Alcoholism Medication

  • Author: Warren Thompson, MD, FACP; Chief Editor: Iqbal Ahmed, MBBS, FRCPsych (UK)   more...
 
Updated: Jan 11, 2012
 

Medication Summary

Treatment of alcohol withdrawal is best accomplished with benzodiazepines. Avoid fixed-dose therapy, and treat patients for symptoms. This results in use of lower doses of benzodiazepines, less patient sedation, and earlier patient discharge. Lorazepam and oxazepam are preferred for patients with significant liver disease because the half-lives of other benzodiazepines can be significantly prolonged. These shorter-acting benzodiazepines require more frequent patient monitoring. Use longer-acting drugs (eg, chlordiazepoxide) when monitoring is not reliable.

Other agents that have been used with some success in the treatment of withdrawal include beta-blockers, clonidine, phenothiazines, and anticonvulsants. All can be used with benzodiazepines, but none has been proven to be adequate as monotherapy. A number of medications have been tried in the treatment of alcoholism. Disulfiram (Antabuse) has been used as an adjunct to counseling and AA with motivated patients to reduce the risk of relapse. Patients are reminded of the risks of adverse effects when tempted to drink. Disulfiram causes nausea, vomiting, and dysphoria with coincident alcohol use. In a large trial, disulfiram did not increase abstinence. If a patient asks for disulfiram and thinks it will help, it might be worth considering.

Naltrexone blocks opiate receptors and works by decreasing the craving for alcohol, resulting in fewer relapses. A recent positron emission tomography study demonstrated that persons with alcoholism have increased opiate receptors in the nucleus accumbens of the brain and that the number of receptors correlates with craving.

Most, but not all, studies found that naltrexone decreases relapses but the effect is modest (12-20%). Combining naltrexone therapy with cognitive behavioral therapy enhanced benefit. One study showed benefit with an intensive primary care intervention. Studies suggest that virtually all placebo patients who sampled alcohol relapsed, while only half the naltrexone patients who sampled alcohol relapsed.

Most studies are of short duration, and more long-term trials are needed. In short-term studies when naltrexone was stopped, patients relapsed. Naltrexone has a greater effect on reducing relapse to heavy drinking than it does on maintaining abstinence. Extended-release intramuscular naltrexone resulted in reduced relapse to heavy drinking in a large, randomized trial. Its effects on complete abstinence were more modest. The main adverse effects are nausea and/or vomiting, abdominal pain, sleepiness, and nasal congestion.

In 2001, Sinclair reviewed 8 studies and suggested that naltrexone is safe to administer in patients who are still drinking and that it will gradually result in the patient consuming less alcohol (this is the case in laboratory animals).[39] Patients should take the naltrexone daily initially and then only when they have a strong urge to drink. Patients should carry naltrexone with them indefinitely. Patients should agree to always take the naltrexone prior to drinking alcohol. Daily naltrexone may be counterproductive in patients who remain abstinent. It is most helpful in those who sample alcohol after stopping (lower chance of a relapse). More data are needed before this approach can be adapted because it challenges the conventional wisdom that complete abstinence is always the goal of treatment.

Nalmefene is another opioid antagonist, and it blocks delta, kappa, and mu receptors; naltrexone acts primarily on mu receptors. One randomized trial with 100 patients using 10 mg PO bid has been completed, and nalmefene appears to have efficacy similar to naltrexone (reduces relapse to heavy drinking in patients who sample alcohol). At present, the drug is approved only for intravenous use for opiate addiction.

The 2010 Cochrane review on opioid antagonists for alcohol dependence included 50 studies with 7793 participants.[40] In most studies, treatment was provided over 3 months. The review showed that more patients who took naltrexone were able to reduce the amount and frequency of drinking compared with patients who took placebo. On average, 1 in 9 patients were helped by naltrexone. For injectable formulations of naltrexone, which can be advantageous for patients who have problems with taking their medication on schedule, and for the second opioid antagonist (nalmefene), the evidence was too limited to allow final conclusions. Nevertheless, available studies indicated that these drugs might have effects on drinking comparable to oral naltrexone.

