Alvarado-Tapias, E. (Edilmar)
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- Bariatric surgery is associated with alcohol-related liver disease and psychiatric disorders associated with AUD(2023) Morales-Arráez, D. (Dalia); Alvarado-Tapias, E. (Edilmar); Clemente-Sánchez, A. (Ana); Atkinson, S.R. (Stephen R.); Martí-Aguado, D. (David); Kennedy, K. (Kevin); Bataller, R. (Ramón); Ventura-Cots, M. (Meritxell); Argemí, J. (Josepmaria); Fernández-Carrillo, C. (Carlos)Background/Aims Bariatric surgery can increase the risk of addictive disorders and nutritional deficiencies. The aim of this study was to evaluate the association between bariatric surgery and alcohol use disorder (AUD), alcohol-related liver disease (ALD), and psychiatric disorders associated with AUD. The impact of vitamin D deficiency in these associations was also investigated.Methods A cross-sectional study was performed using the National Inpatient Sample database and its ICD-9 codes information. Diagnostic and comorbidity data from hospital discharges were obtained from patients with bariatric surgery and other abdominal surgeries between 2005 and 2015. The two groups were then compared for alcohol-related outcomes after propensity-score matching.Results The final study cohort included 537,757 patients with bariatric surgery and 537,757 with other abdominal surgeries. The bariatric surgery group had an increased risk of AUD [odds ratio (OR): 1.90; 95% CI: 1.85-1.95], ALD [OR: 1.29; 95% CI: 1.22-1.37], cirrhosis [OR, 1.39; 95% CI: 1.37-1.42], and psychiatric disorders associated with AUD [OR, 3.59; 95% CI: 3.37-3.84]. Vitamin D deficiency did not impact in the association between bariatric surgery and AUD, ALD, or psychiatric disorders associated with AUD.Conclusions Bariatric surgery is associated with an increased prevalence of AUD, ALD, and psychiatric disorders associated with AUD. These associations appear to be independent from vitamin D deficiency.
- Integrated multiomics reveals glucose use reprogramming and identifies a novel hexokinase in alcoholic hepatitis(Baltimore, 2021) Massey, V. (Veronica); Parrish, A. (Austin); Argemí, J. (Josepmaria); Moreno, M. (Montserrat); Mello, A. (Aline); García-Rocha, M. (Mar); Altamirano, J. (Jose); Odena, G. (Gemma); Dubuquoy, L. (Laurent); Louvet, A. (Alexandre); Martínez, C. (Carlos); Adrover, A. (Anna); Affò, S. (Silvia); Morales-Ibanez, O. (Oriol); Sancho-Bru, P. (Pau); García-Millán, C. (Cristina); Alvarado-Tapias, E. (Edilmar); Morales-Arráez, D. (Dalia); Caballeria, J. (Juan); Mann, J. (Jelena); Cao, S. (Sheng); Sun, Z. (Zhaoli); Shah, V.H. (Vijay H.); Cameron, A. (Andrew); Mathurin, P. (Philippe); Snider, N. (Natasha); Villanueva, C. (Càndid); Morgan, T.R. (Timothy R.); Guinovart, J. (Joan); Vadigepalli, R. (Rajanikanth); Bataller, R. (Ramón)Background & aims: We recently showed that alcoholic hepatitis (AH) is characterized by dedifferentiation of hepatocytes and loss of mature functions. Glucose metabolism is tightly regulated in healthy hepatocytes. We hypothesize that AH may lead to metabolic reprogramming of the liver, including dysregulation of glucose metabolism. Methods: We performed integrated metabolomic and transcriptomic analyses of liver tissue from patients with AH or alcoholic cirrhosis or normal liver tissue from hepatic resection. Focused analyses of chromatin immunoprecipitation coupled to DNA sequencing was performed. Functional in vitro studies were performed in primary rat and human hepatocytes and HepG2 cells. Results: Patients with AH exhibited specific changes in the levels of intermediates of glycolysis/gluconeogenesis, the tricarboxylic acid cycle, and monosaccharide and disaccharide metabolism. Integrated analysis of the transcriptome and metabolome showed the used of alternate energetic pathways, metabolite sinks and bottlenecks, and dysregulated glucose storage in patients with AH. Among genes involved in glucose metabolism, hexokinase domain containing 1 (HKDC1) was identified as the most up-regulated kinase in patients with AH. Histone active promoter and enhancer markers were increased in the HKDC1 genomic region. High HKDC1 levels were associated with the development of acute kidney injury and decreased survival. Increased HKDC1 activity contributed to the accumulation of glucose-6-P and glycogen in primary rat hepatocytes. Conclusions: Altered metabolite levels and messenger RNA expression of metabolic enzymes suggest the existence of extensive reprogramming of glucose metabolism in AH. Increased HKDC1 expression may contribute to dysregulated glucose metabolism and represents a novel biomarker and therapeutic target for AH.
