Alcohol (Hanover, York County, Pa.)最新文献

Background: Racial discrimination has been identified as a contributing risk factor for alcohol use among racially minoritized individuals. The aims of this study were to quantify the relationship between racial discrimination and alcohol use among Asian Americans, examine gender, age and generational status as moderators, and characterize ethnic group representation across the literature.

Methods: A systematic literature search was conducted using PsycINFO, CINAHL, Web of Science, PubMed, Embase, and OpenDissertations. A random effects model using Pearson's r effect sizes was conducted on separate alcohol outcomes. Meta-regression analyses tested for moderating effects, and heterogeneity was examined by identifying outliers and subgroup differences. Risk of bias was assessed using a funnel plot and Egger's regression test.

Results: Twenty-two effect sizes were extracted from 18 studies, representing 8926 participants. A significant positive association was found between racial discrimination and alcohol consumption (k = 9, r = 0.13, 95% CI = [0.07, 0.19], I² = 80.7%, p = 0.002) and problematic alcohol use (k = 12, r = 0.27, 95% CI = [0.12, 0.40] I² = 93.7%, p = 0.002), but not binge use (k = 3, r = 0.08, 95% CI = [-0.49, 0.60], I² = 95.0%, p = 0.64). Age, gender, and generational status were not significant moderators (p's > 0.10). When ethnic groups were reported, Chinese Americans were most represented (36.9%), while Indian Americans were notably underrepresented (1.18%).

Conclusions: There is a small positive association between racial discrimination and alcohol consumption and problematic alcohol use among Asian Americans. Research should seek to fill gaps identified by this review, including the dearth of longitudinal work needed to establish temporal precedence, the limited understanding of racial discrimination on binge use and underrepresented ethnic groups in this field of research, and reducing heterogeneity between studies.

Background: Alcohol-related liver disease (ALD) is the leading indication for liver transplantation in the United States. The aim of this study was to describe the impact of phosphatidylethanol (PEth) in the surveillance for alcohol use after liver transplantation.

Methods: We conducted a single-center retrospective study to assess the impact of phosphatidylethanol (PEth) for the surveillance of alcohol use and its correlation to health outcomes. We compared orthotopic liver transplant (OLT) recipients for ALD transplanted between 2016 and 2018, before the introduction of PEth, to those transplanted between 2019 and 2022, after the introduction of PEth. Alcohol relapse versus nonrelapse cohorts were also compared. Follow-up time for all cohorts was limited to 3 years post-OLT. Continuous variables were analyzed with an independent t-test and categorical variables with Fischer's exact test and chi-square test. The Kaplan-Meier method and log-rank test were used to assess alcohol-free survival.

Results: We reviewed 263 patients who were transplanted for ALD; 46 (17.5%) patients were noted to have at least one episode of alcohol relapse after their transplant. Patients with alcohol relapse had more frequent episodes of elevated liver enzymes compared with nonrelapsed patients (4.35 episodes vs. 2.46 episodes respectively, p < 0.001). The number of hospitalizations was also noted to be elevated among relapsed versus nonrelapsed patients; however, this was not statistically significant (2.85 vs. 2.50 respectively, p = 0.307). When comparing relapse rates before and after the introduction of PEth, relapses were notably detected more frequently after the introduction of PEth (17% vs. 7%, p = 0.012). No difference was noted in rates of mortality between patients who did or did not relapse.

Conclusions: Overall, PEth is an effective surveillance tool in the postliver transplant population to monitor for alcohol relapse. Early detection of relapse can lead to opportunities for early intervention to avoid alcohol-related complications.

Background: Alcohol use disorder (AUD) is associated with imbalanced bone turnover and psychological symptoms, but the relationship between bone and brain remains unclear. The study analyzed serum levels of a bone formation marker, procollagen type 1 N-terminal propeptide (P1NP), and bone resorption marker, C-terminal telopeptide of type I collagen (CTX-1), in AUD patients before and after 2 weeks of alcohol withdrawal and investigated their correlation with psychological symptoms.

Methods: Ninety patients with AUD and 117 healthy controls were recruited. P1NP and CTX-1 levels were measured using Enzyme-Linked Immunosorbent Assay. The Penn Alcohol Craving Scale (PACS), Beck Depression Inventory (BDI), and Beck Anxiety Inventory (BAI) were assessed in the AUD group at baseline, week 1, and week 2 of withdrawal.

Results: Baseline CTX-1 levels, along with the CTX-1/P1NP and P1NP/CTX-1 ratio, were higher in the AUD group than controls. Over the 2-week withdrawal, PACS, BDI, and BAI scores demonstrated significant reductions. P1NP (p < 0.001) and P1NP/CTX-1 ratio increased (p < 0.001), while CTX-1/P1NP ratio decreased (p < 0.001), indicating a propensity toward bone formation. Univariate analysis revealed that reductions in PACS, BDI, and BAI scores during withdrawal correlated with increased P1NP levels and decreased CTX-1/P1NP ratios. However, multivariate analysis indicated that only PACS score reductions correlated with these changes.

Conclusions: Bone metabolism shifted toward increased bone formation and decreased bone resorption during 2-week alcohol withdrawal. The correlation between improvements in bone turnover markers and reduction in craving scores during withdrawal supports the concept of the bone-brain axis.

Background: This study shows the first evidence for pannexin 1 channels as a new target to develop medications for alcohol use disorder (AUD). Due to its history of long-term safe clinical use and preclinical evidence of reducing excessive alcohol intake in rodents, probenecid has clinical potential for AUD.

Methods: We conducted a Phase I/IIa randomized, double-blind, placebo-controlled, crossover trial investigating the safety, tolerability, and efficacy of an oral dose of probenecid (2 g) when administered with alcohol (0.08 g/dL) in individuals who regularly consume alcohol to the 0.08 g/dL level (N = 35) and in individuals with mild to severe AUD. Alcohol pharmacokinetics and subjective responses were evaluated to assess potential interactions between probenecid and alcohol. Alcohol craving, inflammatory biomarkers, cognitive assessments, and hemodynamics were assessed as additional alcohol research domains. All outcomes were assessed both in the ascending and descending limb of alcohol intoxication using Generalized Estimating Equation.

Results: Probenecid did not exert any significant effect on alcohol pharmacokinetics and did not affect alcohol stimulation or sedation. Probenecid, compared to placebo, significantly decreased alcohol craving during the alcohol ascending limb. Inflammatory biomarkers, cognitive performance following alcohol ingestion, and hemodynamics were likewise not affected by probenecid administration. Analysis of sex as a biological variable revealed no differences of probenecid compared to placebo.

Conclusions: Taken together, our data support the potential of probenecid for treatment of AUD and suggest that pannexin 1 channels represent a novel emerging therapeutic target for the development of new pharmacotherapies for treating AUD.