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1.
The aim of this study was to assess the expression of several metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in exudative pleural effusions, and their relationship with inflammatory and fibrinolytic mediators in parapneumonic effusions. The study included 51 parapneumonic effusions (30 empyema or complicated parapneumonic, 21 noncomplicated parapneumonic), 28 tuberculous, 30 malignant and 30 transudates. Inflammatory markers (tumour necrosis factor-alpha, interleukin-8, polymorphonuclear elastase), fibrinolytic system variables (tissue plasminogen activator (PA), urokinase PA (u-PA), plasminogen activation inhibitor (PAI)-1, PAI-2), and several MMPs (MMP-1, MMP-2, MMP-8, MMP-9) and TIMPs (TIMP-1, TIMP-2) were determined by ELISA in plasma and pleural fluid. Elevated MMP-2 and TIMP-1 concentrations were observed in all the pleural fluid samples studied. The group of empyema or complicated parapneumonic effusions showed higher MMP-1, MMP-8 and MMP-9 concentrations than the remaining exudates. There was no correlation between MMP and TIMP levels in plasma and pleural fluid in this group of effusions. In parapneumonic effusions, MMP-1, MMP-8 and MMP-9 showed a positive correlation with the inflammatory markers and with u-PA and PAI-1. Moreover, there was a relationship between MMP-8 concentration in pleural fluid and pleural thickening at the end of treatment. In conclusion, elevated metalloproteinase-1, -8 and -9 expression was found in parapneumonic pleural effusions. These metalloproteinases could be implicated in the local inflammatory response existing in this group of effusions.  相似文献   

2.
目的 探讨基质金属蛋白酶9(MMP-9)、基质金属蛋白酶组织抑制物1(TIMP-1)及MMP-9/TIMP-1比值在结核性和仲瘤性胸腔积液形成过程中的作用及在上述胸腔积液诊断和鉴别诊断中的价值.方法 采用ELISA法测定36例结核性胸膜炎、38例恶性肿瘤和14例漏出液患者胸水中MMP-9和TIMP-1的浓度.结果 ①结核性胸腔积液组胸水中MMP-9浓度、TIMP-1浓度和MMP-9/TIMP-1比值均高于恶性胸腔积液组和漏出液组(P值均<0.05),恶性胸腔积液组上述指标均高于漏出液组(P值均<0.05).②恶性胸水脱落细胞学检查阳性组MMP-9浓度、MMP-9/TIMP-1 均高于细胞学检查阴性组(P值均<0.05),TIMP-1浓度低于细胞学检查阴性组(P<0.05).③MMP-9和TIMP-1之间呈正相关(r=0.239,P=0.025);MMP-9、MMP-9/TIMP-1分别与胸水乳酸脱氢酶、腺苷脱氨酶、蛋白质、白细胞总数、淋巴细胞比例之间显著正相关(P值均<0.01);MMP-9、MMP-9/TIMP-1分别与胸水葡萄糖、氯化物之间呈显著负相关(P值均<0.01);TIMP-1与乳酸脱氢酶、腺苷脱氨酶、蛋白质、淋巴细胞比例之间呈显著正相关(P值均<0.01).④胸水中MMP9、TIMP-1、MMP-9/TIMP-1比值在恶性胸腔积液诊断中的敏感性分别为63.2%、71.1%和65.8%,特异性分别为83.3%、63.9%和80.6%.采用胸水MMP-9和TIMP-1串联联合检测的敏感性和特异性分别为39.5%和91.7%,并联联合检测的敏感性和特异性分别为94.7%和55.6$%.结论 MMP-9和TIMP-1与结核性胸膜炎和恶性胸腔积液的形成密切相关,MMP-9/TIMP-1比例的失衡在此过程中扮演了重要角色,胸水MMP-9、TIMP-1及MMP-9/TIMP-1比值的检测有助于结核性胸膜炎和恶性肿瘤所致胸腔积液的鉴别诊断.  相似文献   

3.
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.  相似文献   

4.
High level of interferon gamma in tuberculous pleural effusion   总被引:6,自引:0,他引:6  
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.  相似文献   

