Vascular endothelial growth factor and proinflammatory cytokines in pleural effusions

To evaluate the predictive value of vascular endothelial growth factor (VEGF) in the differential diagnosis of pleuritis and its association with other proinflammatory cytokines in pleural effusion, we measured VEGF together with interleukin-1beta (IL-1beta), tumor necrosis factor alpha (TNF-alpha) and soluble intercellular adhesion molecule-1 (sICAM-1) in pleural effusions. We investigated 127 patients with pleural effusion (congestive heart failure: 21; parapneumonic: 27; tuberculous: 41; malignant: 38). We examined standard parameters of pleural effusion and measured pleural effusion VEGF, IL-1beta, TNF-alpha and sICAM-1 using enzyme-linked immunosorbent assay. VEGF level was significantly higher in malignant effusion than in other groups. TNF-alpha level was significantly higher in tuberculous pleurisy than in other groups. In tuberculous pleurisy VEGF level showed significant positive correlations with mononuclear cell counts and all investigated cytokines. The sensitivity and specificity of VEGF in the diagnosis of malignancy was 100 and 84%, respectively (cutoff = 2000 pg/ml). The sensitivity and specificity of VEGF and TNF-alpha in the diagnosis of tuberculous pleurisy (VEGF titer <2000 pg/ml and TNF-alpha titer > 55 pg/ml) was 88.9 and 77.1%, respectively. We propose that measurement of VEGF together with TNF-alpha is helpful in differentiating between tuberculous pleurisy and malignant pleural effusion and that VEGF correlates with proinflammatory cytokines especially in tuberculous pleurisy. We also propose that measurement of pleural VEGF is helpful for the diagnosis of malignant pleural effusion.     

Diagnostic value of interleukin-1alpha, interleukin-6, and tumor necrosis factor in pleural effusions

STUDY OBJECTIVES: Interleukin (IL)-1alpha, IL-6, and tumor necrosis factor (TNF)-alpha were measured in pleural fluid from 57 patients with pleural effusion in order to evaluate the diagnostic utility of these cytokines. We studied 20 patients with malignant pleural effusion, 11 patients with parapneumonic pleural effusion, 9 patients with tuberculous pleural effusion, and 17 patients with transudative pleural effusion. Cytokines were measured by radioimmunoassay. SETTING: University tertiary hospital. RESULTS: The mean values of the three cytokines measured in pleural fluid or in serum were significantly higher in patients with exudates than with transudates (p < 0.05). The ratio of IL-6 in pleural fluid to serum was significantly higher in exudates than in transudates (p < 0.05). The level of IL-6 in pleural fluid was significantly higher in tuberculous than malignant (p < 0.007) or parapneumonic pleural effusions (p < 0.04). No significant difference between the three types of exudates was found in pleural fluid levels of IL-1alpha or TNF-alpha. CONCLUSIONS: Serum levels of IL-1alpha, TNF-alpha, and in particular IL-6 can distinguish exudates from transudates, while pleural fluid IL-6 levels could be useful as an additional marker in the differential diagnosis of tuberculous, malignant, and parapneumonic exudates. Finally, our results suggest that there is local cytokine production in exudative pleural effusions.     

Proinflammatory cytokines and fibrinolytic enzymes in tuberculous and malignant pleural effusions

