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1. A polygenic risk score for alcohol-associated cirrhosis among heavy drinkers with European ancestry.

Author

Schwantes-An, Tae-Hwi, Whitfield, John, Aithal, Guruprasad, Atkinson, Stephen, Bataller, Ramon, Botwin, Greg, Chalasani, Naga, Cordell, Heather, Daly, Ann, Darlay, Rebecca, Day, Christopher, Eyer, Florian, Foroud, Tatiana, Gawrieh, Samer, Gleeson, Dermot, Goldman, David, Haber, Paul, Jacquet, Jean-Marc, Lammert, Craig, Liang, Tiebing, Liangpunsakul, Suthat, Masson, Steven, Mathurin, Philippe, Moirand, Romain, McQuillin, Andrew, Moreno, Christophe, Morgan, Marsha, Mueller, Sebastian, Müllhaupt, Beat, Nagy, Laura, Nahon, Pierre, Nalpas, Bertrand, Naveau, Sylvie, Perney, Pascal, Pirmohamed, Munir, Seitz, Helmut, Soyka, Michael, Stickel, Felix, Thompson, Andrew, Thursz, Mark, Trépo, Eric, Morgan, Timothy, and Seth, Devanshi

Subjects
Humans, Polymorphism, Single Nucleotide, Liver Cirrhosis, Alcoholic, Male, Female, Middle Aged, Genome-Wide Association Study, White People, Multifactorial Inheritance, Aged, Risk Assessment, Alcohol Drinking, Adult, Risk Factors, Genetic Predisposition to Disease, United Kingdom, Genetic Risk Score
Abstract

BACKGROUND: Polygenic Risk Scores (PRS) based on results from genome-wide association studies offer the prospect of risk stratification for many common and complex diseases. We developed a PRS for alcohol-associated cirrhosis by comparing single-nucleotide polymorphisms among patients with alcohol-associated cirrhosis (ALC) versus drinkers who did not have evidence of liver fibrosis/cirrhosis. METHODS: Using a data-driven approach, a PRS for ALC was generated using a meta-genome-wide association study of ALC (N=4305) and an independent cohort of heavy drinkers with ALC and without significant liver disease (N=3037). It was validated in 2 additional independent cohorts from the UK Biobank with diagnosed ALC (N=467) and high-risk drinking controls (N=8981) and participants in the Indiana Biobank Liver cohort with alcohol-associated liver disease (N=121) and controls without liver disease (N=3239). RESULTS: A 20-single-nucleotide polymorphisms PRS for ALC (PRSALC) was generated that stratified risk for ALC comparing the top and bottom deciles of PRS in the 2 validation cohorts (ORs: 2.83 [95% CI: 1.82 -4.39] in UK Biobank; 4.40 [1.56 -12.44] in Indiana Biobank Liver cohort). Furthermore, PRSALC improved the prediction of ALC risk when added to the models of clinically known predictors of ALC risk. It also stratified the risk for metabolic dysfunction -associated steatotic liver disease -cirrhosis (3.94 [2.23 -6.95]) in the Indiana Biobank Liver cohort -based exploratory analysis. CONCLUSIONS: PRSALC incorporates 20 single-nucleotide polymorphisms, predicts increased risk for ALC, and improves risk stratification for ALC compared with the models that only include clinical risk factors. This new score has the potential for early detection of heavy drinking patients who are at high risk for ALC.

Published
2024

2. SAT-129 Sub-optimal global public health policies and strategies to combat hepatocellular carcinoma

Author

Diaz, Luis Antonio, Norero, Blanca, Corsi, Oscar, Ayares, Gustavo, Idalsoaga, Francisco, García, Sergio, Vázquez, Valeria, Lacalle, Lucas, Lazo, Mariana, Ferreccio, Catterina, Mendizabal, Manuel, Piñero, Federico, Martinez, Edmundo, Ijeoma, Ifeorah, Louvet, Alexandre, Piano, Salvatore, Cortez-Pinto, Helena, Wong, Vincent Wai-Sun, Kulkarni, Anand, Cotter, Thomas, Brahmania, Mayur, roblero, Juan Pablo, Dirchwolf, Melisa, Pollarsky, Florencia, George, Jacob, Stauber, Rudolf E, Francque, Sven, Guerra, Patricia, Oliveira, Claudia, Araujo, Roberta, Álvares-da-Silva, Mario, Blaise, Nkegoum, Abraldes, Juan G, Zheng, Ming-Hua, Toro, Luis, Restrepo, Juan Carlos, Ramirez, Wagner, Grgurević, Ivica, Infante, Mirtha, Mbendi, Charles, Carrera, Enrique, Kassas, Mohamed El, Mahmoud, Abdelmajeed, Tesfaye, Yonas Gedamu, Tadesse, Sewale Anagaw, Akalu, Tiruwork Fekadu, Desalegn, Hailemichael, Allaire, Manon, Patrizia, Carrieri, Schattenberg, Jörn, Aguyire, Joan, Micah, Eileen Akonobea, Tachi, Kenneth, Cardona, Katherine Emilia Maldonado, Sanchez, Abel, Sánchez, Marco, Björnsson, Einar S, Iavarone, Massimo, Okamoto, Ryuichi, Some, Fatuma, Hellani, Mohammad Fadel, Gonzalez, Veronica Enith Prado, Chávez-Tapia, Norberto Carlos, Méndez-Sánchez, Nahum, Mucumbi, Sheila Constância Mabote, Ugiagbe, Rose Ashinedu, Akande, Kolawole, Nwoko, Chinenye, Ezenkwa, Uchenna Simon, Okoye, Ifeoma Joy, Hamid, Saeed Sadiq, Quezada, Julissa Lombardo, Girala, Marcos, Padilla, P Martin, Diaz-Ferrer, Javier, Tagle, Martin, Kukla, Michał, Odeghe, Emuobor, wemimo, Rasheed mumini, Reis, Daniela, Mozgovoi, Sergei, Ismail, Mona, Koller, Tomas, Spearman, Wendy, Elhassan, Moawia, Stal, Per, Pazi, Swaleh, Ocanit, Anthony, Masson, Steven, Dunn, Winston, Kamath, Patrick S, Singal, Ashwani, Debes, Jose, Reig, María, Loomba, Rohit, Bataller, Ramon, Lazarus, Jeffrey, Arrese, Marco, and Arab, Juan Pablo