5.
Liu CL  Hsieh WY  Wu CL  Kuo HT  Lu YT 《Respiratory medicine》2007,101(5):903-909
BACKGROUND: Triggering receptor expressed on myeloid cells (TREM)-1 is a recently described molecule that plays an important role in myeloid cell-activated inflammatory responses. The aim of this study was to investigate the expression of TREM-1 in pleural effusions of various causes. METHODS: For this cross-sectional, observational study conducted between February and August 2005 in Taiwan, 74 patients with pleural effusions of varying etiology were investigated. Soluble TREM-1 (sTREM-1) was measured in pleural fluid samples, and cells in the fluid were assessed for surface expression of TREM-1. RESULTS: Concentrations of sTREM-1 were significantly higher in infectious and neoplastic pleural effusions (189.1+/-36.7 and 69.9+/-22.8ng/ml, mean+/-sem) than in transudates (10.1+/-5.3ng/ml; P<0.001). Among infectious effusions, the sTREM-1 levels were significantly higher in parapneumonic than in tuberculous effusions (301.8+/-49.8 vs. 38.9+/-17.3ng/ml; P<0.001). TREM-1 was expressed on a portion of the myeloid (CD11b positive) cells in each type of effusion, without significant differences among them (transudative, 34.7%; neoplastic, 36.0%; parapneumonic, 27.7%; tuberculous, 21.2%; P=0.861). Non-myeloid cells expressed very little TREM-1 (transudative, 6.3%; neoplastic, 0.5%; parapneumonic, 1.0%; tuberculous, 0.7%; P=0.192). CONCLUSIONS: sTREM-1 expression in pleural fluids is highest in parapneumonic and neoplastic effusions but low in transudates. In infectious effusions, a high concentration of sTREM-1 may exclude tuberculous pleurisy.  相似文献   

6.
OBJECTIVE: Matrix metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP) have been found in high concentrations in pleural effusions. Because MMP and TIMP may play a part in the causation of the fibrosis seen in tuberculous (TB) pleuritis their occurrence was examined. DESIGN: Pleural effusion fluid and plasma concentrations of MMP-1, MMP-2, MMP-3, MMP-8, MMP-9, TIMP-1 and TIMP-2 were determined by ELISA in 21 patients with TB pleuritis. To adjust for the total protein content, respective ratios were calculated. Activities of MMP-2 and MMP-9 were measured by gelatine zymography and the MMP-9/MMP-2 ratios calculated. Pleural effusions and plasma of 15 patients with congestive heat failure (CHF) and plasma of 15 healthy persons (CON) served as controls. RESULTS: Immunoreactive pleural fluid concentrations of MMP-1, MMP-2, MMP-8, and MMP-9 were higher in TB compared to CHF, but plasma concentrations were not different between the groups. TB pleural fluid concentrations of MMP-1, MMP-2, TIMP-1, and TIMP-2 were higher compared to TB plasma. MMP-3 was found in trace amounts only. The MMP-9/total protein ratios in pleural fluid were higher in TB compared to CHF (0.4492+/-0.1633 vs 0.0364+/-0.0145, P<0.005) but the TIMP-1 ratios were lower (139.0+/-28.7 vs 517.8+/-183.7, P<0.0005). In TB pleural fluid vs TB plasma, the respective MMP-1, MMP-2, TIMP-1, and TIMP-2 ratios were increased (0.46+/-0.10 vs 0.17+/-0.02; 25.2+/-2.8 vs 4.2+/-0.9; 139.0+/-28.7 vs 27.8+/-8.2; 0.67+/-0.13 vs 0.18+/-0.04, P<0.0005 each). Gelatine zymography demonstrated MMP-2 and MMP-9 bands of different brightness in TB effusions but in CHF effusions the MMP-9 band was barely visible. The MMP-9/MMP-2 effusion ratios were therefore higher in TB compared to CHF (0.46+/-0.15 vs 0.05+/-0.04, P<0.0005). CONCLUSION: Compartmentalized MMP-1, MMP-2, TIMP-1, and TIMP-2 and, compared to CHF, a surplus of MMP-1, MMP-2, MMP-8, and MMP-9 in the pleural space obviously contribute to the fibrotic reactions in TB pleuritis.  相似文献   