OBJECTIVES: To measure tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in pleural effusions caused by tuberculosis (TB) and malignancy and their relationship with plasminogen activator inhibitor type I (PAI-1) and tissue type plasminogen activator (tPA), and to compare the differences between tuberculous and malignant pleural effusions. In addition, the relationship between the effusion levels of these parameters and the development of residual pleural thickening was evaluated in the patients with tuberculous pleurisy. DESIGN: Prospective study. MATERIALS AND METHODS: TNF-alpha, IL-1beta, PAI-1, and tPA were measured simultaneously in blood and pleural fluid using an enzyme-linked immunosorbent assay in 33 patients with tuberculous and in 30 patients with malignant pleural effusions. Residual pleural thickening was measured and defined as a pleural thickness of >/= 10 mm found on chest radiographs at the completion of anti-TB chemotherapy in tuberculous pleurisy patients. RESULTS: In both groups, the levels of proinflammatory cytokines and fibrinolytic enzymes were significantly higher in pleural fluid than in blood. The levels of TNF-alpha and PAI-1 were significantly higher in tuberculous than in malignant effusions. In contrast, malignant pleural fluid had significantly higher values of tPA than did tuberculous pleural fluid. In tuberculous effusions, the values of PAI-1 and the PAI-1/tPA ratio correlated positively and the levels of tPA correlated negatively with those of TNF-alpha and IL-1beta. In malignant pleural fluid, positive correlations were found between the values of proinflammatory cytokines (TNF-alpha and IL-1beta) and PAI-1. Residual pleural thickening was found in 9 of 33 patients (27. 3%) with tuberculous pleurisy. The pleural fluid values of TNF-alpha, IL-1beta, and PAI-1 were significantly higher and the concentrations of tPA were significantly lower in tuberculous pleurisy patients with residual pleural thickening. CONCLUSIONS: Compared to malignant pleural effusion, fibrinolytic activity in pleural fluid was reduced in tuberculous effusion. Pleural inflammation caused by TB may enhance the release of proinflammatory cytokines, particularly TNF-alpha, which subsequently may increase PAI-1 and decrease tPA in pleural fluid. The imbalance of PAI-1 and tPA in pleural space may lead to fibrin deposition and pleural thickening.     

Role of pleural viscosity in the differential diagnosis of exudative pleural effusion

OBJECTIVE AND BACKGROUND: Determining the aetiology of an effusion involves assessing if it is an exudate or a transudate. However, a reliable test for determining the aetiology of a pleural effusion is lacking. Pleural viscosity has a high sensitivity and specificity and a high positive and negative predictive value for discriminating exudative and transudative pleural effusions. The aim of this study was to use pleural fluid viscosity to discriminate between various aetiologies of exudative effusions, namely malignant, parapneumonic and tuberculous. METHODS: Seventy consecutive patients (24 women, 46 men, mean age = 67 years) with exudative pleural effusion due to pneumoniae in 24 patients, tuberculous pleurisy in 21 and lung cancer in 25 were studied prospectively. Measurements of pleural fluid and plasma viscosity were performed using Brookfield DV-II viscometer. RESULTS: Pleural viscosity and pleural LDH were highest in the tuberculous pleurisy patients and lowest in the lung cancer patients. Pleural viscosity > or = 1.57 was found to be indicative of tuberculous pleurisy with a sensitivity of 100% and specificity of 95%. Pleural viscosity < 1.39 was found to be indicative of lung cancer with a sensitivity of 100% and specificity of 94%. Pleural viscosity was significantly correlated with pleural albumin (r = 0.34, P = 0.004), protein (r = 0.40, P = 0.001), LDH (r = 0.70, P < 0.001) and plasma viscosity (r = 0.44, P < 0.001), having the most significant value with pleural LDH. CONCLUSION: The pleural fluid viscosity of patients with parapneumonic, tuberculous and malignant effusions are significantly different from each other. Among these groups, tuberculous effusions had the highest viscosity, and malignant effusions from lung cancer the lowest.     

Simultaneous measurement of T-helper 1 cytokines in tuberculous pleural effusion.

OBJECTIVE: Tuberculosis, the leading cause of death among infectious diseases worldwide, is a major cause of lymphocytic exudative pleural effusion. T-helper 1 cytokines, including interferon-gamma (IFN-gamma), interleukin (IL)-12p40 and IL-18 are predominantly associated with cell-mediated immune responses, and play an important role in immunity to Mycobacterium tuberculosis. DESIGN: We studied 55 patients presenting with pleural effusion at the National Sanyo Hospital between April 2000 and September 2001 (42 men and 13 women; mean age 67 years). Twenty patients (36%) had tuberculous pleurisy, while 18 (33%) had malignant effusions and 17 (31%) had an effusion with another aetiology. Pleural fluid concentrations of IL-12p40 and IL-18 as well as IFN-gamma measured by enzyme-immunoassays. RESULTS: Concentrations of all three cytokines were significantly higher in tuberculous than other pleural effusions. Significant correlations were evident between IFN-gamma and IL-12. We found particularly high concentrations of IL-12p40 and IFN-gamma in tuberculous patients with high fever. CONCLUSION: The results indicate that T-helper 1 cytokines are involved in intrapulmonary cellular immune responses to M. tuberculosis, and suggest that the interactions between them may play an important role in the pathogenesis and severity of the pleural effusion. Understanding the development of this response may enhance our understanding of the pathogenesis of tuberculous pleural effusion and suggest new therapies.     