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Public Health and Health Services, Gastroenterology & Hepatology, Clinical sciences
Published
2023

3. All‐cause and liver‐related mortality risk factors in excessive drinkers: Analysis of data from the UK biobank

Author

Whitfield, John B, Seth, Devanshi, Morgan, Timothy R, Aithal, Guruprasad P, Atkinson, Stephen R, Bataller, Ramon, Botwin, Gregory, Chalasani, Naga P, Cordell, Heather J, Daly, Ann K, Darlay, Rebecca, Day, Christopher P, Eyer, Florian, Foroud, Tatiana, Gleeson, Dermot, Goldman, David, Haber, Paul S, Jacquet, Jean‐Marc, Liang, Tiebing, Liangpunsakul, Suthat, Masson, Steven, Mathurin, Philippe, Moirand, Romain, Moreno, Christophe, Morgan, Marsha Y, Mueller, Sebastian, Müllhaupt, Beat, Nagy, Laura E, Nahon, Pierre, Nalpas, Bertrand, Naveau, Sylvie, Perney, Pascal, Pirmohamed, Munir, Schwantes‐An, Tae‐Hwi, Seitz, Helmut K, Soyka, Michael, Stickel, Felix, Thompson, Andrew, Thursz, Mark R, and Trepo, Eric

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Digestive Diseases, Substance Misuse, Liver Disease, Nutrition, Brain Disorders, Alcoholism, Alcohol Use and Health, Clinical Research, Cancer, Oral and gastrointestinal, Good Health and Well Being, Humans, Male, Female, Alcoholism, Alcohol Drinking, Biological Specimen Banks, Risk Factors, Cardiovascular Diseases, Liver, United Kingdom, alcohol, alcohol dependence, all-cause mortality, excessive drinking, liver disease, GenomALC Consortium, Neurosciences, Psychology, Substance Abuse, Clinical sciences, Biological psychology, Clinical and health psychology
Abstract

BackgroundHigh alcohol intake is associated with increased mortality. We aimed to identify factors affecting mortality in people drinking extreme amounts of alcohol.MethodsWe obtained information from the UK Biobank on approximately 500,000 participants aged 40-70 years at baseline assessment in 2006-2010. Habitual alcohol intake, lifestyle and physiological data, laboratory test results, and hospital diagnoses and death certificate data (to June 2020) for 5136 men (2.20% of male participants) and 1504 women (0.60%) who reported consuming ≥80 or ≥50 g/day, respectively, were used in survival analysis.ResultsMortality hazard ratios for these excessive drinkers, compared to all other participants, were 2.02 (95% CI 1.89-2.17) for all causes, 1.89 (1.69-2.12) for any cancer, 1.87 (1.61-2.17) for any circulatory disease, and 9.40 (7.00-12.64) for any liver disease. Liver disease diagnosis or abnormal liver function tests predicted not only deaths attributed to liver disease but also those from cancers or circulatory diseases. Mortality among excessive drinkers was also associated with quantitative alcohol intake; diagnosed alcohol dependence, harmful use, or withdrawal syndrome; and current smoking at assessment.ConclusionsPeople with chronic excessive alcohol intake experience decreased average survival, but there is substantial variation in their mortality, with liver abnormality and alcohol dependence or other alcohol use disorders associated with a worse prognosis. Clinically, patients with these risk factors and high alcohol intake should be considered for early or intensive management. Research can usefully focus on the factors predisposing to dependence or liver abnormality.

Published
2022

4. Liver transplantation for critically ill patients with acute on chronic liver failure: a prospective national programme of waitlist prioritisation

Author

Bernal, William, Taylor, Rhiannon, Rowe, Ian A., Chauhan, Abhishek, Armstrong, Matthew J., Allison, Michael E.D., Webb, Gwilym, Pirani, Tasneem, Moore, Joanna, Burke, Laura, Masson, Steven, Cressy, David, Hogan, Brian J., Westbrook, Rachel, Jalan, Rajiv, Simpson, Kenneth J., Isaac, John, and Thorburn, Douglas

Published
2024
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5. A genetic risk score and diabetes predict development of alcohol-related cirrhosis in drinkers

Author

Whitfield, John B, Schwantes-An, Tae-Hwi, Darlay, Rebecca, Aithal, Guruprasad P, Atkinson, Stephen R, Bataller, Ramon, Botwin, Greg, Chalasani, Naga P, Cordell, Heather J, Daly, Ann K, Day, Christopher P, Eyer, Florian, Foroud, Tatiana, Gleeson, Dermot, Goldman, David, Haber, Paul S, Jacquet, Jean-Marc, Liang, Tiebing, Liangpunsakul, Suthat, Masson, Steven, Mathurin, Philippe, Moirand, Romain, McQuillin, Andrew, Moreno, Christophe, Morgan, Marsha Y, Mueller, Sebastian, Müllhaupt, Beat, Nagy, Laura E, Nahon, Pierre, Nalpas, Bertrand, Naveau, Sylvie, Perney, Pascal, Pirmohamed, Munir, Seitz, Helmut K, Soyka, Michael, Stickel, Felix, Thompson, Andrew, Thursz, Mark R, Trépo, Eric, Morgan, Timothy R, Seth, Devanshi, and Consortium, GenomALC

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Rare Diseases, Liver Cancer, Genetics, Liver Disease, Clinical Research, Substance Misuse, Genetic Testing, Cancer, Alcoholism, Alcohol Use and Health, Digestive Diseases, Chronic Liver Disease and Cirrhosis, Metabolic and endocrine, Oral and gastrointestinal, Good Health and Well Being, Adult, Alcohol Drinking, Case-Control Studies, Cohort Studies, Diabetes Mellitus, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Liver Cirrhosis, Alcoholic, Male, Middle Aged, Polymorphism, Single Nucleotide, Risk Assessment, Hepatocellular carcinoma, risk stratification, chronic alcohol use, genome-wide association, single nucleotide polymorphism, coffee, GenomALC Consortium, Public Health and Health Services, Gastroenterology & Hepatology, Clinical sciences
Abstract

