears to be more specific by avoiding false positive results in benign effusions as compared with determination by conventional RIA. In conclusion, evaluation of pleural CEA levels in patients with malignant effusions by using an EIA because of its high specificity is a valuable adjunct to pleural cytology in improving the diagnosis of malignant effusions. However, a normal CEA level in either pleural effusion or in serum is of no clinical significance. Simultaneous measurement in pleural effusion and serum is of greater value.     

Diagnostic approach to pleural effusion in adults

The first step in the evaluation of patients with pleural effusion is to determine whether the effusion is a transudate or an exudate. An exudative effusion is diagnosed if the patient meets Light's criteria. The serum to pleural fluid protein or albumin gradients may help better categorize the occasional transudate misidentified as an exudate by these criteria. If the patient has a transudative effusion, therapy should be directed toward the underlying heart failure or cirrhosis. If the patient has an exudative effusion, attempts should be made to define the etiology. Pneumonia, cancer, tuberculosis, and pulmonary embolism account for most exudative effusions. Many pleural fluid tests are useful in the differential diagnosis of exudative effusions. Other tests helpful for diagnosis include helical computed tomography and thoracoscopy.     

Quantitative analysis of pleural fluid cell-free DNA as a tool for the classification of pleural effusions

BACKGROUND: Recently, much interest has been focused on the quantification of DNA in miscellaneous body fluids. In this study, the application is extended to classifying pleural effusions by measuring cell-free DNA in pleural fluid. METHODS: We recruited 50 consecutive patients with pleural effusions with informed consent. Pleural fluids were centrifuged at 13000 g, with supernatants aliquoted for extraction and analysis of beta-globin DNA sequence by quantitative real-time PCR. Serum and pleural fluid biochemistries were performed to classify pleural effusions using the modified criteria of Light et al. (Ann Intern Med 1972;77:507-13). The ROC curve was plotted to determine the cutoff DNA concentration for classifying pleural fluids as transudates or exudates. Indicators of diagnostic accuracy were calculated for both pleural fluid DNA and modified criteria of Light et al., using the discharge, microbiologic, and histologic diagnoses as the reference standard. RESULTS: The area under the ROC curve was 0.95 [95% confidence interval (CI), 0.84-0.99]. At 509 genome-equivalents/mL, pleural fluid DNA alone correctly classified 46 of 50 pleural effusions with 91% sensitivity (95% CI, 76-98%), 88% specificity (95% CI, 64-98%), and positive and negative likelihood ratios of 7.7 (95% CI, 3.1-19.5) and 0.10 (95% CI, 0.04-0.27), respectively. With the modified criteria of Light et al., 43 of 50 pleural effusions were correctly classified with 97% sensitivity (95% CI, 91-100%) and 67% specificity (95% CI, 45-89%). There were significant correlations between cell-free DNA and both lactate dehydrogenase and total protein in pleural fluid, suggesting their common origin. CONCLUSIONS: Pleural fluid DNA concentrations are markedly increased in exudative effusions, making it a potential new tool to evaluate the etiologic causes of pleural effusions.     

Diagnostic value of leptin in tuberculous pleural effusions

It is suggested that leptin may be involved in inflammation. Although relation between leptin levels and active pulmonary tuberculosis has been studied, there is no information about relation between leptin levels and tuberculous pleural effusions (TPE). We evaluated the diagnostic value of pleural fluid and serum leptin levels in TPE and compared them with adenosine deaminase (ADA). Forty-five patients, 17 tuberculous effusion and 28 nontuberculous effusion, with exudative pleural effusions were included. Leptin and ADA levels were measured from serum and pleural fluid in all patients. There were no statistically significant differences between tuberculous and nontuberculous groups with respect to the serum ADA activity and pleural fluid/serum leptin ratio. On the contrary, pleural fluid leptin level, pleural fluid ADA activity, serum leptin level and pleural fluid/serum ADA activity ratio were statistically different between tuberculous and nontuberculous groups. When leptin levels were corrected for body mass index, serum leptin levels did not reach statistical significance. Cut-off points to predict tuberculosis were calculated as 9.85 ng/ml and 35.55 U/l for pleural fluid leptin level and pleural fluid ADA activity, respectively. Sensitivity, specificity and area under the curve +/- standard error were 82.4%, 82.1%, 0.83 +/- 0.07 for pleural fluid leptin levels and 100%, 100%, 1.00 +/- 0.00 for pleural fluid ADA activity, respectively; the difference between these curves was significant (p = 0.01). Pleural fluid leptin levels were lower in tuberculous effusions than in other exudates. Pleural fluid leptin has a diagnostic value for TPE but not as good as that of ADA.     

