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International Journal of Environmental... Jan 2023No single effective therapy for alcohol abuse has been found, despite it being a serious sociological and economic problem for hundreds of years. It seems difficult to... (Review)
Review
No single effective therapy for alcohol abuse has been found, despite it being a serious sociological and economic problem for hundreds of years. It seems difficult to find a single drug as a panacea for the alcohol problem due to the complexity of the pathophysiology of alcohol dependence. The purpose of this narrative review is to review existing and potentially future pharmaceuticals for the treatment of alcohol dependence in the most affordable way possible. Psychotherapy is the mainstay of treatment for alcoholism, while few drugs approved by legislators are available in the augmentation of this treatment, such as acamprosate, disulfiram, and naltrexone, approved by the FDA, and nalmefene by the EMA. There are recent reports in the literature on the possibility of using baclofen, topiramate, varenicline, and gabapentin in the treatment of alcohol dependence. Moreover, the results of recent clinical trials using psychoactive substances such as psilocybin and MDMA appear to be a breakthrough in the modern treatment of alcohol abuse. Despite this initial optimism, a lot of scientific effort is still needed before new pharmacological methods supporting the treatment of alcohol dependence syndrome will be widely available.
Topics: Humans; Alcoholism; Public Health; Acamprosate; Disulfiram; Pharmaceutical Preparations; Alcohol Deterrents; Taurine
PubMed: 36767234
DOI: 10.3390/ijerph20031870 -
BMC Gastroenterology Feb 2023Alcohol cessation is the cornerstone of treatment for alcohol-related cirrhosis. This study evaluated associations between medical conversations about alcohol use...
BACKGROUND
Alcohol cessation is the cornerstone of treatment for alcohol-related cirrhosis. This study evaluated associations between medical conversations about alcohol use disorder (AUD) treatment, AUD treatment engagement, and mortality.
METHODS
This retrospective cohort study included all patients with ICD-10 diagnosis codes for cirrhosis and AUD who were engaged in hepatology care in a single healthcare system in 2015. Baseline demographic, medical, liver disease, and AUD treatment data were assessed. AUD treatment discussions and initiation, alcohol cessation, and subsequent 5-year mortality were collected. Multivariable models were used to assess the factors associated with subsequent AUD treatment and 5-year mortality.
RESULTS
Among 436 patients with cirrhosis due to alcohol, 65 patients (15%) received AUD treatment at baseline, including 48 (11%) receiving behavioral therapy alone, 11 (2%) receiving pharmacotherapy alone, and 6 (1%) receiving both. Over the first year after a baseline hepatology visit, 37 patients engaged in AUD treatment, 51 were retained in treatment, and 14 stopped treatment. Thirty percent of patients had hepatology-documented AUD treatment recommendations and 26% had primary care-documented AUD treatment recommendations. Most hepatology (86%) and primary care (88%) recommendations discussed behavioral therapy alone. Among patients with ongoing alcohol use at baseline, AUD treatment one year later was significantly, independently associated with AUD treatment discussions with hepatology (adjusted odds ratio (aOR): 3.23, 95% confidence interval (CI): 1.58, 6.89) or primary care (aOR: 2.95; 95% CI: 1.44, 6.15) and negatively associated with having Medicaid insurance (aOR: 0.43, 95% CI: 0.18, 0.93). When treatment was discussed in both settings, high rates of treatment ensued (aOR: 10.72, 95% CI: 3.89, 33.52). Over a 5-year follow-up period, 152 (35%) patients died. Ongoing alcohol use, age, hepatic decompensation, and hepatocellular carcinoma were significantly associated with mortality in the final survival model.
CONCLUSION
AUD treatment discussions were documented in less than half of hepatology and primary care encounters in patients with alcohol-related cirrhosis, though such discussions were significantly associated with receipt of AUD treatment.
Topics: United States; Humans; Retrospective Studies; Alcoholism; Liver Cirrhosis, Alcoholic; Longitudinal Studies
PubMed: 36732709
DOI: 10.1186/s12876-023-02656-z -
The Cochrane Database of Systematic... Jan 2023Alcohol use disorder (AUD) is one of the most widespread psychiatric disorders leading to detrimental consequences to people with this disorder and others. Worldwide,... (Review)
Review
BACKGROUND
Alcohol use disorder (AUD) is one of the most widespread psychiatric disorders leading to detrimental consequences to people with this disorder and others. Worldwide, the prevalence of heavy episodic drinking (30-day prevalence of at least one occasion of 60 g of pure alcohol intake among current drinkers) is estimated at 20% and the prevalence of AUD at 5% of the adult general population, with highest prevalence in Europe and North America. Therapeutic approaches, including pharmacotherapy, play an important role in treating people with AUD. This is an update of a Cochrane Review first published in 2018.