Background & aimsOnly a minority of excess alcohol drinkers develop cirrhosis. We developed and evaluated risk stratification scores to identify those at highest risk.MethodsThree cohorts (GenomALC-1: n = 1,690, GenomALC-2: n = 3,037, UK Biobank: relevant n = 6,898) with a history of heavy alcohol consumption (≥80 g/day (men), ≥50 g/day (women), for ≥10 years) were included. Cases were participants with alcohol-related cirrhosis. Controls had a history of similar alcohol consumption but no evidence of liver disease. Risk scores were computed from up to 8 genetic loci identified previously as associated with alcohol-related cirrhosis and 3 clinical risk factors. Score performance for the stratification of alcohol-related cirrhosis risk was assessed and compared across the alcohol-related liver disease spectrum, including hepatocellular carcinoma (HCC).ResultsA combination of 3 single nucleotide polymorphisms (SNPs) (PNPLA3:rs738409, SUGP1-TM6SF2:rs10401969, HSD17B13:rs6834314) and diabetes status best discriminated cirrhosis risk. The odds ratios (ORs) and (95% CIs) between the lowest (Q1) and highest (Q5) score quintiles of the 3-SNP score, based on independent allelic effect size estimates, were 5.99 (4.18-8.60) (GenomALC-1), 2.81 (2.03-3.89) (GenomALC-2), and 3.10 (2.32-4.14) (UK Biobank). Patients with diabetes and high risk scores had ORs of 14.7 (7.69-28.1) (GenomALC-1) and 17.1 (11.3-25.7) (UK Biobank) compared to those without diabetes and with low risk scores. Patients with cirrhosis and HCC had significantly higher mean risk scores than patients with cirrhosis alone (0.76 ± 0.06 vs. 0.61 ± 0.02, p = 0.007). Score performance was not significantly enhanced by information on additional genetic risk variants, body mass index or coffee consumption.ConclusionsA risk score based on 3 genetic risk variants and diabetes status enables the stratification of heavy drinkers based on their risk of cirrhosis, allowing for the provision of earlier preventative interventions.Lay summaryExcessive chronic drinking leads to cirrhosis in some people, but so far there is no way to identify those at high risk of developing this debilitating disease. We developed a genetic risk score that can identify patients at high risk. The risk of cirrhosis is increased >10-fold with just two risk factors - diabetes and a high genetic risk score. Risk assessment using this test could enable the early and personalised management of this disease in high-risk patients.

Published
2022

6. IL-1 Signal Inhibition in Alcohol-Related Hepatitis: A Randomized, Double-Blind, Placebo-Controlled Trial of Canakinumab

Author

Vergis, Nikhil, Patel, Vishal, Bogdanowicz, Karolina, Czyzewska-Khan, Justyna, Keshinro, Rosemary, Fiorentino, Francesca, Day, Emily, Middleton, Paul, Atkinson, Stephen, Tranah, Thomas, Cross, Mary, Babalis, Daphne, Foster, Neil, Lord, Emma, Quaglia, Alberto, Lloyd, Josephine, Goldin, Robert, Rosenberg, William, Parker, Richard, Richardson, Paul, Masson, Steven, Whitehouse, Gavin, Sieberhagan, Cyril, Patch, David, Naoumov, Nikolai, Dhanda, Ashwin, Forrest, Ewan, and Thursz, Mark

Published
2024
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8. Evaluation of laboratory tests for cirrhosis and for alcohol use, in the context of alcoholic cirrhosis.

Author

Whitfield, John, Masson, Steven, Liangpunsakul, Suthat, Hyman, Jessica, Mueller, Sebastian, Aithal, Guruprasad, Eyer, Florian, Gleeson, Dermot, Thompson, Andrew, Stickel, Felix, Soyka, Michael, Daly, Ann, Cordell, Heather, Liang, Tiebing, Foroud, Tatiana, Lumeng, Lawrence, Pirmohamed, Munir, Nalpas, Bertrand, Bence, Camille, Jacquet, Jean-Marc, Louvet, Alexandre, Moirand, Romain, Nahon, Pierre, Naveau, Sylvie, Perney, Pascal, Podevin, Philippe, Haber, Paul, Seitz, Helmut, Day, Christopher, Mathurin, Philippe, Morgan, Timothy, and Seth, Devanshi

Subjects
Abstinence, Alcohol, Aspartate aminotransferase, Cirrhosis, Gamma glutamyl transferase, Adult, Alcohol Abstinence, Alcohol Drinking, Area Under Curve, Aspartate Aminotransferases, Bilirubin, Biomarkers, Case-Control Studies, Clinical Enzyme Tests, Europe, Female, Humans, International Normalized Ratio, Liver Cirrhosis, Alcoholic, Liver Function Tests, Male, Middle Aged, Predictive Value of Tests, ROC Curve, Reproducibility of Results, Risk Factors, Sex Factors, United States, gamma-Glutamyltransferase
Abstract

Laboratory tests can play an important role in assessment of alcoholic patients, including for evaluation of liver damage and as markers of alcohol intake. Evidence on test performance should lead to better selection of appropriate tests and improved interpretation of results. We compared laboratory test results from 1578 patients between cases (with alcoholic cirrhosis; 753 men, 243 women) and controls (with equivalent lifetime alcohol intake but no liver disease; 439 men, 143 women). Comparisons were also made between 631 cases who had reportedly been abstinent from alcohol for over 60 days and 364 who had not. ROC curve analysis was used to estimate and compare tests ability to distinguish patients with and without cirrhosis, and abstinent and drinking cases. The best tests for presence of cirrhosis were INR and bilirubin, with areas under the ROC curve (AUCs) of 0.91 ± 0.01 and 0.88 ± 0.01, respectively. Confining analysis to patients with no current or previous ascites gave AUCs of 0.88 ± 0.01 for INR and 0.85 ± 0.01 for bilirubin. GGT and AST showed discrimination between abstinence and recent drinking in patients with cirrhosis, including those without ascites, when appropriate (and for GGT, sex-specific) limits were used. For AST, a cut-off limit of 85 units/L gave 90% specificity and 37% sensitivity. For GGT, cut-off limits of 288 units/L in men and 138 units/L in women gave 90% specificity for both and 40% sensitivity in men, 63% sensitivity in women. INR and bilirubin show the best separation between patients with alcoholic cirrhosis (with or without ascites) and control patients with similar lifetime alcohol exposure. Although AST and GGT are substantially increased by liver disease, they can give useful information on recent alcohol intake in patients with alcoholic cirrhosis when appropriate cut-off limits are used.