- Clinical, histological and molecular profiling of different stages of alcohol-related liver disease(British Medical Assn, 2022) Ventura-Cots, M. (Meritxell); Argemí, J. (Josepmaria); Jones, P.D. (Patricia D.); Lackner, C. (Carolin); Hag, M. (Mohamed) El; Abraldes, J.G. (Juan G.); Alvarado-Tapias, E. (Edilmar); Clemente-Sánchez, A. (Ana); Ravi, S. (Samhita); Alves, A. (Antonio); Alboraie, M. (Mohamed); Altamirano, J. (Jose); Barace, S. (Sergio); Bosques, F. (Francisco); Brown, R. (Robert); Caballeria, J. (Juan); Cabezas, J. (Joaquín); Carvalhana, S. (Sofia); Cortez-Pinto, H. (Helena); Costa, A. (Adilia); Degré, D. (Delphine); Fernández-Carrillo, C. (Carlos); Ganne-Carrie, N. (Nathalie); Garcia-Tsao, G. (Guadalupe); Genesca, J. (Joan); Koskinas, J. (John); Lanthier, N. (Nicolas); Louvet, A. (Alexandre); Lozano, J.J. (Juan J.); Lucey, M.R. (Michael R.)Objective: Alcohol-related liver disease (ALD) ranges from never-decompensated ALD (ndALD) to the life-threatening decompensated phenotype, known as alcohol-related hepatitis (AH). A multidimensional study of the clinical, histological and molecular features of these subtypes is lacking. Design: Two large cohorts of patients were recruited in an international, observational multicentre study: a retrospective cohort of patients with ndALD (n=110) and a prospective cohort of patients with AH (n=225). Clinical, analytical, immunohistochemistry and hepatic RNA microarray analysis of both disease phenotypes were performed. Results: Age and mean alcohol intake were similar in both groups. AH patients had greater aspartate amino transferase/alanine amino transferase ratio and lower gamma-glutamyl transferase levels than in ndALD patients. Patients with AH demonstrated profound liver failure and increased mortality. One-year mortality was 10% in ndALD and 50% in AH. Histologically, steatosis grade, ballooning and pericellular fibrosis were similar in both groups, while advanced fibrosis, Mallory-Denk bodies, bilirubinostasis, severe neutrophil infiltration and ductular reaction were more frequent among AH patients. Transcriptome analysis revealed a profound gene dysregulation within both phenotypes when compare to controls. While ndALD was characterised by deregulated expression of genes involved in matrisome and immune response, the development of AH resulted in a marked deregulation of genes involved in hepatocyte reprogramming and bile acid metabolism. Conclusions: Despite comparable alcohol intake, AH patients presented with worse liver function compared with ndALD patients. Bilirubinostasis, severe fibrosis and ductular reaction were prominent features of AH. AH patients exhibited a more profound deregulation of gene expression compared with ndALD patients.