T-helper type 1/T-helper type 2 balance in malignant pleural effusions compared to tuberculous pleural effusions

STUDY OBJECTIVES: Malignant and tuberculous pleurisies are two major causes of lymphocyte-dominant pleurisy. Several studies have already reported that tuberculous pleurisy is a T-helper type 1(Th1)-dominant disease. In this study, we sought to examine the Th1/T-helper type 2 (Th2) balance, especially focusing on the polarizing status of T-cells to Th1/Th2 in malignant pleural effusions by measuring cytokines in pleural effusions and by evaluating the polarizing status of T-cells on the point of stimulation with interleukin (IL)-12 and/or IL-18. Furthermore, we evaluated inhibitors of interferon (IFN)-gamma production in effusions to rule out the possibility of direct inhibition of T-cell polarization. PATIENTS: Effusion samples were collected from 19 patients with malignant pleurisy caused by lung cancer and from 7 patients with tuberculous pleurisy. MEASUREMENTS: Concentrations of pleural fluid IFN-gamma, IL-12, and IL-4 were measured. IFN-gamma production of T-cells enriched from malignant pleural effusions in the presence of IL-12 and/or IL-18 was also examined. We further compared the inhibitory activity of malignant pleural effusions against IFN-gamma production and analyzed the expression of T-cell immunoglobulin mucin, mucin domain (Tim-3), a Th1-specific molecule in pleural fluid T-cells. RESULTS: Although malignant pleural effusions showed low levels of Th1 and Th2 cytokines and ratios of IFN-gamma and IL-12 to IL-4 were low, isolated T-cells produced a significant level of IFN-gamma in the presence of IL-12 and IL-18. Soluble factors were not found to inhibit IFN-gamma production in malignant pleural effusions. In tuberculous pleural effusion, ratios of IFN-gamma and IL-12 to IL-4 were significantly higher, and T-cells showed the expression of Tim-3 messenger RNA. CONCLUSIONS: We confirmed that T-cells in the malignant pleural effusions are mainly na?ve or not definitely polarized to Th1. Moreover, malignant tumor does not actively distort the cytokine condition through production of soluble inhibitors within effusions. The present study indicates that antitumor immunity may be enhanced by restored IFN-gamma activity through combination of IL-12 and IL-18, and that it will lead to new therapies for malignant effusion.     

胸水ADA、TB-DNA联合检测在结核性胸膜炎中的诊断运用

目的分析胸水ADA、TB-DNA联合检测对结核性胸膜炎诊断运用价值。方法对我院收治的结核性胸膜炎患者183例、癌性胸水患者65例以及炎性胸水患者49例作为研究对象,分别进行ADA、TB-DNA的检测,并对ADA、TB-DNA在三种疾病中的阳性率以及对结核性胸膜炎的敏感度、特异性以及准确性进行分析。结果结核性胸膜炎患者的ADA含量(72.3±23.2 IU/L)明显高于炎性胸水患者(38.4±12.9 IU/L)以及癌性胸水患者(24.3±6.5 IU/L);ADA、TB-DNA联合检测对结核性胸膜炎的特异性84.2%,敏感性98.91%以及准确性为93.26%。结论对结核性胸膜炎患者采用胸水ADA、TB-DNA联合检测可明显提高其检出率,并有助于对结核性胸膜炎胸水、癌性胸水以及炎性胸水的鉴别。     

