Objective To investigate the expression of aquaporin-1( AQP-1) in pleural mesothelial cells ( PMCs) and the influence of glucose thereupon. Methods Rat PMCs were isolated, cultured, and divided into two groups, ie. a glucose group, cultured with glucose of different concentrations for 24 hours,and a control group, cultured in D-MEM/ F-12 medium. The 100 mmol / L glucose group was administered at the time points of 6, 12, 18, and 24 hours respectively. RT-PCR and Western blotting were used to analyze the mRNA and protein expression of AQP-1. Results The absorbance values of AQP-1 protein expression were 54. 02 ±4. 61, 127. 84 ±9. 41, and 231. 62 ±22. 63, respectively in the PMCs treated with glucose of the concentrations of 50, 100, and 200 mmol / L, all significantly higher than those in the control group( 22. 45 ±2. 16, all P lt; 0. 01) . The absorbance values of AQP-1 protein expression were 24. 68 ±2. 56, 58. 68 ±3. 67, 89. 61 ±6. 62, and 113. 41 ±7. 65 in the PMCs treated with glucose of the concentration of 100 mmol / L after 6, 12, 18, and 24 hours, all significantly higher than those in the control group ( 11. 81 ±1. 45, P lt;0. 01) .Conclusions Glucose induces the expression of AQP-1 mRNA and protein. AQP-1 participates in the pleural fluid formation.
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 investigate the etiology of pleural effusions. Methods All adult patients with pleural effusions of unknown etiology admitted to this hospital between January 2011 and December 2013 were investigated. The etiological data of these patients with pleural effusion were retrospectively reviewed. Results During the 3-year period, 1 541 patients eventually were included in this study. The most frequent cause of pleural effusions was bacterial infection (38.7%), followed by malignancy (23.7%), congestive heart failure (13.1%), and tuberculosis (10.7%). The etiology of 120 patients (7.8%) remained uncertain. Conclusions The most frequent cause of pleural effusion is bacterial infection, followed by malignancy, cardiac failure, and tuberculosis. These four etiologies account for over 85 percent of all pleural effusions.
Abstract: Objective To summarize the method and effective result of thoracoscopic intrapleural perfusion hyperthermochemotherapy(TIPHC) for treating malignant pleural effusion caused by lung cancer. Methods Fiftyeight patients with malignant pleural effusion caused by lung cancer were randomly divided into therapeutic group(30 cases) and control group(28 cases) between February 1999 and March 2005. Pleural biopsy and TIPHC under general ansthesia with unilateral ventilation were performed in the therapeutic group, and intrapleural injection of cisplatin was administered in control group after drainage of pleural effusion. The effect on malignant pleural effusion， the change for the concentration of carcinoembryonic antigen(CEA)， cytokeratin-19 fragments (CYFRA21-1)， neuronspecific enolase (NSE) and the side effect were compared before and after the treatment. Results The therapeutic group achieved total response rate of 100.0%, but only 53.6% in control group, with significant difference(χ 2=3.863, Plt;0.05). Furthermore, the concentration of CEA， CYFRA21-1， NSE in therapeutic group dramatically descended than control group(t=2.562,Plt;0.05). But there was no significant difference in side effect (Pgt;0.05). The pathological diagnosis of all the patients were determined in the therapeutic group. Conclusion TIPHC has the advantage of both diagnosis and treatment of malignant pleural effusions. It is safe and effective, and also able to determine the diagnosis. Furthermore, it offers the superiority of small wound， best visualization and convenient pleural biopsy.
Objective To evaluate the value of Sysmex XT-4000i hematology analyzer in its body-fluid mode in cell count and cell differential count of pleural effusion, ascites and cerebrospinal fluid samples. Methods A total of 95 pleural effusion, ascites and cerebrospinal fluid samples were collected from patients hospitalized between May and September 2015. The samples were tested by Sysmex XT-4000i hematology analyzer (instrument method) and modified Neubauer hemocytometer (manual method) for cell count, and the results of them were compared and analyzed. Results The instrument method and the manual method had a good consistency in nuclear cell count and erythrocyte count (kappa=0.965,P< 0.001; kappa=0.988,P<0.001). There was no significant difference in the count of mononuclear cells (P> 0.05). However, there was a significant difference in the count of multiple nuclear cells (P<0.05). Conclusions Hematology analyzer in its body-fluid mode may replace manual method in cell count of pleural effusion, ascites and cerebrospinal fluids for its high precision, high efficiency and easy operation. However, cell differential count of this method needs microscopic examination assistance.
