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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:The prevalence of alcohol use disorder (AUD) has been steadily increasing over the past decade. In parallel, alcohol-associated liver disease (ALD) has been increasing at an alarming rate, especially among young patients. Data suggest that most patients with ALD do not receive AUD therapy. Although liver transplantation is the only curative therapy for end-stage ALD, transplant candidacy is often a matter of debate given concerns about patients being under-treated for AUD and fears of post-transplantation relapse affecting the allograft. In this Review, we discuss diagnosis, predictors and effects of relapse, behavioural therapies and pharmacotherapies, and we also propose an integrative, multidisciplinary and multimodality approach for treating AUD in patients with cirrhosis, especially in the setting of liver transplantation. Notably, this approach takes into account the utility of AUD pharmacotherapy in patients on immunosuppressive medications and those with renal impairment after liver transplantation. We also propose a comprehensive and objective definition of relapse utilizing contemporary biomarkers to guide future clinical trials. Future research using the proposed approach and definition is warranted with the goal of optimizing AUD treatment in patients with cirrhosis, the transplant selection process and post-transplantation care of patients with AUD. In this Review, Arab and colleagues discuss management of alcohol use disorder in patients with alcohol-associated liver disease, particularly in the setting of liver transplantation. An integrative, multidisciplinary approach is proposed. Key points The prevalence of alcohol use disorder (AUD) and alcohol-associated liver disease has increased over the past few decades globally. Definitions of relapse after liver transplantation vary widely. Currently, our understanding of the predictors and effects of relapse after liver transplantation is growing and together with a multidisciplinary approach might improve patient outcomes. The use of pharmacotherapies for AUD is feasible in patients with cirrhosis after tailoring the regimen to account for comorbid illnesses such as renal dysfunction. Relapse-prevention medications do not have notable interactions with immunosuppressants commonly used after liver transplantation. Combining medications and behavioural treatments with medical care at the transplant centre might maximize relapse prevention potential.

Project description:BACKGROUND & AIMS:Cardiovascular 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. METHODS:We 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. RESULTS:Of 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). CONCLUSIONS:In 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 ?M vs. 616 ?M 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 ?M vs. 322 ?M; 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.

Dataset Information

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

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

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