Published
2018

9. Restoring cellular magnesium balance through Cyclin M4 protects against acetaminophen-induced liver damage

Author

González-Recio, Irene, Simón, Jorge, Goikoetxea-Usandizaga, Naroa, Serrano-Maciá, Marina, Mercado-Gómez, Maria, Rodríguez-Agudo, Rubén, Lachiondo-Ortega, Sofía, Gil-Pitarch, Clàudia, Fernández-Rodríguez, Carmen, Castellana, Donatello, Latasa, Maria U., Abecia, Leticia, Anguita, Juan, Delgado, Teresa C., Iruzubieta, Paula, Crespo, Javier, Hardy, Serge, Petrov, Petar D., Jover, Ramiro, Avila, Matías A., Martín, César, Schaeper, Ute, Tremblay, Michel L., Dear, James W., Masson, Steven, McCain, Misti Vanette, Reeves, Helen L., Andrade, Raul J., Lucena, M. Isabel, Buccella, Daniela, Martínez-Cruz, Luis Alfonso, and Martínez-Chantar, Maria L

Published
2022
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11. SAT-285-YI Incorporation of cholestasis into prognostic models improves predictive outcome in alcohol-related liver disease: a retrospective multicenter study

Author

Subhani, Mohsan, primary, Chen, Minjun, additional, Hagström, Hannes, additional, Allison, Michael, additional, Brahmania, Mayur, additional, Forrest, Ewan H., additional, McCune, Anne, additional, Masson, Steven, additional, Rajoriya, Neil, additional, Arab, Juan Pablo, additional, Aithal, Guruprasad, additional, and Parker, Richard, additional

Published
2024
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13. SAT-280 Emergence of co-morbidities in alcohol-related hepatitis over time: insights from the WALDO cohort

Author

Corrigall, Douglas, primary, Naik, Keval, additional, Aithal, Guruprasad, additional, Brahmania, Mayur, additional, Forrest, Ewan H., additional, Hagström, Hannes, additional, McCune, Anne, additional, Masson, Steven, additional, Rajoriya, Neil, additional, Arab, Juan Pablo, additional, Parker, Richard, additional, and Allison, Michael, additional

Published
2024
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14. THU-317 Alcohol-related hepatitis is associated with a distinctive pattern of disordered bile acid metabolism and reduced bile acid transporter expression

Author

Tyson, Luke D., primary, Atkinson, Stephen R., additional, Mullish, Benjamin H., additional, Pechlivanis, Alexandros, additional, Allison, Michael, additional, Austin, Andrew, additional, Chappell, Katie, additional, Forbes, Stuart J., additional, Forrest, Ewan H., additional, Kilpatrick, Alastair M., additional, Martinez-Gili, Laura, additional, Masson, Steven, additional, McPhail, Mark J.W., additional, Richardson, Paul, additional, Torres, Daniel Rodrigo, additional, Ryder, Stephen D., additional, Wright, Mark, additional, Patel, Vishal C., additional, Vergis, Nikhil, additional, Holmes, Elaine, additional, and Thursz, Mark R., additional

Published
2024
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15. SAT-274 Serum proteomic analyses reveal elevated HGFand IL-8 in patients with alcohol-related hepatitis compared to decompensated alcohol-related cirrhosis and can differentiate patients with AH at risk of infection from those at risk of acute kidney injury

Author

Tyson, Luke D., primary, Atkinson, Stephen R., additional, Patel, Vishal C., additional, Allison, Michael, additional, Austin, Andrew, additional, Dear, James W., additional, Forrest, Ewan H., additional, Hunter, RobertW., additional, Liu, Tong, additional, Masson, Steven, additional, McPhail, Mark J.W., additional, Nunes, Joao, additional, Richardson, Paul, additional, Ryder, Stephen D., additional, Wright, Mark, additional, Holmes, Elaine, additional, Thursz, Mark R., additional, and Vergis, Nikhil, additional

Published
2024
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16. Non-invasive alloimmune risk stratification of long-term liver transplant recipients

Author

Vionnet, Julien, Miquel, Rosa, Abraldes, Juan G., Wall, Jurate, Kodela, Elisavet, Lozano, Juan-Jose, Ruiz, Pablo, Navasa, Miguel, Marshall, Aileen, Nevens, Frederik, Gelson, Will, Leithead, Joanna, Masson, Steven, Jaeckel, Elmar, Taubert, Richard, Tachtatzis, Phaedra, Eurich, Dennis, Simpson, Kenneth J., Bonaccorsi-Riani, Eliano, Feng, Sandy, Bucuvalas, John, Ferguson, James, Quaglia, Alberto, Sidorova, Julia, Elstad, Maria, Douiri, Abdel, and Sánchez-Fueyo, Alberto

Published
2021
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18. The mitochondrial negative regulator MCJ is a therapeutic target for acetaminophen-induced liver injury.

Author

Barbier-Torres, Lucía, Iruzubieta, Paula, Fernández-Ramos, David, Delgado, Teresa C, Taibo, Daniel, Guitiérrez-de-Juan, Virginia, Varela-Rey, Marta, Azkargorta, Mikel, Navasa, Nicolas, Fernández-Tussy, Pablo, Zubiete-Franco, Imanol, Simon, Jorge, Lopitz-Otsoa, Fernando, Lachiondo-Ortega, Sofia, Crespo, Javier, Masson, Steven, McCain, Misti Vanette, Villa, Erica, Reeves, Helen, Elortza, Felix, Lucena, Maria Isabel, Hernández-Alvarez, Maria Isabel, Zorzano, Antonio, Andrade, Raúl J, Lu, Shelly C, Mato, José M, Anguita, Juan, Rincón, Mercedes, and Martínez-Chantar, María Luz

Subjects
Liver, Mitochondria, Liver, Hepatocytes, Animals, Mice, Inbred C57BL, Humans, Mice, Disease Models, Animal, Acetaminophen, Rotenone, Electron Transport Complex I, Mitochondrial Proteins, Molecular Chaperones, RNA, Small Interfering, Uncoupling Agents, Adolescent, Adult, Middle Aged, Female, Male, HSP40 Heat-Shock Proteins, Gene Knockout Techniques, Young Adult, Primary Cell Culture, Drug Overdose, Chemical and Drug Induced Liver Injury, Mitochondria, Inbred C57BL, Disease Models, Animal, RNA, Small Interfering
Abstract

