Treatment of Alcohol Use Disorder in Patients with Alcoholic Liver Disease
Alcohol is a leading cause of liver disease worldwide. Although alcohol abstinence is the crucial therapeutic goal for patients with alcoholic liver disease, these patients have less access to psychosocial, behavioral, and/or pharmacologic treatments for alcohol use disorder. Psychosocial and behavioral therapies include 12-step facilitation, brief interventions, cognitive behavioral therapy, and motivational enhancement therapy. In addition to medications approved by the US Food and Drug Administration for alcohol use disorder (disulfiram, naltrexone, and acamprosate), recent efforts to identify potential new treatments have yielded promising candidate pharmacotherapies. Finally, more efforts are needed to integrate treatments across disciplines toward patient-centered approaches in the management of patients with alcohol use disorder and alcoholic liver disease.
Despite the mortality and morbidity resulting from alcohol use disorder,1 <10% of patients receive treatment for alcohol use disorder.2 There is a paucity of clinical trials in patients with alcoholic liver disease and little integration of addiction specialists into the medical teams that care for these patients. This deficiency reflects nihilism, stigma, and a failure to link behavioral and traditional medical research.
Alcohol Use Disorder
Neurobiology of Alcohol Use Disorder
Alcohol use disorder is characterized by loss of control over alcohol consumption, accompanied by changes in brain regions responsible for the execution of motivated behaviors (eg, midbrain and limbic and prefrontal cortex).3 Positive and negative reinforcement mechanisms play a role in the maladaptive pattern of alcohol consumption. As the severity of alcohol use disorder worsens, negative reinforcement mechanisms predominate whereby negative affective state is relieved by alcohol consumption, thus leading to relapse.
Alcohol’s reinforcing effects are primarily mediated by dopamine, opioid peptides, γ-aminobutyric acid, and endocannabinoids,4 whereas negative reinforcement involves increased recruitment of corticotropin-releasing factor and glutamatergic systems and down-regulation of γ-aminobutyric acid transmission.3, 4
Screening and Diagnosis of Alcohol Use Disorder
Screening instruments for problematic drinking include the Cut down-Annoyed-Guilty-Eye opener (CAGE) and the Alcohol Use Disorders Identification Test (AUDIT) (Tables 1 and 2).5, 6 The CAGE is short, may be easily implemented in primary care settings, and assesses consequences of drinking. The latter makes it less sensitive as a screening tool for at-risk drinking and gives inconsistent results across different ethnicities.7 The AUDIT actually quantifies alcohol consumption and has been validated across different ethnicities.7 There is a brief version of the AUDIT, developed for use in primary care settings.8
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-Lorenzo Leggio, MD, PhD, MSc, Mary R. Lee, MD
This article originally appeared in the February 2017 issue of The American Journal of Medicine.