7.
OBJECTIVE: To determine whether measurement of the complement activation products SC5b-9 and C3a-desArg in pleural fluid can reliably differentiate tuberculous from malignant pleural effusions. DESIGN: Twenty-four patients with tuberculous pleuritis, 29 with malignant pleural effusion, and 30 control subjects with transudates were enrolled in the study. SCSb-9 and C3a-desArg were measured in pleural fluid using commercial ELISA tests, and their performances were evaluated using receiver operating characteristic (ROC) analysis. RESULTS: Patients with tuberculous pleuritis had higher mean levels of pleural SC5b-9 (5052 microg/L) and C3a-desArg (7436 microg/L) than those with malignant effusions (1048 and 2835 microg/L, respectively), whereas only SC5b-9 concentrations in the latter were comparable with controls. The area under the ROC curve (AUC) was 0.84 for SC5b-9 and 0.81 for C3a-desArg. Pleural SC5b-9 showed an accuracy of 80.8%, compared with 78.8% for C3a-desArg, when cut-off points of 1500 and 4500 microg/L, respectively, were used. Using a stepwise logistic regression model, the combination of pleural SCSb-9 > or =1500 microg/L, age < or =35 years, and pleural monocyte percentage > or =90% provided the highest accuracy for tuberculous pleurisy (88.5%, AUC 0.95). CONCLUSION: This pilot study suggests that pleural SC5b-9 is clinically useful for differentiating tuberculous and malignant pleural effusions.  相似文献   

8.
Background: The alteration of Th1 and Th2 cytokine levels is the subject of controversy in pleural effusions caused by malignancy, a situation that favors a Th2 immune response. Objective: To examine the different levels of IL-4 and IL-10 (Th2 cytokines), and IL-2 and interferon-γ (IFN-γ) (Th1 cytokines) in malignant and non-malignant pleural effusions. Method: The cytokine levels in pleural fluid of 62 patients with malignant pleural effusion (44 with lung cancer and 18 with extrathoracic tumors), 8 with tuberculous and 8 with congestive heart failure pleural effusion were analyzed using enzyme-linked immunosorbent assays. Results: IL-2 was below the detectable concentration of the assay. A significant decrease in IFN-γ level was observed in malignant but not in congestive heart failure cases compared to tuberculous cases. IL-10 levels were higher in malignant and tuberculous pleural effusions than in congestive heart failure pleural effusions, however, this difference did not reach the significant level. IL-4 levels were also increased non-significantly in lung cancer pleural effusions compared to the other groups. Conclusion: Our results show a wide variation in IL-4, IL-10, and IFN-γ levels in malignant pleural effusions, a pattern which was not convincing enough to differentiate the cause of effusion.  相似文献   

9.
OBJECTIVE: We aimed to investigate adenosine deaminase (ADA) activity and the activities of its ADA1 and ADA2 isoenzymes in pleural effusions and also sera with different aetiological origins. METHODOLOGY: The pleural effusions of 87 patients were examined. The patients were separated into four groups: transudates, parapneumonic, malignant, and tuberculous effusions. The cases were also designated as tuberculous or non-tuberculous group. Adenosine deaminase activity was determined by the colorimetric method described by Giusti and Galanti. RESULTS: The intermean differences were statistically significant for total ADA, ADA1 and ADA2, except for pleural fluid ADA1 in the malignant group when compared to the tuberculous effusion group. The intermean differences between the tuberculous and non-tuberculous group were statistically significant for all three parameters except for pleural fluid and serum ADA1 activity. The sensitivities of total ADA, ADA1 and ADA2 activities for tuberculosis were 91, 57 and 93%, respectively; their specificities 89, 88 and 92%, respectively; their positive predictive values 82, 70 and 86%; and their diagnostic accuracies 89, 76 and 92%, respectively, in pleural fluid. CONCLUSIONS: Determination of ADA and its isoenzymes can help to differentiate the causes of pleural effusion. Increased ADA2 activity is a striking marker of tuberculous effusions. In contrast, increased ADA1 activity was significantly elevated in parapneumonic effusions.  相似文献   

10.
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.  相似文献   

11.
Matrix metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP) have been found by ELISA and gelatine zymography in different concentrations in pleural fluid in tuberculous (TB) pleuritis. For further differentiation MMP and TIMP were localized in pleural biopsies by immunhistochemical staining with antibodies directed against MMP-1, MMP-2, MMP-3, MMP-9, TIMP-1, and TIMP-2 using the Labelled-Avidin-Biotin (LAB). Immunohistological reactivity of MMP-1 was found in epitheloidcellular histiocytes, Langhans' giant cells, lymphocytes, macrophages, as well as in fibroblasts of granulomatous reactions. MMP-2 was found in a few epitheloid cellular histiocytes, fibroblasts, and inflammatory cells. MMP-3 was weakly positive in a few lymphocytes only. MMP-9 was found in a few fibroblasts, epitheloid cells, and inflammatory cells, foremost, however, in pleural mesothial cells. A few fibroblasts only showed immunoreactivity of TIMP-1 and TIMP-2. The observed inhomogenous staining pattern could be explained by the different state of activation of individual cellular units. In conclusion, the immunohistochemical demonstration of MMP and TIMP in pleural cells and tissue structures indicates their local involvement in fibrosing reactions in TB-pleuritis.  相似文献   