OBJECTIVES
To evaluate the benefits and harms of baclofen on achieving and maintaining abstinence or reducing alcohol consumption in people with AUD compared to placebo, no treatment or any other pharmacological relapse prevention treatment.
SEARCH METHODS
We used standard, extensive Cochrane search methods. The latest search was 22 November 2021.
SELECTION CRITERIA
Randomised controlled trials (RCTs) of at least four weeks' treatment duration and 12 weeks' overall study duration comparing baclofen for AUD treatment with placebo, no treatment or other treatments.
DATA COLLECTION AND ANALYSIS
We used standard Cochrane methods. Our primary outcomes were 1. relapse, 2. frequency of use, 3. amount of use, 4. adverse events, 5. dropouts from treatment and 6. dropouts from treatment due to adverse events. Our secondary outcomes were 7. craving, 8. anxiety, 9. depression and 10. frequency of most relevant adverse events.
MAIN RESULTS
We included 17 RCTs (1818 participants) with a diagnosis of alcohol dependence according to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition or International Classification of Diseases 10th edition criteria. Mean age was 46.5 years and 70% were men. Ten studies compared baclofen to placebo or another medication; seven compared two baclofen doses to placebo or another medication. Globally, 15 studies compared baclofen to placebo, two baclofen to acamprosate and two baclofen to naltrexone. In 16 studies, participants received psychosocial treatments. We judged most studies at low risk of selection, performance, detection (subjective outcome), attrition and reporting bias. Ten studies detoxified participants before treatment; in seven studies, participants were still drinking at the beginning of treatment. Treatment duration was 12 weeks for 15 RCTs and longer in two studies. Baclofen daily dose was 30 mg to 300 mg: 10 RCTs used low doses (30 mg or less); eight RCTs medium doses (above 30 and 100 mg or less) and four RCTs high doses (above 100 mg). Compared to placebo, moderate-certainty evidence found that baclofen probably decreases the risk to relapse (risk ratio (RR) 0.87, 95% confidence interval (CI) 0.77 to 0.99; 12 studies, 1057 participants). This result was confirmed among detoxified participants but not among other subgroups of participants. High-certainty evidence found that baclofen increases the percentage of days abstinent (mean difference (MD) 9.07, 95% CI 3.30 to 14.85; 16 studies, 1273 participants). This result was confirmed among all subgroups of participants except non-detoxified or those who received medium doses. There was no difference between baclofen and placebo in the other primary outcomes: heavy drinking days (standardised mean difference (SMD) -0.18, 95% CI -0.48 to 0.11; 13 studies, 840 participants; moderate-certainty evidence); number of drinks per drinking days (MD -0.45, 95% CI -1.20 to 0.30; 9 studies, 392 participants; moderate-certainty evidence); number of participants with at least one adverse event (RR 1.05, 95% CI 0.99 to 1.11; 10 studies, 738 participants; high-certainty evidence); dropouts (RR 0.88, 95% CI 0.74 to 1.03; 17 studies, 1563 participants; high-certainty evidence); dropouts due to adverse events (RR 1.39, 95% CI 0.89 to 2.18; 16 studies, 1499 participants; high-certainty evidence). These results were confirmed by subgroup analyses except than for the dropouts that resulted lower among participants who received high doses of baclofen and studies longer than 12 weeks. Compared to placebo, there was no difference in craving (SMD -0.16, 95% CI -0.37 to 0.04; 17 studies, 1275 participants), anxiety (MD -0.01, 95% CI -0.14 to 0.11; 15 studies, 1123 participants) and depression (SMD 0.07, 95% CI -0.12 to 0.27; 11 studies, 1029 participants). Concerning the specific adverse events, baclofen increases fatigue, dizziness, somnolence/sedation, dry mouth, paraesthesia and muscle spasms/rigidity. There was no difference in the other adverse events. Compared to acamprosate, one study (60 participants) found no differences in any outcomes but the evidence was very uncertain: relapse (RR 1.25, 95% CI 0.71 to 2.20; very low-certainty evidence); number of participants with at least one adverse event (RR 0.63, 95% CI 0.23 to 1.69; very low-certainty evidence); dropouts (RR 0.56, 95% CI 0.21 to 1.46; very low-certainty evidence); dropouts due to adverse events (RR 0.33, 95% CI 0.01 to 7.87; very low-certainty evidence) and craving (MD 5.80, 95% CI -11.84 to 23.44); and all the adverse events evaluated. Compared to naltrexone, baclofen may increase the risk of relapse (RR 2.50, 95% CI 1.12 to 5.56; 1 study, 60 participants; very low-certainty evidence) and decrease the number of participants with at least one adverse event (RR 0.35, 95% CI 0.15 to 0.80; 2 studies, 80 participants; very low-certainty evidence) but the evidence is very uncertain. One study (60 participants) found no difference between baclofen and naltrexone in the dropouts at the end of treatment (RR 1.00, 95% CI 0.32 to 3.10; very low-certainty evidence), craving (MD 2.08, 95% CI -3.71 to 7.87), and all the adverse events evaluated.
