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·循证药学·


          ADRB1 Arg389Gly多态性对比索洛尔疗效影响的Meta分析                                                        Δ


          张天齐 ,李 婷,张 田,赵紫楠,纪立伟(北京医院药学部/国家老年医学中心/中国医学科学院老年医学研究
                *
                                               #
          院/北京市药物临床风险与个体化应用评价重点实验室,北京 100730)


          中图分类号  R969.3      文献标志码  A      文章编号  1001-0408(2024)05-0601-06
          DOI  10.6039/j.issn.1001-0408.2024.05.16

          摘  要  目的  探索ADRB1 Arg389Gly多态性对比索洛尔疗效的影响,为比索洛尔个体化药物治疗提供参考。方法  从PubMed、
          Embase、Cochrane Library、中国生物医学文献服务系统、中国知网、万方等数据库系统性搜索与比索洛尔和ADRB1 Arg389Gly多
          态性相关的文献,检索时间为建库至2023年5月。根据研究制定的纳入与排除标准筛选、提取相关文献并进行文献质量评估。使
          用RevMan 5.4软件对相关结局指标进行Meta分析。结果  最终纳入7项研究,共计1 339人次。其中4项研究涉及比索洛尔治疗
          前后收缩压(SBP)和舒张压(DBP)的变化量(ΔSBP 和 ΔDBP),有 4 项研究涉及治疗前后左室射血分数(LVEF)的变化量
         (ΔLVEF)。研究结果显示,比索洛尔对 ADRB1 Arg389Gly 野生组(AA)和突变组(AG+GG)血压改善的差异均无统计学意义
          {ΔSBP[SMD=0.17,95%CI(-0.97,1.31),P=0.77]、ΔDBP[SMD=-0.01,95%CI(-0.65,0.62),P=0.97]};比索洛尔对两组
          ΔLVEF 改善的差异亦无统计学意义[SMD=-0.61,95%CI(-2.74,1.53),P=0.58]。结论  ADRB1 Arg389Gly 多态性对比索洛尔
          改善心血管患者SBP、DBP和LVEF的作用无显著影响。
          关键词  比索洛尔;β1肾上腺素受体;ADRB1 Arg389Gly;基因多态性;Meta分析

          Meta-analysis about ADRB11 Arg389Gly polymorphism on the efficacy of bisoprolol
          ZHANG Tianqi,LI Ting,ZHANG Tian,ZHAO Zinan,JI Liwei(Dept.  of  Pharmacy,  Beijing  Hospital/National
          Center  of  Gerontology/Institute  of  Geriatric  Medicine,  Chinese  Academy  of  Medical  Science/Beijing  Key
          Laboratory of Assessment for Clinical Risk and Individual Application of Drugs, Beijing 100730, China)


          ABSTRACT   OBJECTIVE  To  explore  the  effects  of  ADRB1  Arg389Gly  polymorphisms  on  the  efficacy  of  bisoprolol,  thus
          providing some information for individualized drug therapy. METHODS  A systematic search was conducted in PubMed, Embase,
          Cochrane  Library,  CBM,  CNKI,  and  Wanfang  Data  to  retrieve  and  find  out  all  relevant  literature  about  bisoprolol  and  ADRB1
          Arg389Gly  polymorphism  from  the  inception  to  May  2023.  The  retrieved  literature  was  screened  and  selected  according  to  the
          inclusive and exclusive criteria, thereafter quality assessment was conducted. RevMan 5.4 software was utilized to perform the meta-
          analysis  for  the  outcome  index.  RESULTS  Overall  7  literature  with  1  339  cases  were  included. Among  them,  4  studies  provided
          the  changes  in  systolic  blood  pressure (SBP),  diastolic  blood  pressure (DBP) (ΔSBP  and  ΔDBP);  4  involving  the  change
         (ΔLVEF)  of  left  ventricular  ejection  fraction (LVEF).  Results  of  the  study  showed  that  there  was  no  statistical  significance  in  the
          improvement  of  blood  pressure  between  wild-type  group (AA)  and  mutation  group (AG+GG)  of ADRB1 Arg389Gly  treated  with
          bisoprolol {ΔSBP [SMD=0.17,95%CI (-0.97,1.31), P=0.77], ΔDBP [SMD=-0.01,95%CI (-0.65,0.62), P=0.97]}; there
          was no statistical significance in the improvement of ΔLVEF [SMD=-0.61, 95%CI (-2.74,1.53), P=0.58] between 2 groups.
          CONCLUSIONS  ADRB1  Arg389Gly  gene  polymorphism  has  no  significant  influence  on  the  improvement  of  SBP,  DBP,  and
          LVEF in cardiovascular patients who use bisoprolol.
          KEYWORDS    bisoprolol; β1-adrenergic receptor; ADRB1 Arg389Gly; gene polymorphism; meta-analysis



             Δ 基金项目 国家重点研发计划项目(No.2020YFC2008305)                比索洛尔是选择性 β1肾上腺素受体(β1-adrenergic
             *第一作者 主管药师,博士。研究方向:临床药学、药事管理。电
                                                             receptor,β1-AR)阻断剂,在临床广泛用于控制血压和心
          话:010-85133637。E-mail:ztqweather@hotmail.com
                                                             率,主要适应证为高血压、冠心病(心绞痛)和慢性稳定
             # 通信作者 主任药师,硕士。研究方向:临床药学、药物警戒。电
          话:010-85133637。E-mail:jlw1228@sina.com             型心衰。β1-AR 是 G 蛋白偶联受体,由 ADRB1 基因编


          中国药房  2024年第35卷第5期                                                 China Pharmacy  2024 Vol. 35  No. 5    · 601 ·
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