Acetaminophen (APAP) is the active component of many medications used to treat pain and fever worldwide. Its overuse provokes liver injury and it is the second most common cause of liver failure. Mitochondrial dysfunction contributes to APAP-induced liver injury but the mechanism by which APAP causes hepatocyte toxicity is not completely understood. Therefore, we lack efficient therapeutic strategies to treat this pathology. Here we show that APAP interferes with the formation of mitochondrial respiratory supercomplexes via the mitochondrial negative regulator MCJ, and leads to decreased production of ATP and increased generation of ROS. In vivo treatment with an inhibitor of MCJ expression protects liver from acetaminophen-induced liver injury at a time when N-acetylcysteine, the standard therapy, has no efficacy. We also show elevated levels of MCJ in the liver of patients with acetaminophen overdose. We suggest that MCJ may represent a therapeutic target to prevent and rescue liver injury caused by acetaminophen.

Published
2017

19. Genetic and pharmacological inhibition of XBP1 protects against APAP hepatotoxicity through the activation of autophagy

Author

Hui, Ye, Chaobo, Chen, Hanghang, Wu, Kang, Zheng, Martín Adrados, Beatriz, Caparros, Esther, Francés, Rubén, Nelson, Leonard J., Gómez Del Moral Martín-Consuegra, Manuel María, Asensio, Iris, Javier Vaquero, Bañares Cañizares, Rafael, Ávila, Matías A., Andrade, Raúl J., Lucena, María Isabel, Martínez Chantar, Maria Luz, Reeves, Helen L., Masson, Steven, Blumberg, Richard S., Gracia Sancho, Jordi, Nevzorova, Yulia, Martínez Naves, Eduardo, Cubero Palero, Francisco Javier, Hui, Ye, Chaobo, Chen, Hanghang, Wu, Kang, Zheng, Martín Adrados, Beatriz, Caparros, Esther, Francés, Rubén, Nelson, Leonard J., Gómez Del Moral Martín-Consuegra, Manuel María, Asensio, Iris, Javier Vaquero, Bañares Cañizares, Rafael, Ávila, Matías A., Andrade, Raúl J., Lucena, María Isabel, Martínez Chantar, Maria Luz, Reeves, Helen L., Masson, Steven, Blumberg, Richard S., Gracia Sancho, Jordi, Nevzorova, Yulia, Martínez Naves, Eduardo, and Cubero Palero, Francisco Javier

Abstract

Acetaminophen (APAP) hepatotoxicity induces endoplasmic reticulum (ER) stress which triggers the unfolded protein response (UPR) in hepatocytes. However, the mechanisms underlying ER stress remain poorly understood, thus reducing the options for exploring new pharmacological therapies for patients with hyperacute liver injury. Eight-to-twelve-week-old C57BL/6J Xbp1-floxed (Xbp1f/f) and hepatocyte-specific knockout Xbp1 mice (Xbp1∆hepa) were challenged with either high dose APAP [500 mg/kg] and sacrificed at early (1–2 h) and late (24 h) stages of hepatotoxicity. Histopathological examination of livers, immunofluorescence and immunohistochemistry, Western blot, real time (RT)-qPCR studies and transmission electron microscopy (TEM) were performed. Pharmacological inhibition of XBP1 using pre-treatment with STF-083010 [STF, 75 mg/kg] and autophagy induction with Rapamycin [RAPA, 8 mg/kg] or blockade with Chloroquine [CQ, 60 mg/kg] was also undertaken in vivo. Cytoplasmic expression of XBP1 coincided with severity of human and murine hyperacute liver injury. Transcriptional and translational activation of the UPR and sustained activation of JNK1/2 were major events in APAP hepatotoxicity, both in a human hepatocytic cell line and in a preclinical model. Xbp1∆hepa livers showed decreased UPR and JNK1/2 activation but enhanced autophagy in response to high dose APAP. Additionally, blockade of XBP1 splicing by STF, mitigated APAP-induced liver injury and without non-specific off-target effects (e.g., CYP2E1 activity). Furthermore, enhanced autophagy might be responsible for modulating CYP2E1 activity in Xbp1∆hepa animals. Genetic and pharmacological inhibition of Xbp1 specifically in hepatocytes ameliorated APAP-induced liver injury by enhancing autophagy and decreasing CYP2E1 expression. These findings provide the basis for the therapeutic restoration of ER stress and/or induction of autophagy in patients with hyperacute liver injury., Ministerio de Economía, Comercio y Empresa, German Research Foundation, Depto. de Inmunología, Oftalmología y ORL, Fac. de Medicina, TRUE, pub

Published
2024

21. Outcomes following SARS-CoV-2 infection in liver transplant recipients: an international registry study

Author

Webb, Gwilym J, Marjot, Thomas, Cook, Jonathan A, Aloman, Costica, Armstrong, Matthew J, Brenner, Erica J, Catana, Maria-Andreea, Cargill, Tamsin, Dhanasekaran, Renumathy, García-Juárez, Ignacio, Hagström, Hannes, Kennedy, James M, Marshall, Aileen, Masson, Steven, Mercer, Carolyn J, Perumalswami, Ponni V, Ruiz, Isaac, Thaker, Sarang, Ufere, Nneka N, Barnes, Eleanor, Barritt, Alfred S, IV, and Moon, Andrew M

Published
2020
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22. Genetic and pharmacological inhibition of XBP1 protects against APAP hepatotoxicity through the activation of autophagy

Author

Ye, Hui, Chen, Chaobo, Wu, Hanghang, Zheng, Kang, Martín-Adrados, Beatriz, Caparros, Esther, Francés, Rubén, Nelson, Leonard J., Gómez del Moral, Manuel, Asensio, Iris, Vaquero, Javier, Bañares, Rafael, Ávila, Matías A., Andrade, Raúl J., Isabel Lucena, M., Martínez-Chantar, Maria Luz, Reeves, Helen L., Masson, Steven, Blumberg, Richard S., Gracia-Sancho, Jordi, Nevzorova, Yulia A., Martínez-Naves, Eduardo, and Cubero, Francisco Javier

