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经皮穿刺肝动脉栓塞化疗治疗肝癌的效果观察及对患者肿瘤标记物CA199、AFP和CEA的影响 被引量:4

The Effect Observation of Transcatheter Hepatic Arterial Chemoembolization in the Treatment of Liver Cancer and Its Effect on Tumor Markers CA199,AFP and CEA
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摘要 目的:探究经皮穿刺肝动脉栓塞化疗(THACE)治疗肝癌的效果及对患者肿瘤标记物CA199、AFP和CEA的影响。方法:将2014年9月-2016年1月本院收治的64例肝癌患者作为研究对象,所有患者(92个病灶)均接受THACE治疗。于治疗前后检测患者肿瘤标记物[糖类抗原(CA199)、甲胎蛋白(AFP)、癌胚抗原(CEA)],以及T细胞亚群水平(CD4^+T细胞、CD8^+T细胞),并采用CT、MRI或B超检查病情,评定临床疗效。结果:THACE治疗肝癌的临床总有效率为90.22%(83/92)。与治疗前比较,治疗后患者的CA199、AFP及CEA均显著下降,CD4^+T细胞水平显著下降,CD8^+T细胞水平显著上升,差异均有统计学意义(P<0.05)。结论:THACE治疗肝癌效果确切,可有效改善T细胞亚群水平并降低CA199、AFP及CEA水平,值得推广。 Objective:To investigate the effect of percutaneous transhepatic arterial chemoembolization(THACE)in the treatment of liver cancer and its influence on tumor markers CA199,AFP and CEA.Method:Sixty-four patients with HCC were enrolled in this study from September 2014 to January 2016,all patients(92 lesions)underwent THACE treatment.The tumor markers[carbohydrate antigen(CA199),alpha fetoprotein(AFP),carcinogenicity antigen(CEA)],and T cell subsets(CD4+T cells,CD8+T cells)were detected before and after treatment,and the clinical efficacy was evaluated by CT,MRI or B ultrasonically.Result:The total effective rate of THACE in the treatment of liver cancer was 90.22%(83/92).Compared before treatment,the CA199,AFP and CEA were significantly decreased in all patients after treatment,the levels of CD4+T cells was significantly decreased,and the levels of CD8+T cells was significantly increased,the differences were statistically significant(P<0.05).Conclusion:THACE is effective in the treatment of liver cancer,can effectively improve the level of T cell subsets,and reduce the levels of CA199,AFP and CEA,so it is worthy of promotion.
作者 何林莉 HE Linli(Qianjiang Center Hosptal,Qianjiang 433100,China)
出处 《中国医学创新》 CAS 2017年第33期120-123,共4页 Medical Innovation of China
基金 湖北省卫生厅立项科研课题(2008Z-B04)
关键词 经皮穿刺 肝动脉栓塞化疗 肝癌 肿瘤标记物 CA199 AFP CEA Percutaneous puncture Transcatheter hepatic arterial chemoembolization Liver cancer Tumor markers CA199 AFP CEA
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