目的分析高耐药性肺癌患者外周静脉置入中心静脉导管(peripherally inserted central catheter,PICC)相关性深静脉血栓形成的危险因素。方法回顾性分析2015年5月至2017年5月本院收治的156例行PICC化疗的高耐药性肺癌患者的临床资料,分...目的分析高耐药性肺癌患者外周静脉置入中心静脉导管(peripherally inserted central catheter,PICC)相关性深静脉血栓形成的危险因素。方法回顾性分析2015年5月至2017年5月本院收治的156例行PICC化疗的高耐药性肺癌患者的临床资料,分析高耐药性肺癌患者PICC置管后深静脉血栓形成的危险因素。结果 156例高耐药性肺癌患者中,发生PICC相关性深静脉血栓18例,发生率为11.54%。多因素Logistic回归分析显示:女性、头静脉置管、PICC留管时间>1个月、纤维蛋白原水平>4 g/L、D-二聚体水平>0.5 mg/ml及腺癌是高耐药性肺癌患者PICC相关性深静脉血栓形成的独立危险因素(P<0.05)。结论性别、穿刺静脉、纤维蛋白原、D-二聚体、留管时间以及病理类型为高耐药性肺癌患者PICC相关性深静脉血栓形成的危险因素,临床需予以重点关注和及早预防,以降低PICC相关性深静脉血栓形成的发生风险。展开更多
原发性非小细胞肺癌（non small cell lung cancer,NSCLC）的病理机制较为复杂,发病隐匿,早期确诊存在困难,80%左右的患者确诊时已为晚期[1]。化疗是晚期NSCLC患者的主要治疗手段,但同时会带来较为严重的毒副反应,且易产生耐药性,影响...原发性非小细胞肺癌（non small cell lung cancer,NSCLC）的病理机制较为复杂,发病隐匿,早期确诊存在困难,80%左右的患者确诊时已为晚期[1]。化疗是晚期NSCLC患者的主要治疗手段,但同时会带来较为严重的毒副反应,且易产生耐药性,影响其临床疗效和应用[2]。中医药治疗可稳定肺癌病灶,提高生活质量,提高免疫功能,起到减毒增效的效果。本文观察了自拟扶正化痰抗癌方联合化疗治疗晚期耐药性非小细胞肺癌的疗效,现报告如下。展开更多
Objective： Recombinant human Endostatin （rh-Endostatin, YH-16） can reverse cisplatin resistance in A549/DDP cells. However, the possible effect of rh-Endostatin in reversing DDP-resistance in A549/DDP cells and the...Objective： Recombinant human Endostatin （rh-Endostatin, YH-16） can reverse cisplatin resistance in A549/DDP cells. However, the possible effect of rh-Endostatin in reversing DDP-resistance in A549/DDP cells and the mechanism are needed to be investigated. Methods： Lung adenocarcinoma cell line A549 and its DDP-resistant cell line A549/DDP were treated with DDP and/or recombinant human Endostatin. Difference in drug resistance was analyzed between different regi- mens and between different cell lines after a 72 h-treatment in vitro. And below the non-cytotoxic concentration of rh-End- ostatin, the possibility of rh-Endostatin in reversing DDP-resistance in A549/DDP was evaluated. The resistance protein which was detected in the study included P glycoprotein （P-gp） and topoisomerase II （Topo-II）. Results： Rh-Endostatin below 400 IJg/mL showed no cytotoxicity in either A549 or A549/DDP after 72 h-treatment with it. The inhibited concentration of 50% （IC50） observed for DDP was （0.79 _＋ 0.05） IJg/mL in A549 and （13.2 ＋ 1.1） in A549/DDP respectively. IC50 was reduced to 2.57 ＋ 0.05 #g/mL in A549/DDP treated by rh-Endostatin below the non-cytotoxic concentrations in combination with DDP, with a reversal fold （RF） of 5.14 and a relative reversal rate of 85.6%. Apoptotic rates were 2.01%, 13.47% and 29.26% re- spectively for cells treated with rh-Endostain, DDP, and the combination. The rate of the A549/DDP control group was 0.99%. The expression level of P-gp or Topo-II was higher in A549/DDP cells than in A549 cells. Rh-Endostatin may partially reverse DDP-resistance in A549/DDP cells in vitro, with a probable mechanism related to lowering expression of P-gp and Topo-II. Conclusien： Rh-Endostatin of non-cytotoxic dose partially reversed cisptatin resistance in cisplatin-resistant human lung adenocarcinoma cell line A549/DDP. Rh-Endostatin reversed the resistance of A549/DDP cells to DDP, which may be related to decreased protein expression of P-gp and Topo-II in A549/DDP cells.展开更多
文摘原发性非小细胞肺癌（non small cell lung cancer,NSCLC）的病理机制较为复杂,发病隐匿,早期确诊存在困难,80%左右的患者确诊时已为晚期[1]。化疗是晚期NSCLC患者的主要治疗手段,但同时会带来较为严重的毒副反应,且易产生耐药性,影响其临床疗效和应用[2]。中医药治疗可稳定肺癌病灶,提高生活质量,提高免疫功能,起到减毒增效的效果。本文观察了自拟扶正化痰抗癌方联合化疗治疗晚期耐药性非小细胞肺癌的疗效,现报告如下。
基金Supported by a grant from the Natural Science Foundation of Liaoning Province(No.201202043)
文摘Objective： Recombinant human Endostatin （rh-Endostatin, YH-16） can reverse cisplatin resistance in A549/DDP cells. However, the possible effect of rh-Endostatin in reversing DDP-resistance in A549/DDP cells and the mechanism are needed to be investigated. Methods： Lung adenocarcinoma cell line A549 and its DDP-resistant cell line A549/DDP were treated with DDP and/or recombinant human Endostatin. Difference in drug resistance was analyzed between different regi- mens and between different cell lines after a 72 h-treatment in vitro. And below the non-cytotoxic concentration of rh-End- ostatin, the possibility of rh-Endostatin in reversing DDP-resistance in A549/DDP was evaluated. The resistance protein which was detected in the study included P glycoprotein （P-gp） and topoisomerase II （Topo-II）. Results： Rh-Endostatin below 400 IJg/mL showed no cytotoxicity in either A549 or A549/DDP after 72 h-treatment with it. The inhibited concentration of 50% （IC50） observed for DDP was （0.79 _＋ 0.05） IJg/mL in A549 and （13.2 ＋ 1.1） in A549/DDP respectively. IC50 was reduced to 2.57 ＋ 0.05 #g/mL in A549/DDP treated by rh-Endostatin below the non-cytotoxic concentrations in combination with DDP, with a reversal fold （RF） of 5.14 and a relative reversal rate of 85.6%. Apoptotic rates were 2.01%, 13.47% and 29.26% re- spectively for cells treated with rh-Endostain, DDP, and the combination. The rate of the A549/DDP control group was 0.99%. The expression level of P-gp or Topo-II was higher in A549/DDP cells than in A549 cells. Rh-Endostatin may partially reverse DDP-resistance in A549/DDP cells in vitro, with a probable mechanism related to lowering expression of P-gp and Topo-II. Conclusien： Rh-Endostatin of non-cytotoxic dose partially reversed cisptatin resistance in cisplatin-resistant human lung adenocarcinoma cell line A549/DDP. Rh-Endostatin reversed the resistance of A549/DDP cells to DDP, which may be related to decreased protein expression of P-gp and Topo-II in A549/DDP cells.
