出 处:《北京医学》2019年第6期455-459,共5页Beijing Medical Journal
摘 要:探讨慢性乙型肝炎(chronic hepatitis B, CHB)患者HBsAg/抗-HBs共存的血清学模式与肝细胞癌(hepatocellularcarcinoma, HCC)的关系。方法在病例对照研究中,选取2017年1月至2018年3月首都医科大学附属北京佑安医院收治的CHB患者412例,分为G1组(HBsAg/抗-HBs共存)和G2组(HBsAg阳性、抗-HBs阴性),每组206例.对HCC发生风险进行logistic回归分析。在队列研究中,选取2010年9月至2013年11月的CHB患者260例,分为G3组(HBsAg/抗-HBs共存)和G4组(HBsAg阳性、抗-HBs阴性),每组130例,采用生存分析法分析两组HCC累计发生率的差异。结果病例对照研究中,年龄M50 岁(OR = 4.486,95% C/:2.592~7.762. P < 0.001),男性(OR = 3.683,95% C/:2.025~6.699,P< 0.001),HBsAg/抗-HBs共存(OR = 2.063,95%CI-. 1.259-3.382,P = 0.004)均可增加HCC发生风险。队列研究中,随访期间85.8%(223/260)的患者接受了规范抗病毒治疗,两组抗病毒治疗患者的比例差异无统计学意义(P =0.214)。基线高病毒载量患者,HBsAg/抗-HBs共存可能增加其HCC发生风险(Log-rank P = 0.018),而低载量患者两组差异无统计学意义(Log-rank P = 0.902)。结论基线高病毒载量的CHB患者,HBsAg/抗-HBs共存可能增加HCC发生风险。该模式与病毒突变有关,对乙肝患者的预后评估有提示作用:建议联合检测反映肝内病毒模板含量的指标及HBV突变位点来评估肝癌风险,拟定治疗及随访策略。To illustrate the association between the serological pattern of coexisting of HBsAg and anti? HBs and hepatocellular carcinoma (HCC) in patients with chronic hepatitis B (CHB). Methods In the case-control study, 206 patients with coexistence of HBsAg and anti-HBs (G1 group) and 206 patients with HBsAg alone (G2 group) were selected. The risk of HCC was analyzed by univariate analysis and multivariate logistic regression analysis. In the cohort study, 130 patients with coexistence of HBsAg and anti-HBs (G3 group) and 130 patients with HBsAg alone (G4 group) were recruited to estimate the cumulative incidence of HCC by Kaplan-Meier analysis. Results In the case-control study, age M 50 years (OR = 4.486, 95% C/:2.592-7.762, P < 0.001), male (OR = 3.683, 95% C/:2.025-6.699, P < 0.001), coexistence of HBsAg and anti-HBs (OR = 2.063, 95% C/: 1.259-3.382, P = 0.004) were risk factors for HCC development. In the cohort study, during the follow-up period, 85.8%(223/260) of the patients received antiviral therapy, and there was no significant difference in the proportion of antiviral therapy between the two groups (P = 0.214). The serological pattern of coexistence of HBsAg and anti- HBs significantly increased the risk of HCC in CHB patients with high HBV load at baseline (Logrank P = 0.018). However, the significance was not showed in patients with low HBV load at baseline (Logrank P = 0.902). Conclusions The serological pattern of coexistence of HBsAg and anti-HBs may increase the risk of HCC in CHB patients with high HBV load. This model is associated with viral mutations and has a promising role in the evaluation of prognosis in CHB patients. It is suggested that the risk of HCC should be assessed by combining the indicators reflecting the content of viral template and the detection of HBV mutation sites, and the treatment and follow-up strategies should be formulated.
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