A number of studies have focused on antidepressants. Early studies with the selective serotonin reuptake inhibitors (SSRIs) have been disappointing. Two fairly good studies used tricyclic antidepressants (ie, desipramine, imipramine), which showed some short-term benefit. More data are needed. SSRIs probably do not benefit patients who are not depressed but might benefit those who are depressed. Topiramate facilitates GABA function and antagonizes glutamate, which should decrease mesocorticolimbic dopamine after alcohol and reduce cravings. One double-blinded trial with 150 subjects for 12 weeks suggests this is the case (decreased drinking, decreased craving, and greater abstinence). Topiramate is not approved for this use by the US Food and Drug Administration.

The largest and longest studies on the treatment of alcohol abuse have been performed in Europe with acamprosate (Campral). At 1 year, the continuous abstinence rates were 18% in the acamprosate group and 7% in the placebo group. At 2 years, the continuous abstinence rates were 12% in the acamprosate group and 5% in the placebo group. Most patients returned to drinking while still using the drug. The drug was recently approved in the United States. It stimulates GABA transmission, inhibits glutamate, and decreases alcohol consumption in alcohol-dependent rats. The main adverse effect is diarrhea.

Two short-term trials have compared acamprosate and naltrexone. Both found naltrexone to be superior. One of these studies compared the combination with either drug alone and with placebo. The combination was statistically superior to placebo and acamprosate alone and superior (but not statistically) to naltrexone alone. Larger and longer trials of the combination therapy are needed.

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Glutamate receptor blockers

Class Summary

Mechanism of action is unknown, but it enhances GABA transmission and inhibits glutamate transmission. Compared with placebo, reduces drinking frequency and effectively increases abstinence in patients with alcoholism.

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Acamprosate (Campral)

 

Synthetic compound with a chemical structure similar to that of the endogenous amino acid homotaurine (structural analogue of GABA). Mechanism of action to maintain alcohol abstinence not completely understood. Hypothesized to interact with glutamate and GABA neurotransmitters centrally to restore neuronal excitation and inhibition balance. Not associated with tolerance or dependence development. Use does not eliminate or diminish alcohol withdrawal symptoms. Indicated to maintain alcohol abstinence as part of a comprehensive management program that includes psychosocial support. Available as a 333-mg tab.

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Aldehyde dehydrogenase inhibitors

Class Summary

Disulfiram inhibits aldehyde dehydrogenase, and, as a result, acetaldehyde accumulates. This leads to nausea, hypotension, and flushing if a person drinks alcohol while taking disulfiram.

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Disulfiram (Antabuse)

 

Decreases number of drinking days but does not increase abstinence. Directly observed therapy might be more beneficial but has not been studied in a good randomized trial.

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Opiate antagonists

Class Summary

Alcohol has been shown to bind to opiate receptors in the brain. Studies show that blocking opiate receptors decreases cravings for alcohol.

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Naltrexone (ReVia, Vivitrol)

 

Patients must be abstinent for 5-7 d before beginning therapy. Monitor liver function during treatment. Expensive, approximately $4.50/pill. Pure antagonist and is not addicting.

IM administration of Vivitrol reduces first-pass hepatic metabolism as compared with oral naltrexone. No significant increase from baseline in mean AST or ALT levels.

Vivitrol does not appear to be a hepatotoxin at recommended doses but patients should be warned of risk of hepatic injury. Preparation is considered nonaddicting.

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Contributor Information and Disclosures
Author

Warren Thompson, MD, FACP  Associate Professor, Department of Internal Medicine, Mayo Medical School

Warren Thompson, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Heart Association, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Coauthor(s)

R Gregory Lande, DO, FACN  Clinical Consultant, Army Substance Abuse Program, Department of Psychiatry, Walter Reed Army Medical Center

R Gregory Lande, DO, FACN is a member of the following medical societies: American Osteopathic Academy of Addiction Medicine and American Osteopathic Association

Disclosure: Nothing to disclose.