Association between inflammatory mediators and the fibrinolysis system in infectious pleural effusions

The response of the fibrinolytic system to inflammatory mediators in empyema and complicated parapneumonic pleural effusions is still uncertain. We prospectively analysed 100 patients with pleural effusion: 25 with empyema or complicated parapneumonic effusion, 22 with tuberculous effusion, 28 with malignant effusion and 25 with transudate effusion. Inflammatory mediators, tumour necrosis factor-alpha (TNF-alpha), interleukin-8 (IL-8) and polymorphonuclear elastase, were measured in serum and pleural fluid. Fibrinolytic system parameters, plasminogen, tissue-type plasminogen activator (t-PA) and urokinase PA, PA inhibitor type 1 (PAI 1) and PAI type 2 concentrations and PAI 1 activity, were quantified in plasma and pleural fluid. The Wilcoxon signed-rank test was used to compare plasma and pleural values and to compare pleural values according to the aetiology of the effusion. The Pearson correlation coefficient was used to assess the relationship between fibrinolytic and inflammatory markers in pleural fluid. Significant differences were found between pleural and plasma fibrinolytic system levels. Pleural fluid exudates had higher fibrinolytic levels than transudates. Among exudates, tuberculous, empyema and complicated parapneumonic effusions demonstrated higher pleural PAI levels than malignant effusions, whereas t-PA was lowest in empyema and complicated parapneumonic pleural effusions. PAI concentrations correlated with TNF-alpha, IL-8 and polymorphonuclear elastase when all exudative effusions were analysed, but the association was not maintained in empyema and complicated parapneumonic effusions. A negative association found between t-PA and both IL-8 and polymorphonuclear elastase in exudative effusions was strongest in empyema and complicated parapneumonic effusions. Blockage of fibrin clearance in empyema and complicated parapneumonic effusions was associated with both enhanced levels of PAIs and decreased levels of t-PA.     

Diagnostic value of ferritin analysis in pleural effusions

Ferritin was analysed with an immunoradiometric assay using anti-spleen ferritin antibodies, in pleural effusions (Pl) from 28 patients with malignant effusions (18 carcinoma, 10 mesothelioma), 15 patients with non-malignant exudative effusions of unknown aetiology, and from 12 patients with transudative effusions due to congestive cardiac failure. Geometric mean Pl-ferritin was 617 micrograms/l in carcinoma, 1301 micrograms/l in mesothelioma (p less than 0.01 against carcinoma), 931 micrograms/l in non-malignant exudates, and 178 micrograms/l in transudates (p less than 0.0001 against malignant and non-malignant exudates). There was no correlation between Pl-ferritin and Pl-protein, Pl-albumin or Pl-cell count. P1-ferritin displayed a wide overlap between the various groups, and was of no value in the discrimination between malignant and non-malignant exudates. In the differentiation between exudates and transudates, the diagnostic accuracy of Pl-ferritin was only slightly lower compared to Pl-protein and Pl-albumin. With the present method, analysis of Pl-ferritin appears to be of limited value in the routine diagnostic evaluation of pleural effusions.     

The value of cells in the pleural fluid in the differential diagnosis.

Fifty samples of pleural fluid, collected from consecutive patients in a thoracic clinic who had diagnostic thoracentesis, were studied prospectively. Pleural fluid protein was of value in differentiating transudates from exudates. Pleural fluid red cell counts, white blood cell counts, and differential white blood cell counts have no specificity and no usefulness in the differential diagnosis of the origin of the effusion. Pleural fluid cytology was positive in 60% of all the malignancies studied in this series; for the group with metastatic breast carcinoma, there was a 78% positive pleural fluid cytology. Differential white cell counts revealed tumor cells in 45% of malignant effusions. In our experience, the finding of tumor cells is the only useful finding in differential cell counts of the pleural fluid.     

The contribution of factor V to the coagulant property of pleural fluid.

Intrapleural fibrin deposition commonly accompanies pleural injury and may contribute to the organization of exudative pleural effusions, which leads to lung entrapment. Previous investigators have observed an increase in procoagulant proteins in pleural effusions but very little thrombin formation. FVa is the protein cofactor in the prothrombinase complex that dramatically enhances the generation of thrombin from prothrombin by the serine protease fXa. The presence of fVa within the pleural space could influence fibrin formation and pleural scarification. We examined pleural fluids obtained from patients who had lung cancer, CHF, and empyema for the presence of fV/fVa. The fV antigen was increased in exudative pleural fluids, in comparison with transudates. However, the specific activity of fV antigen present in exudates was significantly less than that observed for the lower concentration of antigen present in transudate and could not be activated to the same degree by thrombin. Immunoblots of fV antigen in exudates indicated that fV was partially cleaved and inactivated by unidentified proteases. We conclude that although fV is present in pleural fluid, it may be present in a degraded form, which may partially account for a lack of thrombin-generating capacity in these pleural fluids. The presence of fV does not necessarily correlate with pleural loculation.     

Biochemical study of the pleural fluid in exudative pleurisy

The authors relate the data on the importance of a biochemical analysis of the pleural fluid for the differential diagnosis of pleurisy and identification of the early signs of pleural fluid suppuration. For the purposes of the differential diagnosis between transudates and exudates measurements are made of the protein content and LDH activity in the pleural fluid. The exudate protein/serum protein and exudate LDH/serum LDH ratios are computed in necessary cases. The high prothrombin index (over 100%) and the level of lysozyme (over 25 (micrograms/ml) in the pleural fluid provide evidence in favour of the tuberculous etiology of pleurisy. The low level of glucose (under 2 mmol/l), high activity of LDH (over 6.2 mmol/l) and the negative ethanol test may point to the initial signs of exudate suppuration.     

