【摘要】 目的 采用循证医学的方法评价甘露聚糖肽联合顺铂对比单用顺铂治疗恶性胸腔积液的有效性和安全性。 方法 计算机检索中国生物医学文献数据库、中国期刊全文数据库、中文科技期刊全文数据库、万方数据库，收集甘露聚糖肽联合顺铂对比单用顺铂治疗恶性胸腔积液的随机对照试验，检索时间为各数据库建库至2011年3月。对文献进行质量评价，用RevMan 5.0软件对数据进行Meta分析。 结果 共纳入6项研究，所有文献质量均为C级。共收入388例患者，Meta分析结果显示甘露聚糖肽联合顺铂组与单用顺铂组相比，总有效率前者高于后者，差异有统计学意义（Plt;0.05）；消化道不良反应发生率两组组间差异无统计学意义（P=0.05）；骨髓抑制发生率前者低于后者，差异有统计学意义（Plt;0.05）；Karnofsky评分提高率前者高于后者，差异有统计学意义（Plt;0.05）。 结论 系统评价表明，甘露聚糖肽联合顺铂治疗恶性胸腔积液的疗效优于单用顺铂的方案。【Abstract】 Objective To assess the clinical efficacy and safety of mannatide plus cisplatin treating malignant pleural effusion. Methods Literatures were retrieved from CBM, VIP, CNKI, Wanfang databases by computer. Literatures were enrolled according to inclusion and exclusion criteria, and the quality of studies was evaluated according to the Cochrane Library handbook. The period duration of searching was between the establishment of the databases and March, 2011. Meta-analysis was conducted by RevMan 5.0 software. Results The meta-analysis of 6 included RCT, all ranked C, which involved 388 patients. The Meta-analysis showed that the total effective rate in mannatide plus cisplatin group significantly differed from that in cisplatin group (P＜0.05). There were no significant difference in the adverse reaction of digestive tract between the two intervention groups (P=0.05). The adverse reaction of marrow depression inmannatide plus cisplatin group was much lower than that in cisplatin group (P＜0.05). The increase of KPS in mannatide plus cisplatin group was higher than that in cisplatin group (P＜0.05). Conclusions The analysis indicates mannatide plus cisplatin has a better effect on malignant pleural effusion than single cisplatin. However, the reliability of this review is affected by poor quality of included studies, and large-scale randomized controlled trials of high quality are needed to confirm the conclusions above.
目的：探讨胸膜活检对胸腔积液病因诊断的价值。方法:对268例胸腔积液患者行经胸壁胸膜活检术。结果:268例患者共行胸膜活检289次，二次及以上活检者19例，获取胸膜组织244例，穿刺成功率91%，经病理检查有18例为正常胸膜组织，阳性诊断者为226例，阳性率92.6%（226/244），其病理诊断为结核104例（46%）、肿瘤54例（23.9%）、慢性炎症68例（30.1%）；发生并发症者19（6.6%），全部为气胸，肺压缩均小于30%，未做特殊处理数日后自行吸收。结论:从本组资料可以看出，经胸壁胸膜活检术对于胸腔积液的病因诊断具有非常好的效果，相比胸水涂片或病理检查具有更高的阳性率。因此经胸壁胸膜活检术由于它的简单、安全、高效等特点，目前在胸腔积液病因诊断方面仍是一项重要的手段。
Objective To investigate the expression of aquaporin-1（AQP-1） on pleura in rats with carrageenan-induced pleural effusion and explore the role of AQP-1 in effusion formation.Methods Fifty-six healthy Wistar rats were randomly divided into a normal control group and 6 pleuritis groups（6，12，24，36，48 and 72 h groups respectively）.The rat model of inflammatory pleurisy was induced by injecting l-Carrageenan into the pleural cavity.The expression of AQP-1 on pleura was detected with immunohistochemistry.The mRNA and protein expression of AQP-1 on visceral pleura and parietal pleura were measured by RT-PCR and Western blot assay respectively.The volume of pleural effusions were measured.Results The volume of pleural effusion was 2.10±0.22，4.10±0.15，4.40±0.36，3.20±0.27，2.60±0.18，0.12±0.02 mL in the 6，12，24，36，48 and 72 h pleuritis groups respectively.AQP-1 were mainly expressed on visceral and parietal pleural mesothelial cells and capillary endothelial cells，and significantly increased in all pleuritic rats The mRNA and protein expression of AQP-1 on parietal pleura increased after 6 h and reached peak level at 24 h in pleuritic groups.The mRNA and protein expression of AQP-1 on visceral pleura increased after 12 h and reached peak level at 24 h in pleuritic groups.The expression of AQP-1 on parietal pleura at 12 h and 24 h in pleuritic groups was correlated positively with the volume of pleural effusion（r=0.857，r=0.846，all Plt;0.01）.The expression of AQP-1 on visceral pleura at 24 h in pleuritic groups was positively correlated with the volume of pleural effusion（r=0.725，Plt;0.05）.Conclusion The expression of AQP-1 on pleura were increased in rats with e carrageenan-induced pleural effusion.AQP-1 may play a role in pleural fluid transportation in pleural effusion.