ObjectivesTo investigate the clinical and imaging characteristics of pleural effusion in patients with acute pulmonary embolism (APE).MethodsComputed tomographic pulmonary angiography (CTPA) scans and clinical data of suspected APE patients from January 2014 to December 2018 were analyzed.ResultsA total of 1024 suspected APE patients underwent CTPA examination in the imaging department of our hospital. Two hundred patients (19.5%) were diagnosed with APE. Imaging findings of pleural effusion were revealed in 70 cases (35.0%). The majority of APE patients without pleural effusion were males (82.3% vs. 64.3%, P<0.01), and the majority of APE patients with pleural effusion were females (35.7% vs. 17.7%, P<0.01). Most of the effusions were bilateral, small to moderate, with peripheral embolism (62.9%, P<0.05). Pulmonary consolidation, atelectasis and ground-glass opacity were common manifestations of CTPA. Compared with patients with simple pulmonary embolism, pulmonary embolism with pleural effusion was more common (62.9% and 33.8%, respectively, OR=3.279 and 95%CI 1.798 - 6.091, P<0.001). Diagnostic thoracic puncture was performed in 6 cases (8.6%). Pleural effusion was exudate in these 6 patients, with normal blood sugar and neutrophils predominated.ConclusionsAbout one third of APE patients are associated with pleural effusion, which most presented with small and bilateral pleural effusions. The main embolism associated with pleural effusion is peripheral embolism. There is a significant correlation between pulmonary consolidation and pleural effusion. Pleural effusion is mostly exudate and neutrophils often predominate.
ObjectiveTo compare the accuracy and safety of semirigid thoracoscopy and rigid thoracoscopy in the diagnosis of unexplained pleural effusion. MethodsA prospective randomized study was conducted, in which the patients with unexplained pleural effusion were enrolled consecutively from March 2012 to March 2014 in West China Hospital. The age of the patients ranged from 18 to 75 years. After informed consent, the subjects were randomized to a semirigid thoracoscopy group or a rigid thoracoscopy group to be examined. ResultsForty-nine patients were assigned to the semirigid thoracoscopy group, and 48 patients were assigned to the rigid thoracoscopy group. After thoracoscopy procedure, 44 patients were confirmed as malignant diseases, and 48 patients were confirmed as benign diseases. The overall diagnostic accuracy was 93.9% for the semirigid procedure and 95.8% for the rigid procedure. The diagnostic sensitivity and specificity for malignancy were 96.0% and 100.0% for the semirigid thoracoscopy, and 95.2% and 100.0% for the rigid thoracoscopy, respectively, without statistical significant differences between two groups. All the patients tolerated well with minor complications after two kinds of thoracoscopy. ConclusionsThe diagnostic accuracy of semirigid thoracoscopy and rigid thoracoscopy is comparable in the diagnosis of unexplained pleural diseases. The samples obtained by semirigid thoracoscopy are smaller, but adequate for pathological examination.
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.
Objective To investigate the value of tumor type M2 pyruvate kinase ( M2-PK) in the differential diagnosis of pleural effusion. Methods A total of 146 patients with pleural effusion during January 2006 to December 2008 were recruited at the department of respiratory medicine of the Shantou Affiliated Hospital and the First Affiliated Hospital of Sun Yat-sen Medical College. Pleural effusion was malignant in 72 cases ( 52 cases with lung cancer and 20 cases with metastatic lung cancer) and benign in 74 cases ( 54 cases with infective pleural effusion and 20 with transudation effusion) . The patients were divided into a malignant pleural effusion group, an infective pleural effusion group, and a transudation group.Then the infective group was further divided into subgroups of tuberculosis pleural effusion group andparapneumonic effusion group. The concentration of tumor M2-PK in pleural fluid obtained during the first thoracocentesis was measured by enzyme-linked immunosorbent assay( ELISA) . Results The concentration of tumor M2-PK was significantly higher in the malignant pleural effusion group compared with the benignpleural effusion groups ( P lt; 0. 01) . Significant differences were also found in the concentration of tumor M2-PK between malignant pleural effusion caused by lung cancer and metastatic lung cancer( P lt; 0. 05) .When the cutoff value of tumor M2-PK was set at 18. 68 U/mL, the sensitivity, specificity, and accuracy for the diagnosis of malignant pleural effusion was 87. 6% , 86. 0% , and 87. 4%, respectively. Furthermore,the detection of tumor M2-PK in combination with CEA showed better diagnostic sensitivity( 96. 0% ) ,specificity ( 85. 0% ) , and accuracy ( 91. 1% ) . Conclusions The detection of tumor M2-PK in pleural effusion is of some clinical significance in the differential diagnosis of benign and malignant pleural effusion.The detection of tumor M2-PK in combination with CEA is a good diagnostic tool with high sensitivity andspecificity.
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.