| Objective The invasion of pleura by tumors directly and tumor associate inflammations induced the vascular hyperpermeability on the pleura, and with the high permeability of the new vessels, the malignant pleural effusion (MPE) generated greatly. In addition, tumor cells blockade the vein and the efferent lymphatic vessel in the parietal pleura, all these factors lead to the formation of MPE. Nowdays, the recommended treatment of MPE in our and foreign countrys is pleurodesis, which is intrapleural injection of sclerosing agent that causing pleural adhesions, and one kind of them is pingyangmycin(PYM), which was approved and recommended, but the exactly mechanisms of that are still unknown completely, In this study, we try to investigate the mechanisms that PYM produces pleurodesis through the research of the levels of monocyte chemoattractant protein (MCP)-1, carcinoembryonic antigen (CEA), and c-reactive protein (CRP) in MPE before and after the PYM administration.Methods In this clinical prospective study, from October 2009 to August 2010, patients who are confirmed MPE by pathology or cytology in the Department of Respiratory Medicine of the First Affiliated Hospital of Anhui Medical University, and more than middle-volume pleural effusion, KPS score≥50, expected survival time>1 month were recruited for the study. Single cavity central venous catheter was placed in the pleural cavity to drain MPE after the location of the ultrasonic wave, when the flow amount was less than 150ml one day or the compressed lung was reinstrate, 24mg PYM with 20 ml saline was administrated into the pleural cavity. Then the catheter was closed for 24 hours, and was removed after the flow amount was less than 150ml in 24 hours. Then all the 29 lung cancer patients were given TP,GP or NP chemical treatment after the PYM intrapleural administration. For each recruited patient, upon the patient's informed consent, 5 ml pleural effusion before and after intrapleural PYM administration 6, 24, 48 hours would be saved simultaneously, the concentrations of MCP-1,CEA and CRP were detected, and the number of leucocyte was tested. The pleurodesis efficacy according to WHO standard was evaluated four weeks later. Then the patients were divided into effective group and failure group. For each eligible case, the MCP-1, CEA and CRP levels of pleural fluid were detected simultaneously by double-antibody sandwich technique (ELISA), radioimmunoassay (RIA), and particle enhanced immunoturbidimetric test, the leucocytes in MPE were tested by Microscope direct counting method. After completion of all the tests of MCP-1,CEA and CRP and the number of leucocyte and clinical data collection, we analyzed the MCP-1,CEA and CRP levels and the number of leucocyte in accordance with those of reference standard. Followed by statistical analysis, the mechanism of pleurodesis which produced by PYM ware assessed.Results Four weeks after PYM administration, the response rate of MPE control was 58.1%; The levels of MCP-1 and CEA were lower 48 h afterwards than those before treatment ( P <0.05). In addition, decrease of them were observed from 6 h after treatment in effective group ( P <0.05). In failure group, MCP-1 level was lower 48 h afterwards (P <0.05), but no differences of CEA were observed; The PYM intraplueral treatment induced a marked increase of CRP and leucocytes, and in both effective and failure groups ( P <0.05); After the administration 6 h and 48 h, the levels of MCP-1 and CRP were higher in effective group than those in failure group respectively ( P < 0.05), and no statistical significances of CEA and leucocytes were found between the different groups at the same time. Conclusions By inducing inflammation and anti-tumor effects, PYM administration into the pleural cavity induces pleurodesis. |
PDF Full Text Request