Pleural effusions. 1. Preliminary evaluation--recognition of the transudate

Part 1 of this two-part article describes how to document the presence and location of pleural effusion, perform thoracentesis, and differentiate transudates from exudates. If the pleural fluid is found to be a transudate, no further tests are indicated. Part 2, starting on page 181, details pleural fluid analysis, describes pleural biopsy and thoracoscopy, and presents a clinical strategy for evaluating pleural effusion.     

Measurement of vitamin D-binding protein in pleural fluids and sera by means of a turbidimetric immunoassay measuring system

BACKGROUND: Vitamin D-binding protein (DBP) has been recognized as a multifunctional plasma protein that can modulate certain immune and inflammatory responses. There may be differences between the DBP concentrations in pleural fluids from various diseases involving a variety of possible responses in the pleural cavity. METHODS: An anti-DBP polyclonal antibody was prepared using commercially available DBP to establish a quantitative measuring system for DBP. With a rabbit antibody, a turbidimetric immunoassay (TIA) was developed for DBP with an automatic analyzer. Using this measuring system, the concentrations of DBP were compared with the protein concentration in pleural fluid and serum specimens from patients with various diseases. RESULTS: The fluid DBP concentrations in transudative (n=11) and exudative (n=41) effusions were 71.9+/-21.2 and 180.7+/-43.7 mg/l, respectively. Among the exudative effusions, the fluid DBP concentrations in the bacterial (n=10), tuberculous (n=13), and malignant (n=18) effusions were 218.8+/-37.3, 186.7+/-26.2, and 155.1+/-41.3 mg/l, respectively. The DBP fluid/serum ratio and the fluid DBP/protein ratio in bacterial effusions were significantly higher than those in tuberculous (p<0.005, p<0.05, respectively) and malignant effusions (p<0.0005, p<0.005, respectively), although no statistically significant differences in the serum DBP/protein ratio between those effusions were found. CONCLUSIONS: Using the TIA assay, the DBP concentrations in bacterial pleural effusions were significantly higher than in tuberculous and malignant effusions.     

Pleural effusion: comparison of clinical judgment and Light's criteria in determining the cause

Pleural fluid analysis is often the initial diagnostic test used to determine the cause of a pleural effusion. We prospectively studied 33 consecutive patients with pleural effusions to determine whether the fluid arose from a transudative or an exudative process. Clinical judgment by an internist before thoracentesis and both serum and pleural fluid protein and lactic dehydrogenase levels (commonly referred to as "Light's criteria") were compared to the patient's final diagnosis. The internist correctly classified 15 of 17 exudative processes and all 16 transudative processes; the presence of any one of Light's three criteria correctly classified 15 of 17 exudative processes, whereas the absence of all three criteria correctly classified 14 of 16 transudative processes. Clinical judgment and Light's criteria are comparable in their ability to predict whether an exudative or transudative process was responsible for the effusion. Both methods are associated with errors, though of different kinds; these errors occurred infrequently. Recognizing the limitations of these methods will permit the most accurate effusion categorization.     

Decreased Heat-Labile Opsonic Activity and Complement Levels Associated with Evidence of C3 Breakdown Products in Infected Pleural Effusions

Heat-labile opsonic activity was measured simultaneously in serum and pleural fluid of patients with transudates, infectious exudates (with positive or negative bacterial culture) and neoplastic exudates, using two different complement-dependent phagocytic tests: the killing of Staphylococcus aureus Wood 46 variant strain (K50 opsonic titers) and the assessment of ingestion rate of endotoxin-coated paraffin particles (Oil Red 0 uptake test). K50 opsonic titers were lower in culture-positive pleural effusions as compared to culture-negative (P < 0.002) or neoplastic effusions (P < 0.002). These results were corroborated by the Oil Red 0 uptake test. The data obtained with the two assays showed a significant correlation (P < 0.001).The hemolytic activity of complement (CH50) as well as the levels of C3 breakdown product, C3d, were measured in the same sera and pleural fluid samples and in an additional group of patients with pleural effusions of the same etiology. Effusions with positive cultures showed lower CH50 values (P < 0.01) and higher C3d values (P < 0.05) when compared to culture-negative pleural fluids. Finally, evidence for immune complexes in pleural effusions and sera was looked for by determination of Clq binding activity. Levels were higher in culture-positive effusions when compared to culture-negative fluids (P = 0.005).K50 opsonic titers showed a positive correlation with CH50 values (P < 0.001) for all fluids tested. Similarly Clq binding activity correlated with C3d levels in effusions of infectious origin (P = 0.05). Recovery experiments using the various bacterial species isolated from culture-positive pleural effusions showed evidence of complement inactivation upon incubation with pooled sera at concentrations of 10(7)-10(8) microorganisms/ml.These results indicate that one important reason for bacterial persistence in empyema may be decreased opsonization secondary to local consumption of complement.