AUTHORS' CONCLUSIONS
Baclofen likely reduces the risk of relapse to any drinking and increases the percentage of abstinent days, mainly among detoxified participants. It does not increase the number of participants with at least one adverse event, those who dropout for any reason or due to adverse events. It probably does not reduce number of heavy drinking days and the number of drinks per drinking days. Current evidence suggests that baclofen may help people with AUD in maintaining abstinence. The results of comparisons of baclofen with acamprosate and naltrexone were mainly based on only one study.
Topics: Adult; Female; Humans; Male; Middle Aged; Acamprosate; Alcohol Drinking; Alcoholism; Baclofen; Chronic Disease; Naltrexone
PubMed: 36637087
DOI: 10.1002/14651858.CD012557.pub3 -
Current Topics in Behavioral... Jan 2023Humans consume ethanol-containing beverages, which may cause an uncontrollable or difficult-to-control intake of ethanol-containing liquids and may result in alcohol use...
Humans consume ethanol-containing beverages, which may cause an uncontrollable or difficult-to-control intake of ethanol-containing liquids and may result in alcohol use disorders. How the transition at the molecular level from "normal" ethanol-associated behaviors to addictive behaviors occurs is still unknown. One problem is that the components contributing to normal ethanol intake and their underlying molecular adaptations, especially in neurons that regulate behavior, are not clear. The fruit fly Drosophila melanogaster and the earthworm Caenorhabditis elegans show behavioral similarities to humans such as signs of intoxication, tolerance, and withdrawal. Underlying the phenotypic similarities, invertebrates and vertebrates share mechanistic similarities. For example in Drosophila melanogaster, the dopaminergic neurotransmitter system regulates the positive reinforcing properties of ethanol and in Caenorhabditis elegans, serotonergic neurons regulate feeding behavior. Since these mechanisms are fundamental molecular mechanisms and are highly conserved, invertebrates are good models for uncovering the basic principles of neuronal adaptation underlying the behavioral response to ethanol. This review will focus on the following aspects that might shed light on the mechanisms underlying normal ethanol-associated behaviors. First, the current status of what is required at the behavioral and cellular level to respond to naturally occurring levels of ethanol is summarized. Low levels of ethanol delay the development and activate compensatory mechanisms that in turn might be beneficial for some aspects of the animal's physiology. Repeated exposure to ethanol however might change brain structures involved in mediating learning and memory processes. The smell of ethanol is already a key component in the environment that is able to elicit behavioral changes and molecular programs. Minimal networks have been identified that regulate normal ethanol consumption. Other environmental factors that influence ethanol-induced behaviors include the diet, dietary supplements, and the microbiome. Second, the molecular mechanisms underlying neuronal adaptation to the cellular stressor ethanol are discussed. Components of the heat shock and oxidative stress pathways regulate adaptive responses to low levels of ethanol and in turn change behavior. The adaptive potential of the brain cells is challenged when the organism encounters additional cellular stressors caused by aging, endosymbionts or environmental toxins or excessive ethanol intake. Finally, to underline the conserved nature of these mechanisms between invertebrates and higher organisms, recent approaches to identify drug targets for ethanol-induced behaviors are provided. Already approved drugs regulate ethanol-induced behaviors and they do so in part by interfering with cellular stress pathways. In addition, invertebrates have been used to identify new compounds targeting molecules involved in the regulation in ethanol withdrawal-like symptoms. This review primarily highlights the advances of the last 5 years concerning Drosophila melanogaster, but also provides intriguing examples of Caenorhabditis elegans and Apis mellifera in support.
