破伤风抗毒素致不良反应2 636例文献分析
x

请在关注微信后,向客服人员索取文件

篇名: 破伤风抗毒素致不良反应2 636例文献分析
TITLE:
摘要: 目的:探讨破伤风抗毒素(TAT)致不良反应(ADR)的一般规律及特点,为临床合理用药提供参考。方法:检索国内外公开发表的TAT致ADR的文献,并就收集到的2 636例ADR相关信息进行统计和分析。结果:记录了性别、年龄的患者中,TAT致ADR男性高于女性,以15~35岁为主,约占70.32%(289/411);溶剂为注射用水的约占28.28%(56/198);用药30 min内发生ADR占5.84%(154/2 636),以皮肤及附件损害、循环系统损害及全身反应为主;临床表现主要为荨麻疹、皮肤瘙痒、胸闷、过敏性休克等。死亡病例10例,留有后遗症7例,其余患者经积极对症治疗后均好转或痊愈。结论:TAT致过敏反应尤其是过敏性休克的比例较高,但罕见的听觉和前庭功能障碍、视力损伤、白细胞升高等ADR仍应引起重视,建议临床加强用药监测,严格按说明书用药,促进合理用药。
ABSTRACT: OBJECTIVE: To investigate general regularity and characteristics of tetanus antitoxin (TAT) induced by ADRs, in order to provide reference for rational drug use in the clinic. METHODS: Domestic and foreign literatures on ADRs induced by TAT were retrieved, and related information of 2 636 case of ADR were analyzed statistically. RESULTS: Among patients whose gender and age were recorded, male with ADR induced by TAT was more than female, mainly aged 15-35 years old, accounting for 70.32%(289/411); 28.28%(56/198) used water for injection; ADR occurred within 30 min after medication in 5.84%(154/2 636)cases; main ADR were lesion of skin and its appendents, circulatory system damage, systemic reaction damage. Main clinical manifestations were urticaria, rash, chest tightness and anaphylactic shock, etc. Ten cases died and 7 cases had sequelae; the rest were all recovered and cured after symptomatic treatment. CONCLUSIONS: TAT has a higher proportion of allergic reactions, especially anaphylactic shock, but great importance should be attached to rare auditory and vestibular dysfunction, visual impairment, elevated white blood cell count and other ADR. It is suggested to strengthen medication monitoring and used drugs strictly in accordance with drug package inserts so as to promote rational drug use.
期刊: 2017年第28卷第36期
作者: 余超,徐玉茗,徐瑾,万凯化,袁兴东,李穗,周鹃
AUTHORS: YU Chao,XU Yuming,XU Jin,WAN Kaihua,YUAN Xingdong,LI Sui,ZHOU Juan
关键字: 破伤风抗毒素;不良反应;文献分析;合理用药
KEYWORDS: Tetanus antitoxin; ADR; Literature analysis; Rational drug use
阅读数: 556 次
本月下载数: 9 次

* 注:未经本站明确许可,任何网站不得非法盗链资源下载连接及抄袭本站原创内容资源!在此感谢您的支持与合作!