Raj K Kalapatapu, MD  Fellow, Addiction Psychiatry, Columbia University College of Physicians and Surgeons

Raj K Kalapatapu, MD is a member of the following medical societies: American Academy of Addiction Psychiatry, American Academy of Child and Adolescent Psychiatry, American Association for Geriatric Psychiatry, American Medical Association, and American Psychiatric Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Denis F Darko, MD  Executive Director, Clinical Research and Development, Global Neuroscience, AstraZeneca

Denis F Darko, MD is a member of the following medical societies: American College of Physicians and American Psychiatric Association

Disclosure: AstraZeneca Salary Management position

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Harold H Harsch, MD  Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin

Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association

Disclosure: lilly Honoraria Speaking and teaching; Forest Labs None None; Pfizer Grant/research funds Speaking and teaching; Northstar None None; Novartis Grant/research funds research; Pfizer Honoraria Speaking and teaching; Sunovion Speaking and teaching; Otsuke Grant/research funds reseach; GlaxoSmithKline Grant/research funds research; Merck Honoraria Speaking and teaching

Chief Editor

Iqbal Ahmed, MBBS, FRCPsych (UK)  Faculty, Department of Psychiatry, Tripler Army Medical Center; Clinical Professor of Psychiatry, Clinical Professor of Geriatric Medicine, University of Hawaii, John A Burns School of Medicine

Iqbal Ahmed, MBBS, FRCPsych (UK) is a member of the following medical societies: Academy of Psychosomatic Medicine, American Association for Geriatric Psychiatry, American Neuropsychiatric Association, American Psychiatric Association, American Society of Clinical Psychopharmacology, and Royal College of Psychiatrists

Disclosure: Nothing to disclose.

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Deaths while intoxicated. Data from the National Institute on Alcohol Abuse and Alcoholism (NIAAA).
Table 1. AUDIT Questions and Scoring System
Questions0 Points1 Point2 Points3 Points4 Points
1. How often do you have a drink containing alcohol?NeverMonthly or less2-4 times a month2-3 times a week4 or more times a week
2. How many drinks containing alcohol do you have on a typical day when you are drinking?1 or 23 or 45 or 67-910 or more
3. How often do you have 6 or more drinks on 1 occasion?NeverLess than monthlyMonthlyWeeklyDaily or almost daily
4. How often during the past year have you found that you were not able to stop drinking once you had started?NeverLess than monthlyMonthlyWeeklyDaily or almost daily
5. How often during the past year have you failed to do what was normally expected of you because of drinking?NeverLess than monthlyMonthlyWeeklyDaily or almost daily
6. How often during the past year have you needed a first drink in the morning to get yourself going after a heavy drinking session? NeverLess than monthlyMonthlyWeeklyDaily or almost daily
7. How often during the past year have you had a feeling of guilt or remorse after drinking?NeverLess than monthlyMonthlyWeeklyDaily or almost daily
8. How often during the past year have you been unable to remember what happened the night before because you had been drinking?NeverLess than monthlyMonthlyWeeklyDaily or almost daily
9. Have you or has someone else been injured as a result of your drinking?NoYes, but not in the past yearYes, during the past year
10. Has a relative, friend, or a doctor or other health care worker been concerned about your drinking or suggested you cut down? NoYes, but not in the past yearYes, during the past



year



Table 2. Sensitivity and Specificity of Alcohol Biomarkers*
BiomarkerSensitivity (%)Specificity (%)
AST15-6947-68
ALT18-5850-57
GGT34-8511-95
MCV34-8926-95
CDT39-9482-100
CDT + GGT90 † 98
Alcohol0-1000-100
EtG76-9177-92
*Values vary considerably according to gender, age, drinking pattern, prevalence of alcohol abuse/dependence, and prevalence of comorbidity, among other factors.[30, 31, 35, 36, 32]



† The sensitivity comes from one study in Finland, which uses a special formula. This study needs to be replicated.[37]



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