PubMed: 36598738
DOI: 10.1007/7854_2022_413 -
Current Neuropharmacology 2024Patients with psychotic disorders (PD) often have comorbid alcohol use disorder (AUD), which is typically treated pharmacologically. Up till now, no systematic review...
BACKGROUND
Patients with psychotic disorders (PD) often have comorbid alcohol use disorder (AUD), which is typically treated pharmacologically. Up till now, no systematic review has examined the effectiveness and safety of AUD treatment in PD patients.
OBJECTIVES
This study aimed to systematically review the literature on (1) the effects of pharmacological treatments for AUD on drinking outcomes, (2) the side effects of the drugs, and (3) the effects of polypharmacy in patients with comorbid AUD and PD.
METHODS
Bibliographic searches were conducted in MEDLINE, Embase, Cochrane Central Register of Controlled Trials, and PsycINFO. At least two reviewers extracted the data, assessed the risk of bias, and performed the qualitative synthesis of the collected evidence.
RESULTS
Twelve eligible studies were identified, half being randomized controlled trials (RCTs). Three studies examined disulfiram, nine naltrexone, two acamprosate, and one nalmefene by comparing the effects of treatment to placebo, baseline, or pharmacological agents. Disulfiram and naltrexone were shown to reduce alcohol intake. Regarding acamprosate, the findings were mixed. Nalmefene decreased alcohol intake. All pharmacological agents appeared safe to use as AUD monotherapy, but cardiac events were reported when combining naltrexone and disulfiram. Nine studies had a high risk of bias, and three had some other concerns.
CONCLUSION
The studies provide tentative support for the use of naltrexone and disulfiram in this population, although combinations of pharmacological AUD treatments and other polypharmacy remain unexplored. The studies had high adherence rates that are hardly replicable in real-world settings. Thus, the findings should be confirmed in larger high quality efficacy and effectiveness RCTs with longer follow-ups.
Topics: Humans; Alcoholism; Naltrexone; Acamprosate; Disulfiram; Alcohol Drinking; Psychotic Disorders
PubMed: 36582063
DOI: 10.2174/1570159X21666221229160300 -
Drug and Alcohol Dependence Jan 2023Acamprosate and naltrexone, evidence-based pharmacotherapies for alcohol use disorder (AUD), are publicly covered by the Ontario Drug Benefit (ODB) programs; however,...
BACKGROUND
Acamprosate and naltrexone, evidence-based pharmacotherapies for alcohol use disorder (AUD), are publicly covered by the Ontario Drug Benefit (ODB) programs; however, their availability has changed over time, with expanded formulary access in July 2018, followed by an acamprosate shortage in February 2019 and ending in July 2020. We evaluated the impact of these events on the use of these medications in Ontario, Canada.
METHODS
We conducted a time-series analysis among individuals with AUD dispensed acamprosate or naltrexone through the ODB from July 2016 to December 2020. Outcomes included monthly rates of those with AUD on therapy (primary), and rate of initiation (secondary) overall and by treatment type. We used autoregressive moving average models to evaluate the impact of expanded coverage and the acamprosate shortage on rates of use, and reported characteristics at first dispensation.
RESULTS
Over the study period, 10,637 individuals (61.0% male) initiated acamprosate or naltrexone. Expanded coverage increased monthly utilization rates of acamprosate (p = 0.0004), naltrexone (p < 0.0001), and either AUD pharmacotherapy (p < 0.0001). The acamprosate shortage led to a 98.1% reduction in acamprosate use (p = 0.0003) but did not impact naltrexone (p = 0.51). Our secondary analysis yielded consistent results with respect to the shortage; however, the expanded formulary listing did not impact the rate of new acamprosate patients (p = 0.3). By December 2020, 5.3% of ODB recipients with AUD were accessing pharmacotherapy.
CONCLUSIONS
Although coverage expansion increased access to medications that treat AUD, the shortage of acamprosate led to large reductions in its use, with no responsive increase in naltrexone prescribing.
Topics: Humans; Male; Female; Acamprosate; Naltrexone; Alcohol Deterrents; Ontario; Taurine; Alcoholism
PubMed: 36463765
DOI: 10.1016/j.drugalcdep.2022.109705 -
Physiology & Behavior Feb 2023Despite the teratogenic effects of alcohol, little is known about the safety of pharmacotherapies such as acamprosate for the treatment of alcohol use disorders in...
