Dataset Information

Alcohol Use after Liver Transplantation is Independent of Liver Disease Etiology.

ABSTRACT: To assess alcohol use after liver transplantation (LT) and compare liver transplant recipients for alcoholic liver disease (ALD) with recipients for non-ALD causes.National Institute of Diabetes and Digestive and Kidney Diseases liver transplant database stratified to ALD and non-ALD causes.Among 488 LT recipients reporting pre-transplant alcohol use (147 ALD), proportion of LT recipients reporting alcohol use was similar comparing ALD and non-ALD transplants (25.4% vs. 27.2%; P = 0.56). Among ALD transplants, of 31 with alcohol use, 23 (74%) relapsed at ?2 year, 25 (80%) reported intermittent drinking and 4 (13%) reported heavy drinking. Among Non-ALD recipients, alcohol use was equally distributed to within 2, 2-5 and after 5 years of LT with 82% reporting intermittent drinking and 9% heavy drinking. Patients with pre-transplant drinking of >20 years and abstinence duration of <2 years were over 2.5-fold likely to report post-transplant alcohol use compared to drinking of >20 years and abstinence of >2 years, 2.56 [95% CI: 1.41-4.67]. Etiology (ALD vs. non-ALD) did not predict post-transplant alcohol use. Of 139 ALD patients with follow-up biopsy data, 13 (7 with post-transplant alcohol use) had steatohepatitis. Histology on 319 non-ALD recipients showed recurrent disease in 91, none due to alcohol. Overall survival was similar between drinkers and abstainers (71% vs. 66%; P = 0.35). Recurrent ALD was cause of death in one ALD and none of non-ALD patients.Alcohol use after LT is independent of LT indication. Patients with non-ALD etiology should be carefully screened for alcohol use prior to LT to identify those at risk for post-LT alcohol use.

SUBMITTER: Russ KB

PROVIDER: S-EPMC5091294 | biostudies-literature | 2016 Nov

REPOSITORIES: biostudies-literature

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Alcohol Use after Liver Transplantation is Independent of Liver Disease Etiology.

Russ Kirk B KB Chen Nai-Wei NW Kamath Patrick S PS Shah Vijay H VH Kuo Yong-Fang YF Singal Ashwani K AK

Alcohol and alcoholism (Oxford, Oxfordshire) 20160606 6

<h4>Aim</h4>To assess alcohol use after liver transplantation (LT) and compare liver transplant recipients for alcoholic liver disease (ALD) with recipients for non-ALD causes.<h4>Methods</h4>National Institute of Diabetes and Digestive and Kidney Diseases liver transplant database stratified to ALD and non-ALD causes.<h4>Results</h4>Among 488 LT recipients reporting pre-transplant alcohol use (147 ALD), proportion of LT recipients reporting alcohol use was similar comparing ALD and non-ALD tran ...[more]

PMID: 27267907

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Project description:PurposeChronic alcohol use is a major cause of liver damage and death. In the United States, multiple factors have led to low utilization of pharmacotherapy for alcohol use disorder (AUD), including lack of provider knowledge and comfort in prescribing medications for AUD. Alcohol consumption has direct effects on the gut microbiota, altering the diversity of bacteria and leading to bacterial overgrowth. Growing evidence suggests that alcohol's effects on the gut microbiome may contribute to increased alcohol consumption and progression of alcohol-associated liver disease (ALD). This article reviews human and preclinical studies investigating the role of fecal microbiota transplantation (FMT) in ameliorating alcohol-associated alterations to the liver, gut, and brain resulting in altered behavior; it also discusses the therapeutic potential of FMT.Search methodsFor this narrative review, a literature search was conducted in September 2022 of PubMed, Web of Science Core Collection, and Google Scholar to identify studies published between January 2012 and September 2022. Search terms used included "fecal microbiota transplantation" and "alcohol."Search resultsMost results of the literature search were review articles or articles on nonalcoholic fatty liver disease; these were excluded. Of the remaining empirical manuscripts, very few described clinical or preclinical studies that were directly investigating the effects of FMT on alcohol drinking or related behaviors. Ultimately, 16 studies were included in the review.Discussion and conclusionsThe literature search identified only a few studies that were directly investigating the effect of FMT on ALD or alcohol drinking and related behaviors. Largely proof-of-concept studies, these findings demonstrate that alcohol can alter the gut microbiome and that the microbiome can be transferred between humans and rodents to alter affective behaviors frequently associated with increased alcohol use. Other studies have shown promise of FMT or other probiotic supplementation in alleviating some of the symptoms associated with ALD and drinking. These results show that the implementation of FMT as a therapeutic approach is still in the investigatory stages.

Project description:Background & aimsCardiovascular disease (CVD) is the leading cause of death among patients with nonalcoholic fatty liver disease (NAFLD). Moderate drinking (vs abstinence) is associated with lower risk of CVD in the general population. We assessed whether alcohol use is associated with CVD risk in patients with NAFLD.MethodsWe analyzed data from participants in the Coronary Artery Risk Development in Young Adults longitudinal cohort study of 5115 black and white young adults, 18-30 years old, recruited from 4 cities in the United States from 1985 through 1986. Participants self-reported alcohol use at study entry and then again after 15, 20, and 25 years. At year 25 (2010-2011), participants underwent computed tomography examination of the thorax and abdomen and tissue Doppler echocardiography with myocardial strain measured by speckle tracking. Coronary artery calcification was defined as an Agatston score above 0. NAFLD was defined as liver attenuation <51 Hounsfield Units after exclusions. Drinkers reported 1-21 (men) or 1-14 (women) standard drinks/week at years 15, 20, or 25. Nondrinkers reported no alcohol use at years 15, 20, and 25.ResultsOf the 570 participants with NAFLD (mean age, 50 years; 54% black; 46% female), 332 (58%) were drinkers; significantly higher proportions of drinkers were white, male, and with higher levels of education compared with nondrinkers (P < .05 for all). Higher proportions of drinkers had obesity, diabetes, and metabolic syndrome compared with nondrinkers (P < .01). There was no difference in liver attenuation between groups (P = .12). After multivariable adjustment, there was no association between alcohol use and CVD risk factors (diabetes, hypertension, hyperlipidemia) or subclinical CVD measures (coronary artery calcification, early transmitral velocity/late (atrial) transmitral velocity (E/A) ratio, global longitudinal strain).ConclusionsIn a population-based sample of individuals with NAFLD in midlife, prospectively assessed alcohol use is not associated with significant differences in risk factors for CVD or markers of subclinical CVD. In contrast to general population findings, alcohol use may not reduce the risk of CVD in patients with NAFLD.