Published
2022
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23. Brief Report: Genetics of Alcoholic Cirrhosis—GenomALC Multinational Study

Author

Whitfield, John B, Rahman, Khairunnessa, Haber, Paul S, Day, Christopher P, Masson, Steven, Daly, Ann K, Cordell, Heather J, Mueller, Sebastian, Seitz, Helmut K, Liangpunsakul, Suthat, Westerhold, Chi, Liang, Tiebing, Lumeng, Lawrence, Foroud, Tatiana, Nalpas, Bertrand, Mathurin, Philippe, Stickel, Felix, Soyka, Michael, Botwin, Gregory J, Morgan, Timothy R, Seth, Devanshi, and Consortium, for the GenomALC

Subjects
Biomedical and Clinical Sciences, Biological Psychology, Clinical and Health Psychology, Clinical Sciences, Psychology, Liver Disease, Alcoholism, Alcohol Use and Health, Substance Misuse, Clinical Research, Chronic Liver Disease and Cirrhosis, Behavioral and Social Science, Digestive Diseases, Genetics, Aetiology, 2.1 Biological and endogenous factors, Oral and gastrointestinal, Good Health and Well Being, Alcohol Drinking, Australia, Case-Control Studies, Clinical Protocols, Family Health, France, Genome-Wide Association Study, Germany, Internationality, Liver Cirrhosis, Alcoholic, Patient Selection, Switzerland, United Kingdom, United States, GenomALC Consortium, Alcoholic Liver Disease, Cirrhosis, Genetic Risk Factors, Genomewide Association, High-Risk Drinkers, Neurosciences, Substance Abuse, Clinical sciences, Biological psychology, Clinical and health psychology
Abstract

BackgroundThe risk of alcohol-related liver cirrhosis increases with increasing alcohol consumption, but many people with very high intake escape from liver disease. We postulate that susceptibility to alcoholic cirrhosis has a complex genetic component and propose that this can be dissected through a large and sufficiently powered genomewide association study (GWAS).MethodsThe GenomALC Consortium comprises researchers from Australia, France, Germany, Switzerland, United Kingdom, and United States, with a joint aim of exploring the genetic and genomic basis of alcoholic cirrhosis. For this National Institutes of Health/National Institute on Alcohol Abuse and Alcoholism funded study, we are recruiting high-risk drinkers who are either cases (with alcoholic cirrhosis) or controls (drinking comparable amounts over similar time, but free of significant liver disease). Extensive phenotypic data are obtained using semistructured interviews and patient records, and blood samples are collected.ResultsWe have successfully recruited 859 participants including 538 matched case-control samples as of September 2014, using study-specific inclusion-exclusion criteria and data collection protocols. Of these, 580 are cases (442 men and 138 women) and 279 are controls (205 men and 74 women). Duration of excessive drinking was slightly greater in cases than controls and was significantly less in women than men. Cases had significantly lower lifetime alcohol intake than controls. Both cases and controls had a high prevalence of reported parental alcohol problems, but cases were significantly more likely to report that a father with alcohol problems had died from liver disease (odds ratio 2.53, 95% confidence interval 1.31 to 4.87, p = 0.0055).ConclusionsRecruitment of participants for a GWAS of alcoholic cirrhosis has proved feasible across countries with multiple sites. Affected patients often consume less alcohol than unaffected ones, emphasizing the existence of individual vulnerability factors. Cases are more likely to report liver disease in a father with alcohol problems than controls, consistent with a potential genetic component to the risk of alcoholic cirrhosis.

Published
2015

27. In severe alcohol‐related hepatitis, acute kidney injury is prevalent, associated with mortality independent of liver disease severity, and can be predicted using IL‐8 and micro‐RNAs

Author

Tyson, Luke D., primary, Atkinson, Stephen, additional, Hunter, Robert W., additional, Allison, Michael, additional, Austin, Andrew, additional, Dear, James W., additional, Forrest, Ewan, additional, Liu, Tong, additional, Lord, Emma, additional, Masson, Steven, additional, Nunes, Joao, additional, Richardson, Paul, additional, Ryder, Stephen D., additional, Wright, Mark, additional, Thursz, Mark, additional, and Vergis, Nikhil, additional

Published
2023
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28. Quality standards for the management of alcohol-related liver disease: consensus recommendations from the British Association for the Study of the Liver and British Society of Gastroenterology ARLD special interest group

Author

Parker, Richard, primary, Allison, Michael, additional, Anderson, Seonaid, additional, Aspinall, Richard, additional, Bardell, Sara, additional, Bains, Vikram, additional, Buchanan, Ryan, additional, Corless, Lynsey, additional, Davidson, Ian, additional, Dundas, Pauline, additional, Fernandez, Jeff, additional, Forrest, Ewan, additional, Forster, Erica, additional, Freshwater, Dennis, additional, Gailer, Ruth, additional, Goldin, Robert, additional, Hebditch, Vanessa, additional, Hood, Steve, additional, Jones, Arron, additional, Lavers, Victoria, additional, Lindsay, Deborah, additional, Maurice, James, additional, McDonagh, Joanne, additional, Morgan, Sarah, additional, Nurun, Tania, additional, Oldroyd, Christopher, additional, Oxley, Elizabeth, additional, Pannifex, Sally, additional, Parsons, Graham, additional, Phillips, Thomas, additional, Rainford, Nicole, additional, Rajoriya, Neil, additional, Richardson, Paul, additional, Ryan, J, additional, Sayer, Joanne, additional, Smith, Mandy, additional, Srivastava, Ankur, additional, Stennett, Emma, additional, Towey, Jennifer, additional, Vaziri, Roya, additional, Webzell, Ian, additional, Wellstead, Andrew, additional, Dhanda, Ashwin, additional, and Masson, Steven, additional

Published
2023
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33. Impact of 5 years of hepatitis C testing and treatment in the North East of England prisons

Author

Johnson, Amy, primary, Shearer, Jessica, additional, Thompson, Craig, additional, Jelley, Ryan, additional, Aldridge, Jodi, additional, Allsop, Caroline, additional, Kerry, Jenna, additional, Jones, Dee, additional, McCullough, Francesca, additional, Miller, Carolyn, additional, Valappil, Manoj, additional, Taha, Yusri, additional, Masson, Steven, additional, Jefferson, Tony, additional, Lawton, Colin, additional, Christensen, Lee, additional, and McPherson, Stuart, additional