BACKGROUND
Despite the teratogenic effects of alcohol, little is known about the safety of pharmacotherapies such as acamprosate for the treatment of alcohol use disorders in pregnancy. The aims of this study were to investigate, in a mouse model, the effects of maternally administered acamprosate on maternal and neonatal health, offspring neurodevelopment and behaviour, as well as examine whether acamprosate reduces the neurological harm associated with alcohol consumption in pregnancy.
METHODS
Dams were randomly allocated to one of four treatment groups: (i) control (water), (ii) acamprosate (1.6 g/L), (iii) alcohol (5% v/v) or (iv) acamprosate and alcohol (1.6 g/L; 5% v/v ethanol) and exposed from 2-weeks pre-pregnancy until postpartum day 7. Gestational outcomes including litter size and sex ratio were assessed, in addition to early-life markers of neurodevelopment. At 8 weeks of age, motor coordination, anxiety, locomotion, and memory of the adult offspring were also examined.
RESULTS
Exposure to acamprosate did not affect maternal and birth outcomes (mating success, gestational weight gain, litter size, sex ratio), neonatal outcomes (head and body length, postnatal weight) or neurodevelopmental markers (righting reflex and negative geotaxis). Acamprosate exposure did not affect offspring motor control, locomotion or anxiety, however the effects on short-term memory remain uncertain. Prenatal alcohol exposed offspring exhibited various alterations, such as lower postnatal weight, smaller head (p = 0.04) and body lengths (p = 0.046) at postnatal day 70 (males only), increased negative geotaxis speed (p = 0.03), an increased time spent in the inner zone of the open field (p = 0.02). Acamprosate mitigated the effects of alcohol for negative geotaxis at postnatal day 7 (p = 0.01) and female offspring weight at postnatal day 70 (p = 0.03).
CONCLUSIONS
Overall, we show that prenatal acamprosate exposure was not associated with poor maternal or neonatal health outcomes or impaired neurodevelopment and behaviour. However, acamprosate's effects on short-term memory remain uncertain. We present preliminary evidence to suggest acamprosate displayed some neuroprotective effects against damage caused by in utero alcohol exposure.
Topics: Pregnancy; Mice; Animals; Male; Humans; Female; Alcoholism; Acamprosate; Prenatal Exposure Delayed Effects; Reproduction; Ethanol
PubMed: 36427542
DOI: 10.1016/j.physbeh.2022.114037 -
Frontiers in Molecular Neuroscience 2022Alcohol use disorder (AUD) is highly prevalent and one of the leading causes of disability in the US and around the world. There are some molecular biomarkers of heavy... (Review)
Review
Alcohol use disorder (AUD) is highly prevalent and one of the leading causes of disability in the US and around the world. There are some molecular biomarkers of heavy alcohol use and liver damage which can suggest AUD, but these are lacking in sensitivity and specificity. AUD treatment involves psychosocial interventions and medications for managing alcohol withdrawal, assisting in abstinence and reduced drinking (naltrexone, acamprosate, disulfiram, and some off-label medications), and treating comorbid psychiatric conditions (e.g., depression and anxiety). It has been suggested that various patient groups within the heterogeneous AUD population would respond more favorably to specific treatment approaches. For example, there is some evidence that so-called reward-drinkers respond better to naltrexone than acamprosate. However, there are currently no objective molecular markers to separate patients into optimal treatment groups or any markers of treatment response. Objective molecular biomarkers could aid in AUD diagnosis and patient stratification, which could personalize treatment and improve outcomes through more targeted interventions. Biomarkers of treatment response could also improve AUD management and treatment development. Systems biology considers complex diseases and emergent behaviors as the outcome of interactions and crosstalk between biomolecular networks. A systems approach that uses transcriptomic (or other -omic data, e.g., methylome, proteome, metabolome) can capture genetic and environmental factors associated with AUD and potentially provide sensitive, specific, and objective biomarkers to guide patient stratification, prognosis of treatment response or relapse, and predict optimal treatments. This Review describes and highlights state-of-the-art research on employing transcriptomic data and artificial intelligence (AI) methods to serve as molecular biomarkers with the goal of improving the clinical management of AUD. Considerations about future directions are also discussed.
