Fernández-Carrillo, C. (Carlos)
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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.
- 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.