12.
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.  相似文献   

13.
Acute-phase markers, such as C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-alpha), have been studied in inflammatory and malignant disorders. We examined the diagnostic value of these markers for the differentiation among parapneumonic, tuberculous and malignant effusions. We studied 124 patients with pleural effusions, classified as exudates [total (n=97), parapneumonic (n=15), tuberculous (n=25), malignant (n=57)] and transudates due to congestive heart failure (n=27). CRP, IL-6 and TNF-alpha were measured in pleural fluid and serum. Pleural fluid CRP was higher in parapneumonic compared to tuberculous and malignant effusions, providing 100% sensitivity for a cut-off point of 5.3mg/dL. IL-6 was higher in both parapneumonic and tuberculous compared to malignant effusions. TNF-alpha was higher in tuberculous compared to malignant effusions, providing 96.0% sensitivity, and 93.0% specificity for a cut-off point of 88.1 pg/mL. Pleural fluid CRP levels were lower than serum in all groups, probably reflecting systemic inflammation, whereas IL-6 and TNF-alpha were higher in pleural fluid indicating local production. Our data suggest that these markers may provide useful information for the differentiation of infectious and malignant effusions in clinical practice. However, further studies are needed for the validation of these findings in usual clinical circumstances.  相似文献   

14.
Hua CC  Chang LC  Chen YC  Chang SC 《Chest》1999,116(5):1292-1296
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.  相似文献   

15.
N Hara  M Abe  S Inuzuka  Y Kawarada  N Shigematsu 《Chest》1992,102(4):1060-1064
A monoclonal antibody against soluble phase-terminal complement complex (SC5b-9) was used to try to differentiate pleural effusions of tuberculous vs malignant and other origin. Effusions of tuberculous origin showed a significantly higher SC5b-9 level than did plasma, suggesting activation of complement in the pleural space. All 26 patients with tuberculous effusions showed SC5b-9 levels in pleural fluid exceeding 2.0 mg/L, while 20 with malignant effusions had levels less than 2.0 mg/L. However, rheumatoid, some parapneumonic, and treated malignant effusions showed SC5b-9 levels above 2.0 mg/L. Considering a value exceeding 2.0 mg/L, the specificity and sensitivity of the SC5b-9 estimation in tuberculosis were 0.74 and 1.0, respectively. The mean values for C4d and Bb fragments of complement were significantly (p < 0.05) higher in the tuberculous than in the malignant effusions. However, the values for Bb in 16 (62 percent) of the 26 patients with tuberculous or malignant effusions were in the same range. The activity of adenosine deaminase (ADA) was higher in the tuberculous than in the malignant effusions. While 18 of 26 patients with tuberculous effusions showed an ADA value exceeding 50 mU/ml, the estimated cutoff point (sensitivity = 0.69), 35 of the 36 nontuberculous effusions showed a true negative value (specificity = 0.97). A correlation between ADA and SC5b-9 values was observed in pleural effusions. These observations suggest that the estimation of SC5b-9 in pleural fluid presents a new approach to differentiating tuberculous vs malignant effusions.  相似文献   

16.
目的探讨细胞角质蛋白19片段(CYFRA21-1)与癌胚抗原(CEA)检测对结核性胸水与癌性胸水的鉴别诊断价值?方法对胸水患者108例(癌性68例?结核性40例)分别测定其血清?胸水中CYFRA21-1和CEA浓度?结果1.两种肿瘤标记物浓度在恶性胸水中明显高于结核性胸水;2.癌性胸水中CYFRA21-1浓度明显高于血清浓度,而胸水中CEA浓度与血清中浓度相比无显著性差异;3.胸水CYFRA21.1的检测结果存在一定的假阳性?结论联合检测CYFRA21-1与CEA对胸水良恶性的鉴别诊断有较高的临床价值?  相似文献   