PubMed: 36407766
DOI: 10.3389/fnmol.2022.1032362 -
Alcohol and Alcoholism (Oxford,... Jan 2023Acamprosate, naltrexone and disulfiram are underprescribed for alcohol use disorder (AUD) with marked variability among primary care providers (PCPs). We aimed to...
AIMS
Acamprosate, naltrexone and disulfiram are underprescribed for alcohol use disorder (AUD) with marked variability among primary care providers (PCPs). We aimed to identify differences between high and low prescribers of medications for AUD (MAUD) with regard to knowledge, experiences, prioritization and attitudes.
METHODS
We surveyed PCPs from a large healthcare system with at least 20 patients with AUD. Prescribing rates were obtained from the electronic health record (EHR). Survey responses were scored from strongly disagree (1) to strongly agree (5). Multiple imputation was used to generate attitude scores for 7 missing subjects. PCPs were divided into groups by the median prescribing rate and attitude. Comparisons were made using Wilcoxon rank-sum and regression.
RESULTS
Of the 182 eligible PCPs, 68 (37.4%) completed the survey. Most indicated willingness to attend an educational course (57.4%). Compared with low prescribers, high prescribers viewed the effectiveness of medications more favorably (short term 4.0 vs 3.7, P = 0.02; long term 3.5 vs 3.2, P = 0.04) and were more likely to view prescribing as part of their job (3.9 vs 3.4, P = 0.04). PCPs with positive attitudes (72.4%, CI 60.9-83.8%) had a prescribing rate of 5.0% (CI 3.5-6.5%) compared to 1.9% (CI 0.5-3.4%) among those with negative attitudes (P = 0.028). When stratified by attitude, belief in effectiveness was associated with higher prescribing among PCPs with positive attitudes but not those with negative attitudes.
CONCLUSIONS
PCPs indicated an interest in learning to prescribe MAUD. However, education alone may not be effective unless physicians have positive attitudes towards patients with AUD.
Topics: Humans; Alcoholism; Attitude of Health Personnel; Physicians; Surveys and Questionnaires; Primary Health Care
PubMed: 36368012
DOI: 10.1093/alcalc/agac057 -
Journal of Substance Abuse Treatment Jan 2023Alcohol use disorder (AUD) represents the most prevalent addiction in the United States. Integration of AUD treatment in primary care settings would expand care access.... (Review)
Review
BACKGROUND
Alcohol use disorder (AUD) represents the most prevalent addiction in the United States. Integration of AUD treatment in primary care settings would expand care access. The objective of this scoping review is to examine models of AUD treatment in primary care that include pharmacotherapy (acamprosate, disulfiram, naltrexone).
METHODS
The team undertook a search across MEDLINE, PsycINFO, CINAHL, the Cochrane Central Register of Controlled Trials, and Web of Science on May 21, 2021. Eligibility criteria included: patient population ≥ 18 years old, primary care-based setting, US-based study, presence of an intervention to promote AUD treatment, and prescription of FDA-approved AUD pharmacotherapy. Study design was limited to controlled trials and observational studies. We assessed study bias using a modified Oxford Centre for Evidence-based Medicine Rating Framework quality rating scheme.
RESULTS
The qualitative synthesis included forty-seven papers, representing 25 primary studies. Primary study sample sizes ranged from 24 to 830,825 participants and many (44 %) were randomized controlled trials. Most studies (80 %) included a nonpharmacologic intervention for AUD: 56 % with brief intervention, 40 % with motivational interviewing, and 12 % with motivational enhancement therapy. A plurality of studies (48 %) included mixed pharmacologic interventions, with administration of any combination of naltrexone, acamprosate, and/or disulfiram. Of the 47 total studies included, 68 % assessed care initiation and engagement. Fewer studies (15 %) explored practices surrounding screening for or diagnosing AUD. Outcome measures included receipt of pharmacotherapy and alcohol consumption, which about half of studies included (53 % and 51 %, respectively). Many of these outcomes showed significant findings in favor of integrated care models for AUD.
CONCLUSIONS
The integration of AUD pharmacotherapy in primary care settings may be associated with improved process and outcome measures of care. Future research should seek to understand the varied experiences across care integration models.
Topics: Humans; United States; Adolescent; Alcoholism; Acamprosate; Naltrexone; Disulfiram; Alcohol Drinking; Primary Health Care; Randomized Controlled Trials as Topic
PubMed: 36332528
DOI: 10.1016/j.jsat.2022.108919