Use of pleural fluid C-reactive protein in diagnosis of pleural effusions

The aims of the study were to assess whether C-reactive protein (CRP) is a sensitive marker for discriminating between transudative and exudative and pleural effusions to evaluate whether it can be used to distinguish inflammatory pleural effusions from other types of effusion. Pleural fluid and serum CRP levels were obtained in 97 patients with pleural effusion, using an immunoturbidimetric method (Olympus AU-600 autoanalyser). We compared CRP levels between transudates and exudates, inflammatory effusions and other types of effusion. According to the criteria used, 16 patients were included in the transudate group and 81 patients in the exudate group. Pleural fluid CRP levels were significantly lower in the transudate group (P<0.04; 14.9 +/- 4.9 mg l(-1) and 35.5 +/- 4.9 mg l(-1) respectively). Also, the ratio of pleural fluid to serum was significantly lower in the transudate group (P<0.009; 0.8 +/- 0.5 mg l(-1) and 2.8 +/- 0.7 mg l(-1), respectively). In the exudate group, 35 patients had neoplastic effusions, 10 chronic non-specific pleurisy, 19 tuberculous pleurisy, 16 parapneumonic effusion and one Dressler Syndrome. When these sub-groups were compared, the parapneumonic effusion subgroup CRP levels (mean 89 +/- 16.3 mg l(-1)) were significantly higher than those in the other subgroups, other exudate of neoplastic effusion, tuberculous pleurisy and chronic non-specific effusion and the transudate group (P<0.0001; P<0.0001; P<0.0004 and P<0.0001, respectively). The ratio between pleural fluid and serum CRP was significantly higher in the parapneumonic effusion subgroup than in the neoplastic subgroup (P<0.0002; 6.6 +/- 2.7 mg l(-1) and 1 +/- 0.2 mg l(-1), respectively). Pleural fluid CRP levels > 30 mg l(-1) had a high sensitivity (93.7%) and specificity (76.5%) and a positive predictive value of 98.4%. In the differential diagnosis of pleural effusions, higher CRP levels may prove to be a rapid, practical and accurate method of differentiating parapneumonic effusions from other exudate types. Although the high level of CRP obtained in the exudate group may be due to the number of patients with parapneumonic effusion who were included, the pleural CRP level may also be helpful in discriminating between exudative and transudative pleural effusions.     

Transforming growth factor beta-1 level in pleural effusion

OBJECTIVE: Transforming growth factor-beta1 is an important immunomodulator. The diagnostic role of TGF-beta1 has not been systematically investigated in pleural effusion. METHODOLOGY: A prospective clinical study of 45 patients (23 men, 22 women; mean age 49 +/- 21 years) with pleural effusion was performed. Of these patients, 19 had malignant pleural effusion, 14 had tuberculous pleural effusion, seven had empyema/parapneumonic pleural effusion, and five had transudative pleural effusion due to congestive heart failure. The concentrations of TGF-beta1 were measured by ELISA in all pleural fluid samples and in serum samples only from patients with malignant and tuberculous pleural effusions. RESULTS: The median TGF-beta1 levels of malignant, tuberculous and empyema/parapneumonic pleural effusions were 7.25 ng/mL, 7.81 ng/mL, and 9.75 ng/mL, respectively. There was no significant difference between them. The median TGF-beta1 level was 5.62 ng/mL in the transudate pleural effusion group and it was significantly lower than that in the empyema/parapneumonic group (P < 0.05). The pleural fluid TGF-beta1 levels did not correlate with cell profiles of the pleural fluid. The median serum TGF-beta1 levels in malignant and tuberculous pleural effusion groups were 7.38 ng/mL and 7.38 ng/mL, respectively. There was no significant difference between the levels of TGF-beta1 in paired samples of serum and pleural fluid. CONCLUSIONS: This study shows that TGF-beta1 concentrations in exudative pleural effusions are higher than those in transudative effusions secondary to congestive heart failure but TGF-beta1 concentrations do not assist in differentiating exudative effusions.     

检测血清和胸液E—选择素对鉴别良恶性疾病的意义

目的 通过检测结核性胸膜炎及癌性胸液患血清及胸液的Ｅ－选择素水平，探讨其对鉴别良恶性疾病的意义。方法 采用酶联免疫吸附法（ＥＬＩＳＡ）检测２５例结核性胸膜炎及２１例癌性胸液患血清及胸液的Ｅ－选择素水平。结果 结核性胸膜炎患血清Ｅ－选择素水平为４４±５μｇ／Ｌ、胸液Ｅ－选择素水平２４±３μｇ／Ｌ。明显高于癌性胸液患血清（２７±４μｇ／Ｌ）及胸液（１１±３μｇ＋Ｌ），且重叠性很小。此外，结核性     

