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Nicotine‐Use/Smoking Is Associated with the Efficacy of Naltrexone in the Treatment of Alcohol Dependence
Author(s) -
Anton Raymond F.,
Latham Patricia K.,
Voronin Konstantin E.,
Randall Patrick K.,
Book Sarah W.,
Hoffman Michaela,
Schacht Joseph P.
Publication year - 2018
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.13601
Subject(s) - naltrexone , nicotine , placebo , medicine , alcohol dependence , randomized controlled trial , smoking cessation , alcohol , pharmacology , opioid , chemistry , biochemistry , receptor , alternative medicine , pathology
Background The opioid antagonist naltrexone is not efficacious for every alcohol treatment seeker. However, various individual factors, such as genetic differences and nicotine‐use/smoking status, have been suggested as predictors of naltrexone response. In a randomized clinical trial, we previously reported that nicotine‐use/smoking status might be a stronger predictor of naltrexone efficacy than OPRM 1 A118G single nucleotide polymorphism ( SNP ) genotype. In this report, we further characterize the nicotine‐users in that trial, examine other drinking outcomes, examine the influence of smoking change on naltrexone effects on drinking, and validate the result in smokers with disialo carbohydrate‐deficient transferrin (% dCDT ) change as an independent biomarker of response. Methods Individuals ( n = 146) meeting DSM ‐ IV criteria for alcohol dependence who were genotyped for the OPRM 1 A118G SNP and who did, or did not, use nicotine/cigarettes were randomized, in a balanced fashion, to naltrexone (50 mg/d) or placebo and provided medical management (MM) over a 16‐week clinical trial. Alcohol use and smoking during the trial were assessed and analyzed. Results Nicotine‐use/smoking status significantly interacted with medication in reducing percent heavy drinking days ( PHDD ) during the trial ( p = 0.003), such that nicotine‐users/smokers showed significantly lower PHDD on naltrexone versus placebo ( p = 0.0001, Cohen's d = 0.89), while nonusers showed no significant difference between naltrexone and placebo ( p = 0.95, Cohen's d = 0.02). Similar effects were shown for drinks per day and percent days drinking. The superiority of naltrexone over placebo on PHDD reduction in nicotine‐users/smokers was confirmed with % dCDT (Cohen's d range 0.3 to 0.9 over the study). Naltrexone did not significantly change cigarette use in smokers, and change in use did not influence naltrexone's effect on PHDD . Conclusions These data confirm past findings that naltrexone is more efficacious in those who use nicotine/cigarettes. Compared to previous work on the OPRM 1 A118G SNP , it appears that nicotine‐use might be a more salient predictor of naltrexone treatment response. While naltrexone did not change cigarette use during the study, and smoking change was not related to alcohol reduction, it should be noted that participants were not seeking smoking cessation and MM did not address this issue.