Published
2023
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35. P127 Impact of 5 years of Hepatitis C testing and treatment in the North-East of England prisons

Author

Johnson, Amy, primary, Shearer, Jessica, additional, Thompson, Craig, additional, Jelley, Ryan, additional, Aldridge, Jodi, additional, Allsop, Caroline, additional, Kerry, Jenna, additional, Jones, Dee, additional, McCullough, Francesca, additional, Miller, Carolyn, additional, Valappil, Manoj, additional, Taha, Yusri, additional, Masson, Steven, additional, Jefferson, Tony, additional, Lawton, Colin, additional, Christensen, Lee, additional, and McPherson, Stuart, additional

Published
2023
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39. In Patients With Severe Alcoholic Hepatitis, Prednisolone Increases Susceptibility to Infection and Infection-Related Mortality, and Is Associated With High Circulating Levels of Bacterial DNA

Author

Vergis, Nikhil, Atkinson, Stephen R., Knapp, Suzanne, Maurice, James, Allison, Michael, Austin, Andrew, Forrest, Ewan H., Masson, Steven, McCune, Anne, Patch, David, Richardson, Paul, Gleeson, Dermot, Ryder, Stephen D., Wright, Mark, and Thursz, Mark R.

Published
2017
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41. Sub-optimal global public health policies and strategies to combat hepatocellular carcinoma

Author

Diaz, Luis Antonio, primary, Norero, Blanca, additional, Corsi, Oscar, additional, Ayares, Gustavo, additional, Idalsoaga, Francisco, additional, García, Sergio, additional, Vázquez, Valeria, additional, Lacalle, Lucas, additional, Lazo, Mariana, additional, Ferreccio, Catterina, additional, Mendizabal, Manuel, additional, Piñero, Federico, additional, Martinez, Edmundo, additional, Ijeoma, Ifeorah, additional, Louvet, Alexandre, additional, Piano, Salvatore, additional, Cortez-Pinto, Helena, additional, Wong, Vincent Wai-Sun, additional, Kulkarni, Anand, additional, Cotter, Thomas, additional, Brahmania, Mayur, additional, roblero, Juan Pablo, additional, Dirchwolf, Melisa, additional, Pollarsky, Florencia, additional, George, Jacob, additional, Stauber, Rudolf E., additional, Francque, Sven, additional, Guerra, Patricia, additional, Oliveira, Claudia, additional, Araujo, Roberta, additional, Álvares-da-Silva, Mario, additional, Blaise, Nkegoum, additional, Abraldes, Juan G, additional, Zheng, Ming-Hua, additional, Toro, Luis, additional, Restrepo, Juan Carlos, additional, Ramirez, Wagner, additional, Grgurević, Ivica, additional, Infante, Mirtha, additional, Mbendi, Charles, additional, Carrera, Enrique, additional, El Kassas, Mohamed, additional, Mahmoud, Abdelmajeed, additional, Tesfaye, Yonas Gedamu, additional, Tadesse, Sewale Anagaw, additional, Akalu, Tiruwork Fekadu, additional, Desalegn, Hailemichael, additional, Allaire, Manon, additional, Patrizia, Carrieri, additional, Schattenberg, Jörn, additional, Aguyire, Joan, additional, Micah, Eileen Akonobea, additional, Tachi, Kenneth, additional, Maldonado Cardona, Katherine Emilia, additional, Sanchez, Abel, additional, Sánchez, Marco, additional, Björnsson, Einar S., additional, Iavarone, Massimo, additional, Okamoto, Ryuichi, additional, Some, Fatuma, additional, Hellani, Mohammad Fadel, additional, Prado Gonzalez, Veronica Enith, additional, Chávez-Tapia, Norberto Carlos, additional, Méndez-Sánchez, Nahum, additional, Mabote Mucumbi, Sheila Constância, additional, Ugiagbe, Rose Ashinedu, additional, Akande, Kolawole, additional, Nwoko, Chinenye, additional, Ezenkwa, Uchenna Simon, additional, Okoye, Ifeoma Joy, additional, Hamid, Saeed Sadiq, additional, Quezada, Julissa Lombardo, additional, Girala, Marcos, additional, Padilla, P. Martin, additional, Diaz-Ferrer, Javier, additional, Tagle, Martin, additional, Kukla, Michał, additional, Odeghe, Emuobor, additional, wemimo, Rasheed mumini, additional, Reis, Daniela, additional, Mozgovoi, Sergei, additional, Ismail, Mona, additional, Koller, Tomas, additional, Spearman, Wendy, additional, Elhassan, Moawia, additional, Stal, Per, additional, Pazi, Swaleh, additional, Ocanit, Anthony, additional, Masson, Steven, additional, Dunn, Winston, additional, Kamath, Patrick S., additional, Singal, Ashwani, additional, Debes, Jose, additional, Reig, María, additional, Loomba, Rohit, additional, Bataller, Ramon, additional, Lazarus, Jeffrey, additional, Arrese, Marco, additional, and Arab, Juan Pablo, additional

Published
2023
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42. Diabetes increases risk of mortality in alcohol-related liver disease

Author

Theodoreson, Mark, primary, Aithal, Guruprasad, additional, Allison, Michael, additional, Brahmania, Mayur, additional, Forrest, Ewan, additional, Hagström, Hannes, additional, Likhitsup, Alisa, additional, Masson, Steven, additional, McCune, Anne, additional, Rajoriya, Neil, additional, Rowe, Ian, additional, and Parker, Richard, additional

Published
2023
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43. Neddylation inhibition recovers drug-induced liver injury through the stabilization of Tamm41

Author

Gil-Pitarch, Claudia, primary, Serrano-Macia, Marina, additional, Espinosa, Jorge Simón, additional, Agudo, Rubén Rodríguez, additional, Lachiondo-Ortega, Sofia, additional, Mercado-Gómez, Maria, additional, González-Recio, Irene, additional, Goikoetxea, Naroa, additional, Delgado, Teresa Cardoso, additional, Martinez-Cruz, Luis Alfonso, additional, Nogueiras, Ruben, additional, Iruzubieta, Paula, additional, Crespo, Javier, additional, Masson, Steven, additional, McCain, Misti, additional, Reeves, Helen Louise, additional, and Martínez-Chantar, María Luz, additional