High level of interferon gamma in tuberculous pleural effusion

It has been observed that T-lymphocytes of patients with tuberculosis produce interferon gamma (IFN gamma) in vitro. Based on this idea, we studied IFN gamma in pleural fluid and serum. We studied 80 patients with pleural effusion; 30 patients with tuberculous pleurisy had high IFN gamma concentrations in pleural fluid. Patients with malignant pleural effusions, nonspecific pleural effusion, parapneumonic effusions and pleural transudates had low levels. The IFN gamma levels were higher in those with massive tuberculous effusion and apparent pulmonary lesion on x-ray film. We found that the T4/T8 lymphocyte ratio was higher in pleural fluid than in peripheral blood. Numbers of T3 and T4 lymphocytes were higher in tuberculous pleural effusions compared with those in other patients. There is no correlation between IFN gamma levels and lymphocyte subsets in pleural effusion. Perhaps pleural T-lymphocytes produce IFN gamma after stimulation by mycobacterial antigens and this lymphokine activates macrophages, increasing their bactericidal activity against Mycobacterium tuberculosis.     

Elevated soluble CD26 levels in patients with tuberculous pleurisy.

SETTING: Several reports have shown that tuberculous infection elicits a Th1-like immune response with increased levels of IFN-gamma. Recently, expression of CD26 on CD4+ lymphocytes has been shown to correlate with the production of Th1-like cytokines. We therefore hypothesized that CD26 expression might increase in tuberculous pleural effusion, and might thus be a possible marker for detecting tuberculous pleurisy. OBJECTIVE AND DESIGN: To test this hypothesis, we measured soluble CD26 levels in the serum and pleural fluid of patients with tuberculous pleurisy (TB; n = 13), carcinomatous pleurisy (CA, n = 17), empyema (EM, n = 6), and congestive heart failure (HF, n = 10). RESULTS: The pleural CD26 levels, but not the serum CD26 levels, in patients with tuberculous pleurisy were significantly higher than those in other groups, and were correlated with levels of adenosine deaminase and interferon-gamma in the tuberculous pleural effusion. Furthermore, when the cut-off value for p-CD26 was set at 544.5 ng/ml, the positive rate for the TB group was significantly higher than that for the CA, EM and HF groups (P < 0.05). CONCLUSION: These results suggest that elevation of soluble CD26 in pleural fluid is implicated in Th1-like immune response, and may be a useful marker for tuberculous pleurisy.     

胸液Cyfra21-1测定对结核性和癌性胸腔积液鉴别诊断的价值

目的为评价Ｃｙｆｒａ２１－１对癌性胸液的诊断价值。方法采用ＥＬＩＳＡ方法测定３０例结核性胸液和３０例癌性胸液患者胸液中的Ｃｙｆｒａ２１－１含量。结果Ｃｙｆｒａ２１－１临界值为≤１４．２３ｎｇ／ｍｌ。当特异性为９０％时,诊断癌性胸液的敏感性７３．３３％。结论胸液Ｃｙｆｒａ２１－１的检测对癌性胸腔积液的鉴别诊断有着重要的意义。     

Vasoactive mediators (VEGF and TNF-alpha) in patients with malignant and tuberculous pleural effusions

OBJECTIVE: Vascular endothelial growth factor (VEGF) is a potent endothelial cell-specific mitogen that promotes angiogenesis, vascular hyperpermeability, and vasodilatation by autocrine mechanisms involving nitric oxide (NO). This study was undertaken to determine the potential role of VEGF in the pathogenesis of pleural effusions, and its relationship with tumour necrosis factor (TNF)-alpha and NO in the pleural fluid and serum of patients with tuberculous and malignant pleural effusions. METHODOLOGY: Pleural fluid and serum (SE) VEGF, TNF-alpha and NO levels were measured in 30 patients with exudative pleural effusion (15 with malignancies and 15 with tuberculosis). Control pleural fluid was obtained from 10 patients with transudative pleural effusion due to congestive heart failure and control serum samples were obtained from 10 healthy individuals. VEGF and TNF-alpha were measured by enzyme-linked immunosorbent assay and NO by a colorimetric method. Pleural biopsy, cytology or microbiological methods were used to make the final diagnosis. RESULTS: In patients with exudative pleural effusions, the mean pleural fluid and serum VEGF levels and their ratios (P < 0.0001 for all) and TNF-alpha levels (P < 0.01, P < 0.0001 and P < 0.05) were significantly elevated compared to those with transudative pleural effusion. In malignant effusions, pleural fluid and serum VEGF levels were significantly elevated (P < 0.001 and P < 0.0001) while pleural fluid, and serum levels and their ratios of TNF-alpha (P < 0.001, P < 0.01 and P < 0.05) were significantly lower than those in tuberculosis. NO levels did not distinguish between tuberculous and malignant effusions. CONCLUSIONS: In patients with malignant pleural effusions, levels of VEGF were significantly higher, while levels of TNF-alpha were significantly lower, than in patients with tuberculous effusions. In malignant pleural effusions, the elevated pleural fluid levels of VEGF and TNF-alpha are noteworthy. Our data support the hypothesis that blockade of VEGF, might benefit cancer patients with recurrent ascites or pleural fluid accumulation.     

