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目的:探讨HBV感染导致肝硬化的过程中可溶性肿瘤坏死因子相关凋亡诱导配体(s TRAIL)介导的免疫损伤及恩替卡韦通过影响s TRAIL及抑制HBV-DNA复制,延缓或阻止乙型肝炎肝硬化发展的作用。方法:选取2013年1月至2014年1月海南医学院附属医院中医科乙型肝炎肝硬化患者40例为治疗组,健康体检者45例为对照组。治疗组予恩替卡韦(0.5 mg,每日一次)口服,疗程48周。两组患者分别于治疗前、治疗12、24、48周使用ELISA检测血清中s TRAIL水平,RT-PCR检测血清中HBV-DNA载量的变化,全自动生化分析仪检测肝功能,全自动血凝仪检测凝血酶原时间。同时在治疗组中随机选取16例患者,Child-Pugh分级分别为A级6例,B级5例,C级5例,于恩替卡韦治疗前及治疗24周时进行肝脏穿刺组织病理检查。结果:治疗组治疗前s TRAIL、HBV DNA及ALT水平均高于健康对照组,差异有统计学意义(P<0.05);经线性相关分析,治疗组患者血清s TRAI与ALT含量呈显著正相关(r=0.736,P=0.000),血清s TRAIL与HBV-DNA载量无相关性(r=-0.0127,P=0.382)。恩替卡韦治疗后,治疗组血清s TRAIL水平下降,ALT恢复正常,HBV-DNA载量降低,肝脏组织病理学改善,与治疗前比较,差异有统计学意义(P<0.05)。结论:s TRAIL介导乙型肝炎肝硬化患者肝脏的免疫损伤过程。经恩替卡韦治疗后s TRAIL与ALT降低,HBV-DNA复制抑制,肝脏组织病理学改善,从而延缓或阻止肝硬化的发展。在恩替卡韦抗病毒过程中动态监测s TRAIL的变化有助于肝硬化预后的判断。
OBJECTIVE: To investigate the immunological injury induced by soluble TRAIL-associated apoptosis-inducing ligand (s TRAIL) during HBV infection-induced cirrhosis and entecavir to delay or stop hepatitis B by affecting s TRAIL and inhibiting HBV-DNA replication Hardening the development of the role. Methods: From January 2013 to January 2014, 40 patients with hepatitis B cirrhosis in the Department of Traditional Chinese Medicine, Affiliated Hospital of Hainan Medical College were selected as the treatment group and 45 healthy people as the control group. The treatment group was given entecavir (0.5 mg once daily) for 48 weeks. Two groups of patients before treatment, respectively, 12,24,48 weeks of treatment using ELISA TRAIL serum levels of s TRAIL, RT-PCR detection of serum HBV-DNA load changes, automatic biochemical analyzer detection of liver function, automatic blood Coagulation test prothrombin time. At the same time, 16 patients were randomly selected from the treatment group. The Child-Pugh grading was Grade A in 6 cases, Grade B in 5 cases and Grade C in 5 cases. Liver biopsy was performed before and 24 weeks after entecavir treatment. Results: The levels of s TRAIL, HBV DNA and ALT before treatment in the treatment group were significantly higher than those in the healthy control group (P <0.05). The linear correlation analysis showed that there was a significant positive correlation between serum s TRAI and ALT (r = 0.736, P = 0.000). No correlation was found between serum s TRAIL and HBV DNA load (r = -0.0127, P = 0.382). After treatment with entecavir, serum TRAIL level decreased, ALT returned to normal, HBV-DNA load decreased and liver histopathology improved. The difference was statistically significant (P <0.05). Conclusion: s TRAIL mediates the hepatic immune injury in patients with hepatitis B cirrhosis. After entecavir treatment s TRAIL and ALT decreased, HBV-DNA replication inhibition, liver histopathology improved, thus slowing or preventing the development of cirrhosis. Dynamic monitoring of TRAIL changes during entecavir antiviral therapy contributes to the prognosis of cirrhosis.