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目的观察恩替卡韦治疗血清HBV DNA阴性乙型肝炎肝硬化对预后的影响。方法将76例血清HBV DNA阴性乙型肝炎肝硬化(代偿期)患者随机分为两组,对照组36例,给予护肝、抗肝纤维化及对症等治疗;治疗组40例,在对照组治疗基础上给予恩替卡韦0.5 mg/d,疗程均为12个月。观察并记录两组患者的肝肾功能、凝血酶原时间(PT)、肝纤扫描肝脏硬度值、Child-Pugh评分及药物不良反应情况。结果在治疗6、12个月时,治疗组生化指标改善较对照组明显,两组患者同期比较差异均有统计学意义(P<0.05)。两组患者肝纤扫描检查提示肝脏纤维化程度较前改善,但治疗组较对照组改善明显,治疗12个月时两组比较差异有统计学意义(P<0.05)。治疗组PTA、Child-Pugh评分无恶化,而对照组部分病例出现恶化,两者比较差异均有统计学意义(P<0.05)。疗程结束时,治疗组患者未出现上消化道出血、肝性脑病、感染及肝肾综合征等严重并发症;而对照组发生率分别为5.56%、8.33%、2.78%、2.78%,两组间差异有统计学意义(P<0.05);对照组有1例患者死于上消化道大出血,1例患者死于肝肾综合征。结论恩替卡韦治疗血清HBV DNA阴性代偿期乙型肝炎肝硬化获得生化应答、组织学改善,减少相关并发症、失代偿期及死亡病例的发生。
Objective To observe the effect of entecavir on the prognosis of patients with serum HBV DNA-negative hepatitis B cirrhosis. Methods Sixty-six patients with serum HBV DNA-negative hepatitis B cirrhosis (decompensated) were randomly divided into two groups. The control group received 36 cases of liver protection, anti-hepatic fibrosis and symptomatic treatment. The treatment group (40 cases) On the basis of group therapy, entecavir 0.5 mg / d was given for 12 months. The liver and renal function, prothrombin time (PT), liver fibrosis liver fibrosis score, Child-Pugh score and adverse drug reactions were observed and recorded. Results At 6 and 12 months of treatment, the improvement of biochemical indexes in the treatment group was more obvious than that in the control group. There was significant difference between the two groups in the same period (P <0.05). Two groups of patients with liver fibrosis scan examination showed that the degree of liver fibrosis improved compared with the previous, but the treatment group improved significantly than the control group, 12 months after treatment, the difference between the two groups was statistically significant (P <0.05). The PTA and Child-Pugh scores of the treatment group did not deteriorate, but some cases of the control group deteriorated. The differences between the two groups were statistically significant (P <0.05). At the end of the treatment period, the patients in the treatment group showed no serious complications such as upper gastrointestinal bleeding, hepatic encephalopathy, infection and hepatorenal syndrome. The incidence rates of the control group were 5.56%, 8.33%, 2.78% and 2.78% There was a significant difference between the two groups (P <0.05). One patient in the control group died of upper gastrointestinal bleeding and one patient died of hepatorenal syndrome. Conclusion Entecavir treatment of serum HBV DNA negative compensated hepatitis B cirrhosis biochemical response, histological improvement, reduce the incidence of complications, decompensation and deaths.