降钙素原与CA125联合检测对结核性胸腔积液的诊断价值

目的探讨联合检测血清和胸腔积液降钙素原(PCT)、CA125对结核性胸腔积液的诊断价值。方法 30例结核性胸腔积液、20例肺炎旁积液、30例恶性胸腔积液,采用化学发光法测定血浆和胸腔积液中的PCT水平,快速发光免疫分析测定CA125的水平。结果结核组、肺炎组血清PCT水平差异无统计学意义(P>0.05),结核组和肺炎组胸腔积液中PCT的表达均较对照组明显升高(均P<0.05)。结核组和恶性组血清及胸腔积液中CA125水平较肺炎组显著升高(P<0.01)。结论联合检测血清及胸腔积液中PCT与CA125水平可提高结核性胸腔积液诊断的敏感性和特异性。     

基因芯片技术检测分枝杆菌和IFN-γ测定对结核性胸膜炎的诊断价值

目的探讨胸腔积液中基因芯片技术检测分枝杆菌和IFN-γ测定对结核性胸膜炎的诊断价值。方法选择2013年9月至2016年11月就诊的260例胸腔积液患者为研究对象,结核性胸腔积液(TPE)组120例,非结核性胸腔积液组140例,其中恶性胸腔积液72例,类肺炎性胸腔积液68例。检测各组患者胸腔积液中IFN-γ水平,并应用基因芯片法行胸腔积液分枝杆菌菌种鉴定,绘制受试者工作特征(ROC)曲线,根据敏感度、特异度和准确度等指标评价其对结核性胸膜炎的诊断价值。结果TPE组胸腔积液IFN-γ水平明显高于其他组,组间比较具有统计学差异(P<0.05)。诊断结核性胸膜炎的ROC曲线下面积(AUC)为0.98,敏感度为78.2%,特异度为94.4%。结论胸腔积液中IFN-γ检测可作为鉴别结核性胸膜炎的一种免疫生物学标志物,但基因芯片法行胸腔积液分枝杆菌菌种鉴定对结核性胸膜炎的诊断价值不大,不建议临床推广应用。     

胸水M1/M2型巨噬细胞比例在结核性胸膜炎与恶性胸腔积液鉴别中的价值

目的探讨巨噬细胞极化在结核性胸膜炎与恶性胸腔积液鉴别中的价值。方法前瞻性收集2018年10月至2019年9月到我院就诊的新发结核性胸膜炎或恶性胸腔积液患者,在治疗前采集胸腔积液与外周血,流式细胞术检测M1型(CD14^+CD86^+)与M2型(CD14^+CD163^+)单核巨噬细胞。并测定外周血细胞计数、血沉、γ-干扰素释放试验及胸腔积液腺苷脱氨酶。结果纳入结核组51例,肿瘤组39例。结核组外周血CD14^+巨噬细胞高于肿瘤组,胸水M1型巨噬细胞高于肿瘤组,M2型巨噬细胞低于肿瘤组(P<0.05)。胸水M1/M2>0.92诊断结核性胸膜炎的敏感性86.3%,特异性94.6%,阳性预测值86.3%,阴性预测值81.7%(曲线下面积0.946)。结论结核性胸水中巨噬细胞向M1极化,恶性胸水巨噬细胞向M2极化,胸水M1/M2>0.92可作为结核性胸膜炎与恶性胸水鉴别的免疫学指标。     