Project description:Nicotinamide adenine dinucleotide (NAD+) and related coenzymes play critical roles in liver function. Although hepatic alcohol metabolism depresses NAD+, current understanding of the NAD+ metabolome in alcohol-related liver disease (ArLD) is based on animal models. We used human liver samples to quantify the NAD+ metabolome in ArLD with samples obtained at the time of liver transplantation or resection at University Hospitals Birmingham National Health Service Foundation Trust. The severity of steatohepatitis in liver from patients with ArLD was assessed with standard liver function tests and histology. NAD-targeted quantitative metabolomic analysis of liver tissue was performed by liquid chromatography-tandem mass spectrometry. Seventy-two human liver specimens were analyzed, including 43 with ArLD. The NAD+ metabolome differed significantly between different types of liver disease (two-way analysis of variance [ANOVA], P = 0.001). ArLD liver tissue showed markedly depressed concentrations of NAD+ (432 μM vs. 616 μM in normal liver) and precursor molecules nicotinic acid and nicotinamide riboside. There was a significant overall difference in the NAD+ metabolome between ArLD samples with and without steatohepatitis (two-way ANOVA, P = 0.018). After correcting for multiple comparisons, a significant difference for individual components of the metabolome was observed for the concentration of NAD+ (mean, 462 μM vs. 322 μM; P < 0.01 in nonsevere vs. severe alcoholic steatohepatitis, respectively). NAD+ concentration was inversely related to serum bilirubin concentration (r 2 = -0.127; P = 0.04) and positively correlated with myeloperoxidase activity (r 2 = 0.31; P = 0.003). The concentration of NAD+ and its precursor molecules are significantly reduced in ArLD and are associated with disease activity. Conclusion: Liver samples from people with ArLD show depressed NAD+ and precursor levels as well as depressed myeloperoxidase activity.

Project description:ImportanceAlcohol-associated liver disease (ALD) is one of the most devastating complications of alcohol use disorder (AUD), an increasingly prevalent condition. Medical addiction therapy for AUD may play a role in protecting against the development and progression of ALD.ObjectiveTo ascertain whether medical addiction therapy was associated with an altered risk of developing ALD in patients with AUD.Design, setting, and participantsThis retrospective cohort study used the Mass General Brigham Biobank, an ongoing research initiative that had recruited 127 480 patients between its start in 2010 and August 17, 2021, when data for the present study were retrieved. The mean follow-up duration from AUD diagnosis was 9.2 years. International Statistical Classification of Diseases and Related Health Problems, Tenth Revision diagnosis codes were used to identify ALD and AUD diagnoses.ExposuresMedical addiction therapy was defined as the documented use of disulfiram, acamprosate, naltrexone, gabapentin, topiramate, or baclofen. Patients were considered to be treated if they initiated medical addiction therapy before the relevant outcome.Main outcomes and measuresAdjusted odds ratios (aORs) for the development of ALD and hepatic decompensation were calculated and adjusted for multiple risk factors.ResultsThe cohort comprised 9635 patients with AUD, of whom 5821 were male individuals (60.4%), and the mean (SD) age was 54.8 (16.5) years. A total of 1135 patients (11.8%) had ALD and 3906 patients (40.5%) were treated with medical addiction therapy. In multivariable analyses, medical addiction therapy for AUD was associated with decreased incidence of ALD (aOR, 0.37; 95% CI, 0.31-0.43; P < .001). This association was evident for naltrexone (aOR, 0.67; 95% CI, 0.46-0.95; P = .03), gabapentin (aOR, 0.36; 95% CI, 0.30-0.43; P < .001), topiramate (aOR, 0.47; 95% CI, 0.32-0.66; P < .001), and baclofen (aOR, 0.57; 95% CI, 0.36-0.88; P = .01). In addition, pharmacotherapy for AUD was associated with lower incidence of hepatic decompensation in patients with cirrhosis (aOR, 0.35; 95% CI, 0.23-0.53, P < .001), including naltrexone (aOR, 0.27; 95% CI, 0.10-0.64; P = .005) and gabapentin (aOR, 0.36; 95% CI, 0.23-0.56; P < .001). This association persisted even when medical addiction therapy was initiated only after the diagnosis of cirrhosis (aOR, 0.41; 95% CI, 0.23-0.71; P = .002).Conclusions and relevanceResults of this study showed that receipt of medical addiction therapy for AUD was associated with reduced incidence and progression of ALD. The associations of individual pharmacotherapy with the outcomes of ALD and hepatic decompensation varied widely.

Dataset Information

Alcohol Use after Liver Transplantation is Independent of Liver Disease Etiology.

Publications

Alcohol Use after Liver Transplantation is Independent of Liver Disease Etiology.

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