17.
K Shimokata  H Saka  T Murate  Y Hasegawa  T Hasegawa 《Chest》1991,99(5):1103-1107
Tuberculous pleurisy is a good model for resolution of local cellular immunity. It would be expected that tuberculous pleural fluid contains a variety of immunologically important cytokines because of the accumulation of immunocompetent cells in the pleural cavity. We studied interleukin 1 (IL-1), interleukin 2 (IL-2), and interferon gamma (IFN-gamma) levels in pleural fluid of 20 patients with tuberculous pleurisy and compared them with those in pleural fluid of 20 patients with malignant pleurisy. We also evaluated adenosine deaminase (ADA) levels in both effusions. Tuberculous pleural fluid had higher levels of IL-1, IL-2, IFN-gamma, and ADA than malignant pleural fluid. Although the difference of IL-1 level between tuberculous and malignant pleural fluid was modest, that of IL-2, IFN-gamma, and ADA was dominant. These findings suggest that activated T lymphocytes in tuberculous pleural fluid concern the production of lymphokines at the morbid site and they effectively exert local cellular immunity through the action of such lymphokines.  相似文献   

18.
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 > 50%) 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 x 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 ADA1 and ADA2 were measured, and in all these cases (100%) ADA1/ADA(p) correctly classified these lymphocytic effusions as nontuberculous (ratio < 0.42). 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 < 40 IU x L(-1) virtually excluded a diagnosis of tuberculosis in lymphocytic pleural effusions. Adenosine deaminase1/adenosine deaminase(p) correctly classified all nontuberculous lymphocytic pleural effusions with high adenosine deaminase levels.  相似文献   

19.
The mesothelial lining of the pleura and malignant mesothelioma promote fibrin deposition in pleural injury or neoplasia via expression of tissue factor (TF). It was hypothesized that these cells might also regulate intrapleural coagulation by elaborating TF pathway inhibitor (TFPI). TFPI activity and antigen in pleural fluids were assayed from patients with congestive heart failure (CHF), pneumonia, empyema, metastatic pleural cancer and malignant mesothelioma. The authors also assessed expression of TF and TFPI messenger ribonucleic acid (mRNA) as well as TFPI activity and antigen by human pleural mesothelial cells, malignant mesothelioma cells (MS-1 cell line) and human lung fibroblasts. Immunohistochemical analyses of normal, fibrotic, and neoplastic pleura were performed to determine whether TFPI antigen was expressed in vivo. The study revealed that TFPI was present in transudates from patients with CHF and exudative pleural effusions from patients with pneumonia, empyema or pleural carcinoma. TFPI mRNA, activity and antigen were expressed by pleural mesothelial cells, MS-1 cells and lung fibroblasts. Cytokines and serum stimulated a significant early increase in TF mRNA levels with minimal enhancement of TFPI mRNA, activity and antigen levels. TFPI antigen was found in normal, fibrotic and neoplastic pleural tissues. The current observations indicate that tissue factor pathway inhibitor is locally expressed in pleural disease, but that it does not prevent the development of a prothrombotic environment favouring local fibrin deposition in pleural inflammation or cancer.  相似文献   

20.
We identified and characterized type IV collagenase and gelatinase activity in pleural fluid from 32 patients. The capacity to substantially degrade type IV collagen was demonstrated in every pleural sample. Comparable results were also noted for the degradation of a radiolabeled gelatin substrate. Gelatin gel zymography of the pleural fluids revealed two prominent zones of lysis at 66 kDa and 92 kDa. These were identified by specific polyclonal antibodies as human matrix metalloproteinases MMP-2 and MMP-9. The concentration of MMP-2 in pleural fluid, as measured by enzyme-linked immunoassay, averaged 1,622 ng/ml whereas those of MMP-9 were 210 ng/ml. Substrate degradation activity was compared in both serum and pleural fluid from three patients and found to be similar. In serum this enzymatic activity was primarily due to MMP-9 whereas in pleural fluid, the predominant gelatinase was MMP-2. This was confirmed by immunoassay that showed that MMP-2 levels were two to five times higher in pleural fluid than in serum. We conclude that substantial amounts of MMP-2 and, to a lesser degree, MMP-9 are present in pleural effusions. The bioactivity and the immunoactivity of these enzymes did not help to distinguish among pleural fluids characterized as transudates, nonmalignant exudates, or malignant exudates. The differences in the distribution of these enzymes in pleural fluid and blood suggest that their presence is not due simply to the ultrafiltration of plasma, but rather to synthesis by the resident cells at the pleural surfaces.  相似文献   

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