瞄准:为肝炎 B 病毒(HBV ) 的 mother-to-child 传播(MTCT ) 的打断在迟了的怀孕决定 lamivudine 的治疗学的效果。方法:研究被寻找可得到的数据库直到 2011 年 1 月识别。包括标准是在迟了的怀孕,和谁的新生儿或婴儿与 lamivudine 治疗涉及了使随机化的控制临床的试用(RCT ) 的 HBV 搬运人母亲浆液肝炎 B 表面抗原(HBsAg ) ,肝炎 B e 抗原(HBeAg ) 或 HBV DNA 被记录了。为由 HBsAg, HBV DNA 或新生儿或婴儿的 HBeAg 显示了的 MTCT 的打断的相对风险(RR ) 与 95% 信心间隔(CI ) 被计算估计 lamivudine 处理的功效。结果:包括 1693 位 HBV 搬运人母亲的十五 RCT 在这元分析被包括。全面 RR 是 0.43 (95% CI, 0.25-0.76;8 RCT;Pheterogeneity = 0.04 ) 并且 0.33 (95% CI, 0.23-0.47;6 RCT;Pheterogeneity = 0.93 ) 由新生的 HBsAg 或 HBV DNA 显示了。RR 是 0.33 (95% CI, 0.21-0.50;6 RCT;Pheterogeneity = 0.46 ) 并且 0.32 (95% CI, 0.20-0.50;4 RCT;Pheterogeneity = 0.33 ) 在出生以后由浆液 HBsAg 或婴儿 6-12 瞬间的 HBV DNA 显示了。RR (lamivudine 对肝炎 B 免疫球蛋白) 是 0.27 (95% CI, 0.16-0.46;5 RCT;Pheterogeneity = 0.94 ) 并且 0.24 (95% CI, 0.07-0.79;3 RCT;Pheterogeneity = 0.60 ) 分别地由新生的 HBsAg 或 HBV DNA 显示了。在有病毒的负担的母亲 < 在 lamivudine 处理以后的 106 copies/mL,功效(RR, 95% CI ) 是 0.33, 0.21-0.53 (5 RCT;Pheterogeneity = 0.82 ) 然而,如果母亲的病毒的负担是,为 MTCT 的打断,这价值不是重要的 > 在 lamivudine 处理以后的 106 copies/mL (P = 0.45, 2 RCT ) 由新生的浆液 HBsAg 显示了。RR (从怀孕期对控制的 28 wk 开始的 lamivudine ) 是 0.34 (95% CI, 0.22-0.52;7 RCT;Pheterogeneity = 0.92 ) 并且 0.33 (95% CI, 0.22-0.50;5 RCT;Pheterogeneity = 0.86 ) 由新生的 HBsAg 或 HBV DNA 显示了。lamivudine 的不利效果的发生不比在控制在母亲是更高的(P = 0.97 ) 。仅仅一研究在新生儿报导?
AIM: To determine the therapeutic effect of lamivu- dine in late pregnancy for the interruption of motherto-child transmission (MTCT) of hepatitis B virus (HBV). METHODS: Studies were identified by searching available databases up to January 2011. Inclusive criteria were HBV-carrier mothers who had been involved in randomized controlled clinical trials (RCTs) with lamivudine treatment in late pregnancy, and newborns or infants whose serum hepatitis B surface antigen (HBsAg), hepatitis B e antigen (HBeAg) or HBV DNA had been documented. The relative risks (RRs) for inerruption of MTCT as indicated by HBsAg, HBV DNA or HBeAg of newborns or infants were calculated with 95% confidence interval (CI) to estimate the efficacy of lamivudine treatment. RESULTS: Fifteen RCTs including 1693 HBV-carrier mothers were included in this meta-analysis. The overall RR was 0.43 (95% CI, 0.25-0.76; 8 RCTs; Phet- erogeneity= 0.04) and 0.33 (95% CI, 0.23-0.47; 6 RCTs; Pheterogeneity = 0.93) indicated by newborn HBsAg or HBV DNA. The RR was 0.33 (95% CI, 0.21-0.50; 6 RCTs; Pheterogeneity = 0.46) and 0.32 (95% CI, 0.20-0.50; 4 RCTs; Pheterogeneity = 0.33) indicated by serum HBsAg or HBV DNA of infants 6-12 mo after birth. The RR (lamivudine vs hepatitis B immunoglobulin) was 0.27 (95% CI, 0.16-0.46; 5 RCTs; Pheterogeneity = 0.94) and 0.24 (95% CI, 0.07-0.79; 3 RCTs; Pheterogeneity = 0.60) indicated by newborn HBsAg or HBV DNA, respectively. In the mothers with viral load 〈 106 copies/mL after lamivudine treatment, the efficacy (RR, 95% CI) was 0.33, 0.21-0.53 (5 RCTs; Pheterogeneity = 0.82) for the interruption of MTCT, however, this value was not significant if maternal viral load was 〉 106 copies/mL after lamivudine treatment (P = 0.45, 2 RCTs), as indicated by newborn serum HBsAg. The RR (lamivudine initiated from 28 wk of gestation vs control) was 0.34 (95% CI, 0.22-0.52; 7 RCTs; Pheterogeneity = 0.92) and 0.33 (95% CI, 0.22-0.50; 5 RCTs; Phetero