Objective To compare the effects of heparin versus urokinase injection intrapleurally in the management of pleural thickening and adhesion due to tuberculous exudative pleurisy. Methods Sixty patients with tuberculous pleurisy were allocated into three groups randomly. Sodium heparin ( heparin group) , urokinase ( urokinase group) , and 0. 9% saline ( control group) were intrapleurally injected respectively. The concentrations of fibrinogen and D-dimer in pleural effusion were measured before and after the injection. The duration of absorption and the total drainage volume of pleural effusion were recorded. The pleural thickness and adhesion were observed two months after the injection. Results In 72 hours after the intrapleural injection, the concentration of fibrinogen( g/L) in the pleural effusion was significantly increased in the heparin group( 1. 13 ±0. 44 vs 0. 34 ±0. 19, P lt; 0. 001) , and significantly decreased in the urokinase group( 0. 25 ±0. 16 vs 0. 38 ±0. 15, P lt; 0. 05) when compared with baseline. Concentrations of D-dimer in the pleural effusions were significantly higher than those at baseline in both the heparin group and the urokinase group( 57. 0 ±17. 6 vs 40. 0 ±15. 4, P lt; 0. 05; 74. 5 ±16. 4 vs 43. 8 ±14. 9, P lt; 0. 001) . There were no significant differences in the absorption duration of pleural effusion among the three groups( P gt;0. 05) . The total drainage volume of pleural effusion was higher in the heparin group and the urokinase group compared to the control group( P lt;0. 01) . And the total volume of pleural effusion was significantly higher in the heparin group and the urokinase group than that in the control group( 2863 mL and 2465 mL vs 1828 mL,P lt;0. 01) . Two months after the intervention, the pleura were thinner[ ( 1. 37 ±0. 82) mm and ( 1. 33 ±0. 85) mmvs ( 3. 06 ±1. 20) mm, P lt; 0. 01] and the incidence of pleural adhesion was significantly lower[ 15% and 20% vs 50% , P lt; 0. 05] in the heparin and the urokinase groups than those in the control group.Conclusion Intrapleural heparin has similar effects with urokinase for prevention pleural thickness andadhesion in tuberculous pleurisy with good availability and safety.
Objective To investigate the expression of aquaporin-1( AQP1 ) in visceral and parietal pleura in SD rats and to examine the effect of AQP1 on pleural fluid turnover. Methods Five groups( n = 24 ) of SD rats were randomly assigned to received intrapleural injection of dexamethasone,lipopolysaccharide, erythromycin, hypertonic saline and normal saline, respectively. The AQP1 protein in pleural was detected with immunohistochemistry. The mRNA expression of AQP1 under stimulations at different time points was measured by real time RT-PCR. Results AQP1 was immunolocalized predominantly to the microvessels and mesothelial cells of visceral and parietal pleura. The extent of AQP1expression in parietal pleura was less than that in visceral pleura[ ( 4. 14 ±1. 12) ×104 copy /μg vs ( 7. 43 ±2. 02) ×104 copy / μg, P lt;0. 05] . AQP1 expression increased at all phases in the dexamethasone group andthe hypertonic saline group, whereas decreased in the erythromycin group and the lipopolysaccharide group.Conclusion The stimulations of dexamethasone, lipopolysaccharide, erythromycin and hypertonic saline can significantly change the AQP1 expression in pleura, which indicate that AQP1 may contribute to the accumulation and clearance of pleuritic fluids.