Published
2023
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44. The Liverpool alcohol-related liver disease algorithm identifies twice as many emergency admissions compared to standard methods when applied to Hospital Episode Statistics for England

Author

Dhanda, Ashwin, Bodger, Keith, Hood, Steve, Henn, Clive, Allison, Michael, Amasiatu, Chioma, Burton, Robyn, Cramp, Matthew, Forrest, Ewan, Khetani, Meetal, MacGilchrist, Alastair, Masson, Steven, Parker, Richard, Sheron, Nick, Simpson, Ken, Vergis, Nikhil, White, Martin, BASL ARLD SIG National Service Evaluation Group, Dhanda, Ashwin [0000-0002-0523-0193], Bodger, Keith [0000-0002-1825-3239], Forrest, Ewan [0000-0002-7293-2574], Masson, Steven [0000-0003-1041-9844], Parker, Richard [0000-0003-4888-8670], and Apollo - University of Cambridge Repository

Subjects
Hospitalization, England, Liver Diseases, Humans, COVID-19, Pandemics, Hospitals, Algorithms
Abstract

BACKGROUND: Emergency admissions in England for alcohol-related liver disease (ArLD) have increased steadily for decades. Statistics based on administrative data typically focus on the ArLD-specific code as the primary diagnosis and are therefore at risk of excluding ArLD admissions defined by other coding combinations. AIM: To deploy the Liverpool ArLD Algorithm (LAA), which accounts for alternative coding patterns (e.g., ArLD secondary diagnosis with alcohol/liver-related primary diagnosis), to national and local datasets in the context of studying trends in ArLD admissions before and during the COVID-19 pandemic. METHODS: We applied the standard approach and LAA to Hospital Episode Statistics for England (2013-21). The algorithm was also deployed at 28 hospitals to discharge coding for emergency admissions during a common 7-day period in 2019 and 2020, in which eligible patient records were reviewed manually to verify the diagnosis and extract data. RESULTS: Nationally, LAA identified approximately 100% more monthly emergency admissions from 2013 to 2021 than the standard method. The annual number of ArLD-specific admissions increased by 30.4%. Of 39,667 admissions in 2020/21, only 19,949 were identified with standard approach, an estimated admission cost of £70 million in under-recorded cases. Within 28 local hospital datasets, 233 admissions were identified using the standard approach and a further 250 locally verified cases using the LAA (107% uplift). There was an 18% absolute increase in ArLD admissions in the seven-day evaluation period in 2020 versus 2019. There were no differences in disease severity or mortality, or in the proportion of admissions with decompensation of cirrhosis or alcoholic hepatitis. CONCLUSIONS: The LAA can be applied successfully to local and national datasets. It consistently identifies approximately 100% more cases than the standard coding approach. The algorithm has revealed the true extent of ArLD admissions. The pandemic has compounded a long-term rise in ArLD admissions and mortality.

Published
2022
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46. British Society of Gastroenterology Best Practice Guidance: outpatient management of cirrhosis - part 3: special circumstances.

Author

Mansour, Dina, Masson, Steven, Hammond, John, Leithead, Joanna A., Johnson, Jill, Rahim, Mussarat Nazia, Douds, Andrew C., Corless, Lynsey, Shawcross, Debbie L., Heneghan, Michael A., Tripathi, Dhiraj, McPherson, Stuart, Bonner, Emily, Botterill, Gemma, West, Rebecca, Donnelly, Mhairi, Grapes, Allison, Hollywood, Coral, and Ross, Valerie

Published
2023
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47. British Society of Gastroenterology Best Practice Guidance: outpatient management of cirrhosis - part 2: decompensated cirrhosis.

Author

Mansour, Dina, Masson, Steven, Corless, Lynsey, Douds, Andrew C., Shawcross, Debbie L., Johnson, Jill, Leithead, Joanna A., Heneghan, Michael A., Rahim, Mussarat Nazia, Tripathi, Dhiraj, Ross, Valerie, Hammond, John, Grapes, Allison, Hollywood, Coral, Botterill, Gemma, Bonner, Emily, Donnelly, Mhairi, McPherson, Stuart, and West, Rebecca

Published
2023
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48. British Society of Gastroenterology Best Practice Guidance: outpatient management of cirrhosis - part 1: compensated cirrhosis.

Author

Mansour, Dina, Masson, Steven, Shawcross, Debbie L., Douds, Andrew C., Bonner, Emily, Corless, Lynsey, Leithead, Joanna A., Hammond, John, Heneghan, Michael A., Rahim, Mussarat Nazia, Tripathi, Dhiraj, West, Rebecca, Johnson, Jill, Botterill, Gemma, Hollywood, Coral, Ross, Valerie, Donnelly, Mhairi, Compston, Juliet E., McPherson, Stuart, and Grapes, Allison

Published
2023
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49. Extra‐hepatic Morbidity and Mortality in Alcohol‐related Liver Disease: Systematic Review and Meta‐analysis

Author

Theodoreson, Mark D., primary, Aithal, Guruprasad P., additional, Allison, Michael, additional, Brahmania, Mayur, additional, Forrest, Ewan, additional, Hagström, Hannes, additional, Johansen, Stine, additional, Krag, Aleksander, additional, Likhitsup, Alisa, additional, Masson, Steven, additional, McCune, Anne, additional, Rajoriya, Neil, additional, Thiele, Maja, additional, Rowe, Ian A., additional, and Parker, Richard, additional

Published
2023
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50. Letter: Algorithmic NIT approaches to identify advanced liver fibrosis in patients with MASLD: Authors' reply.

Author

McPherson, Stuart, Dyson, Jessica K., Jopson, Laura, Masson, Steven, Patel, Preya, and Anstee, Quentin M.

Subjects
HEPATIC fibrosis, AUTHORS
Abstract

LINKED CONTENT: This article is linked to McPherson et al papers. To view these articles, visit https://doi.org/10.1111/apt.18061 and https://doi.org/10.1111/apt.18176 [ABSTRACT FROM AUTHOR]

Published
2024
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