结核性和恶性胸膜炎患者VEGF的水平及意义

目的 通过检测结核性胸膜炎及恶性胸膜炎患者血清和胸水中血管内皮生长因子（VEGF）含量,分析VEGF在两组患者血清、胸水中的差异,探讨VEGF在二者中的意义和诊断价值.方法 对确诊结核性胸膜炎和恶性胸膜炎各30例的患者在同一日留取胸水标本10 ml及静脉血5 ml,采用双抗体夹心酶联免疫吸附试验检测患者胸水及血清中VEGF水平,分析其差异及相关性.结果 结核组血清和胸水VEGF检测值分别为（45.33±18.33） ng/L、（62.73±24.65） ng/L;恶性组血清和胸水VEGF检测值分别为（66.00±29.83） ng/L、（95.54±42.11） ng/L;恶性组血清及胸水中VEGF含量均高于结核组（t值分别为3.9、5.2,P值均＜0.05）.VEGF在两组的血清和胸水中均呈正相关性（r值分别为0.53、0.38,P值均＜0.05）.结论 在结核性胸膜炎及恶性胸膜炎患者血清、胸水中VEGF水平有差异,恶性高于结核性;两组患者胸水中VEGF含量均高于血清,胸水VEGF含量随着血清VEGF含量增高而增高.检测胸腔积液患者血清和胸水中VEGF含量对结核性胸膜炎和恶性胸膜炎的诊断和鉴别诊断有一定的价值.     

胸腔积液中IL-27及Gene Xpert MTB/RIF联合检测有助于结核性胸膜炎的快速诊断

目的：观察胸腔积液中白介素-27（IL-27）、结核杆菌利福平耐药基因（Gene Xpert MTB/RIF）表达水平在结核性胸膜炎快速诊断中的应用价值。方法：回顾性分析128例结核性胸膜炎患者的临床资料，另选择同期收治的128例非结核性胸膜炎胸腔积液患者为对照（恶性胸腔积液组、类肺炎性胸腔积液组与漏出性胸腔积液组分别61例、36例与31例），采用酶联免疫吸附法检测患者胸腔积液中IL-27水平，并予以Gene Xpert MTB/RIF试验，以临床综合诊断结果为金标准，评估IL-27、Gene Xpert MTB/RIF水平在结核性胸膜炎诊断中的应用价值。结果：结核性胸膜炎组胸腔积液中IL-27水平显著高于恶性胸腔积液组、类肺炎性胸腔积液组与漏出性胸腔积液组（F=112.944，P均<0.05）；IL-27诊断结核性胸膜炎的AUC值为0.875，敏感度为73.43%、特异性为85.16%；Gene Xpert MTB/RIF诊断结核性胸膜炎敏感度、特异性分别为77.34%、100.00%；两者联合诊断结核性胸膜炎的敏感度为86.72%，特异性为100.00%。结论：胸腔积液中IL-27、Gene Xpert MTB/RIF水平对结核性胸膜炎的诊断有一定意义，联合检测有助于结核性胸膜炎的诊断。     

The management of pleural space infections

Pleural infection is responsible for significant morbidity and mortality worldwide, and its clinical management is challenging. The diagnosis of empyema and tuberculous pleurisy may be difficult, and these conditions may be confused with other causes of exudative pleural effusions. Complicated parapneumonic effusion or empyema may present with 'atypical' clinical features; delays in diagnosis are common and may contribute to the high mortality of these infections. Pleural aspiration is the key diagnostic step; pleural fluid that is purulent or that has a pH < 7.2, or organisms on Gram stain or culture, is an indication for formal intercostal drainage. In order to achieve a definitive diagnosis of tuberculous pleurisy, Mycobacterium tuberculosis must be isolated in the culture of pleural fluid, pleural tissue or sputum; demonstration of granulomas in pleural tissue is also suggestive of tuberculosis. The use of pleural fluid biochemical markers, such as adenosine deaminase, in the diagnosis of tuberculous pleurisy varies among clinicians; the diagnostic value of such markers is affected by the background prevalence of tuberculosis and the likelihood of an alternative diagnosis. Uncertainties also remain regarding the treatment of pleural infection. Treatment of complicated parapneumonic effusion and empyema involves prolonged courses of antibiotics and attention to the patient's nutritional state. The role of intrapleural fibrinolytics and the optimal timing of surgical intervention are unknown. The lack of clear predictors of clinical outcome in empyema contributes to the difficulty in treating this condition. The pharmacological treatment of tuberculous pleurisy is the same as for pulmonary tuberculosis; the precise role of steroids in the treatment of tuberculous pleurisy remains uncertain.