【Abstract】Objective To explore the differential diagnostic value of major fibrinolytic parameters in pleural fluid. Methods Tissue-type plasminogen activator( t-PA) and plasminogen activator inhibitor-1( PAI-1) in pleural fluid at the first thoracentesis were measured with ELISA and D-dimer was measured with immunoturbidimetry. Results Eighty-four patients with pleural effusion were enrolled, among which 40 with malignant effusion, 33 with infectious effusion and 11 with transudative effusion. t-PA level was higher in malignant and transudative pleural fluid than that in infectious pleural fluid[ ( 52. 49 ±31. 46) ng /mL and ( 58. 12 ±23. 14) ng /mL vs ( 37. 39 ±22. 44) ng /mL, P lt; 0. 05] , but was not statistically different between malignant pleural fluid and transudative ( P gt; 0. 05) . PAI-1 level was higher in malignant and infectious pleural fluid than that in transudative [ ( 164. 86 ±150. 22) ng/mL and ( 232. 42 ±175. 77) ng/mL vs ( 46. 38 ±16. 13) ng/mL, P lt; 0. 01] , but was not statistically different between malignant and infectious pleural fluid( P gt;0. 05) . D-dimer levels in the three types of pleural fluid were significantly different, which was ( 23. 66 ±25. 18) mg/L, ( 6. 36 ±10. 87) mg/L and ( 66. 90 ±42. 17) mg/L in malignant, transudative and infectious pleural fluid, respectively. As single-item detection for malignant pleural fluid, the cutoff of t-PA was gt; 38. 7 ng/mL( area under ROC curve was 64. 0 ) , with sensitivity of 60. 0% , specificity of 63. 6%, positive predictive value of 66. 7%, negative predictive value of 56. 8% and accuracy of 61. 6% .The cutoff of D-dimer was lt; 27. 0 mg/L( area under ROC curve was 85. 5) , with sensitivity of 84. 8% ,specificity of 72. 5% , positive predictive value of 85. 3% , negative predictive value of 71. 8% and accuracy of78.1%. The sensitivity, specificity, positive predictive value, negative predictive value and accuracy of combined examination( t-PA + D-dimer) were 92. 5% , 60. 6% , 74. 0% , 87. 0% , 78. 1% , respectively.Conclusions The t-PA, PAI-1 and D-dimer levels are significantly different in the three types of pleural fluid. The detection of fibrinolytic parameters in pleural fluid, especially the value of D-dimer,may be helpful in the differential diagnosis of pleural effusion.
Objective To investigate the feasibility of detection of epidermal growth factor receptor ( EGFR) exon 19 deletions and exon 21 L858R mutations in pleural effusion fromnon-small-cell lung cancer ( NSCLC) patients by mutant enriched PCR assay. Methods The mutations of exon 19 and 21 of EGFR gene in pleural samples fromthirty NSCLC patients were analyzed using both the mutant-enriched PCR assay and the non-enriched PCR assay. Results Ten ( 33. 3% , 10/ 30) exon 19 deletions and five ( 16. 7% , 5/30) exon 21 L858R mutation were detected by the mutant-enriched PCR assay, while only 6 cases ( 20. 0% ) and 1 case ( 3. 3% ) were detected by the non-enriched PCR assay respectively. The difference of mutation detection rate of EGFR gene between the two methods was statistically significant ( P = 0. 032) . Mutations were detected in all of partial responders ( 2 /4) among the four patients who received gefitinib therapy. Conclusions Mutant-enriched PCR assay can detect EGFR exon 19 deletions and exon 21 L858R mutation in pleural effusion from NSCLC patients effectively, economically and accurately. It may be a valuable biomarker for gefitinib therapy in advanced NSCLC.
Objective To elucidate the clinical features and treatment of parapneumonic effusions ( PPE) . Methods Ninety-seven patients were analyzed retrospectively in Guangzhou First Municipal People’s Hospital fromJanuary 2004 to July 2008. The data of 54 patients with complicated parapneumonic effusion ( CPPE) and 9 cases with empyema were compared with 49 patients with tuberculosis pleural effusions. Results Of 97 cases, 34 patients with uncomplicated parapneumonic effusion ( UPPE) were treated with antibiotics only, whose hospitalization time was ( 14. 8 ±7. 6) days, and 27 cases were cured ( 79. 4% ) . Of 54 CPPE patients, 42 were treated with antibiotics and pleural space drainage with central venous catheter, whose hospitalization time was ( 21. 7 ±13. 0) days, and 32 were cured ( 76. 2% ) . Another12 CPPE patients were treated with interapleural urokinase and drainage from the chest tube, whose hospitalization time was ( 22. 5 ±9. 3) days, and 8 were cured ( 66. 7% ) . Nine cases with empyema were rinsed the pleural with metronidazole solution, whose hospitalization time was ( 25. 7 ±17. 4) days, and 8 were cured( 89. 0% ) . Compared with the tuberculous pleurisy patients, most CPPE and empyema occurred in middle and old aged patients with an average age of ( 63. 3 ±19. 3) years. Polykaryocyte and lactate dehydrogenase increased significantly. Adenosine deaminase ( ADA) was lt; 45 U/L in most UPPE and empyema patients, but was gt; 45 U/L in 7 cases ( 11% ) . Conclusions UPPE is simple and preferably treated with antibiotics alone. While CPPE and empyema should be drainaged as early as possible, and the low-dose urokinase may be helpful. The level of ADA can not absolutely distinguish parapneumonic effusion from tuberculous pleural effusion.