氟哌啶醇与安慰剂为精神分裂症。

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亚当斯CE,伯格曼H,欧文CB,洛瑞

氟哌啶醇与安慰剂为精神分裂症。

科克伦数据库系统启2013 11月15;(11):CD003082。cd003082.pub3 doi: 10.1002/14651858.。

PubMed ID
24242360 (在PubMed
]
文摘

背景:氟哌啶醇是在1950年代末开发的麻醉领域的使用。随后研究了影响幻觉、妄想,攻击性,冲动和兴奋的状态,导致作为一个抗精神病药物氟哌啶醇的引入。目的:探讨精神分裂症的临床影响氟哌啶醇的管理与安慰剂比较,和其他类似的严重的精神疾病。搜索方法:最初,我们电子搜索生物抽象的数据库(1985 - 1998),CINAHL (1982 - 1998), Cochrane图书馆(1998年,问题4),Cochrane精神分裂症组的寄存器(1998年12月),EMBASE (1980 - 1998), MEDLINE (1966 - 1998), PsycLIT(1974 - 1998),和SCISEARCH。我们还检查引用的所有识别研究为进一步试验引文的作者和联系试验和制药公司进行进一步的信息和档案材料。2012年更新,2012年5月15日,我们搜查了Cochrane精神分裂症组的试验注册。选择标准:我们包括所有相关随机对照试验比较使用氟哌啶醇与安慰剂(任何口服剂量)对于那些患有精神分裂症或其他类似的严重,非情感性精神病疾病(然而诊断)。我们感兴趣的主要成果是死亡,失去随访,临床和社会反应、复发和不利影响的严重性。数据收集和分析:我们独立评估数据和提取,重新和质量评估数据。我们分析了两个数据使用风险比(RR),并计算其95%可信区间(CI)。对于连续数据,我们计算意味着差异(MD)。 We excluded continuous data if loss to follow-up was greater than 50% and inspected data for heterogeneity. We used a fixed-effect model for all analyses. For the 2012 update, we assessed risk of bias of included studies and used the GRADE approach to create a 'Summary of findings' table. MAIN RESULTS: Twenty-five trials randomising 4651 people are now included in this review. We chose seven main outcomes of interest for the 'Summary of findings' table. More people allocated haloperidol improved in the first six weeks of treatment than those given placebo (4 RCTs n = 472, RR 0.67 CI 0.56 to 0.80, moderate quality evidence). A further eight trials also found a difference favouring haloperidol across the six weeks to six months period (8 RCTs n = 307 RR 0.67 CI 0.58 to 0.78, moderate quality evidence). Relapse data from two trials favoured haloperidol at < 52 weeks but the evidence was very low quality (2 RCTs n = 70, RR 0.69 CI 0.55 to 0.86). Moderate quality evidence showed about half of those entering studies failed to complete the short trials (six weeks to six months), although, at up to six weeks, 16 studies found a difference that marginally favoured haloperidol (n = 1812, RR 0.87 CI 0.80 to 0.95). Adverse effect data does, nevertheless, support clinical impression that haloperidol is a potent cause of movement disorders, at least in the short term. Moderate quality evidence indicates that haloperidol caused parkinsonism (5 RCTs n = 485, RR 5.48 CI 2.68 to 11.22), akathisia (6 RCTs n = 695, RR 3.66 CI 2.24 to 5.97, and acute dystonia (5 RCTs n = 471, RR 11.49 CI 3.23 to 10.85). Discharge from hospital was equivocal between groups (1 RCT n = 33, RR 0.85 CI 0.47 to 1.52, very low quality evidence). Data were not reported for death and patient satisfaction. AUTHORS' CONCLUSIONS: Haloperidol is a potent antipsychotic drug but has a high propensity to cause adverse effects. Where there is no treatment option, use of haloperidol to counter the damaging and potentially dangerous consequences of untreated schizophrenia is justified. However, where a choice of drug is available, people with schizophrenia and clinicians may wish to prescribe an alternative antipsychotic with less likelihood of adverse effects such as parkinsonism, akathisia and acute dystonias. Haloperidol should be less favoured as a control drug for randomised trials of new antipsychotics.

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