背景:酒精给药和提示反应性范例经常用于筛选酒精使用障碍(AUD)药物的初始功效。虽然药物对这些范式的主要结果的影响被认为是定性相关的,严重缺乏支持这一假设的定量证据。
目的:该研究旨在测试对酒精给药的主观反应的药物效应大小与提示引起的对提示暴露的渴望的药物效应大小之间的关系,使用荟萃分析。
方法:进行了系统的文献检索,以确定随机试验,其中AUD药物使用酒精施用和/或提示反应性范例进行测试。从这些研究中,我们收集了描述性统计数据,以计算每个范式对主要结局的药物效应大小.以药物为分析单位,使用Williamson-York回归对酒精给药研究中的药物效应大小与提示反应性研究中的药物效应大小进行了比较,该回归允许跨独立样本进行meta回归.
结果:对酒精诱导的刺激和酒精诱导的渴望的药物效应大小与提示诱导的酒精渴望的药物效应大小没有显着相关(k刺激=10种药物,[配方:见正文]和k渴望=11种药物,[公式:见正文](SE=0.237),[公式:见正文]),分别。药物对酒精诱导的镇静作用大小与药物对提示诱导的渴望的作用显着相关(k=10种药物,[公式:见正文](SE=0.258),[公式:见正文]),这样,增加酒精引起的镇静作用的药物更有可能减少提示引起的酒精渴望。
结论:除酒精引起的镇静作用外,几乎没有定量证据表明药物对酒精给药过程中测量的主观反应域的影响。为当前研究提供更多背景,未来的工作应该检查提示反应性结果是否能预测临床试验结果.
BACKGROUND: Alcohol administration and cue-reactivity paradigms are frequently used to screen for the initial efficacy of medications for alcohol use disorder (AUD). While medication effects on the primary outcomes for these paradigms are assumed to be qualitatively related, there is a critical lack of quantitative evidence to support this hypothesis.
OBJECTIVE: The study aims to test the relationship between medication effect sizes on subjective response to alcohol administration and medication effect sizes for cue-induced craving to cue exposure, using meta-analysis.
METHODS: Systematic literature searches were conducted to identify randomized trials, wherein AUD medications were tested using the alcohol administration and/or cue-reactivity paradigms. From these studies, descriptive statistics were collected to compute medication effect sizes on the primary outcomes for each respective paradigm. With medication as the unit of analysis, medication effect sizes in alcohol administration studies were compared with medication effect sizes in cue-reactivity studies using the Williamson-York regression which allows for meta-regression across independent samples.
RESULTS: Medication effect sizes on alcohol-induced stimulation and alcohol-induced craving were not significantly associated with medication effect sizes on cue-induced alcohol craving (k stimulation = 10 medications, [Formula: see text] and k craving = 11 medications, [Formula: see text] (SE = 0.237), [Formula: see text]), respectively. Medication effect sizes on alcohol-induced sedation were significantly associated with medication effects on cue-induced craving (k = 10 medications, [Formula: see text] (SE = 0.258), [Formula: see text]), such that medications that increased alcohol-induced sedation were more likely to reduce cue-induced alcohol craving.
CONCLUSIONS: With the exception of alcohol-induced sedation, there is little quantitative evidence of medication effects on subjective response domains measured during alcohol administration parallel medication effects on cue-induced alcohol craving. To provide additional context to the current study, future work should examine whether cue-reactivity findings predict clinical trial outcomes.