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1. Alcohol-Associated Liver Disease Outcomes: Critical Mechanisms of Liver Injury Progression

Author

Osna, Natalia A, Tikhanovich, Irina, Ortega-Ribera, Martí, Mueller, Sebastian, Zheng, Chaowen, Mueller, Johannes, Li, Siyuan, Sakane, Sadatsugu, Weber, Raquel Carvalho Gontijo, Kim, Hyun Young, Lee, Wonseok, Ganguly, Souradipta, Kimura, Yusuke, Liu, Xiao, Dhar, Debanjan, Diggle, Karin, Brenner, David A, Kisseleva, Tatiana, Attal, Neha, McKillop, Iain H, Chokshi, Shilpa, Mahato, Ram, Rasineni, Karuna, Szabo, Gyongyi, and Kharbanda, Kusum K

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Digestive Diseases, Liver Disease, Hepatitis, Chronic Liver Disease and Cirrhosis, Alcoholism, Alcohol Use and Health, Substance Misuse, Aetiology, 2.1 Biological and endogenous factors, Oral and gastrointestinal, Good Health and Well Being, alcohol-associated liver disease, epigenetics, cell death, hemolysis, MetAld, hepatic stellate cells, fibrosis, fatty acid binding protein 4, hepatocellular carcinoma, models, Liver, Animals, Humans, Liver Diseases, Alcoholic, Disease Progression, Epigenesis, Genetic, Hepatic Stellate Cells, Biochemistry and cell biology, Bioinformatics and computational biology, Medical biotechnology
Abstract

Alcohol-associated liver disease (ALD) is a substantial cause of morbidity and mortality worldwide and represents a spectrum of liver injury beginning with hepatic steatosis (fatty liver) progressing to inflammation and culminating in cirrhosis. Multiple factors contribute to ALD progression and disease severity. Here, we overview several crucial mechanisms related to ALD end-stage outcome development, such as epigenetic changes, cell death, hemolysis, hepatic stellate cells activation, and hepatic fatty acid binding protein 4. Additionally, in this review, we also present two clinically relevant models using human precision-cut liver slices and hepatic organoids to examine ALD pathogenesis and progression.

Published
2024

4. Prolonged hypoxia alleviates prolyl hydroxylation-mediated suppression of RIPK1 to promote necroptosis and inflammation

Author

Zhang, Tao, Xu, Daichao, Liu, Jianping, Wang, Min, Duan, Li-Juan, Liu, Min, Meng, Huyan, Zhuang, Yuan, Wang, Huibing, Wang, Yingnan, Lv, Mingming, Zhang, Zhengyi, Hu, Jia, Shi, Linyu, Guo, Rui, Xie, Xingxing, Liu, Hui, Erickson, Emily, Wang, Yaru, Yu, Wenyu, Dang, Fabin, Guan, Dongxian, Jiang, Cong, Dai, Xiaoming, Inuzuka, Hiroyuki, Yan, Peiqiang, Wang, Jingchao, Babuta, Mrigya, Lian, Gewei, Tu, Zhenbo, Miao, Ji, Szabo, Gyongyi, Fong, Guo-Hua, Karnoub, Antoine E., Lee, Yu-Ru, Pan, Lifeng, Kaelin, Jr., William G., Yuan, Junying, and Wei, Wenyi

Published
2023
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5. Randomized trial of anakinra plus zinc vs. prednisone for severe alcohol-associated hepatitis

Author

Chalasani, Naga, Patidar, Kavish R., Vuppalanchi, Raj, Samala, Niha, Yoder, Lindsey, Nephew, Lauren, Shah, Vijay H., Simonetto, Douglas A., Kamath, Patrick, Vargas, Hugo E., Yang, Liu, Dasarathy, Srinivasan, Welch, Nicole, Bellar, Annette, Attaway, Amy, Dasarathy, Jaividhya, Growley, Ashley, Streem, David, Nagy, Laura E., Mitchell, Mack C., Herlong, H. Franklin, Kerr, Thomas, Cotter, Thomas, Sanyal, Arun, O'Connor, Sara, Luketic, Velimir, Asgharpour, Amon, Taylor, Stephanie, McClain, Craig J., Vatsalya, Vatsalya, Jophlin, Loretta, Cave, Matt, Jha, Suman Kumar, Marsano, Luis, Barve, Ashutosh, Frimodig, Jane, Bataller, Ramon, Ravi, Samhita, Behari, Jaideep, Shivanekar, Sharvari, Novelli, Paula, Duarte-Rojo, Andres, Jonassaint, Naudia, Szabo, Gyongyi, Curry, Jiang, Zhenghui G., Agarwal, Ushma, Hazel, Mia, Schnabl, Bernd, Gawrieh, Samer, Tu, Wanzhu, Kamath, Patrick S., Chalasani, Naga P., Tang, Qing, Radaeva, Svetlana, Barton, Bruce, and Sanyal, Arun J.

Published
2024
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6. Provider Attitudes and Practices for Alcohol Screening, Treatment, and Education in Patients With Liver Disease: A Survey From the American Association for the Study of Liver Diseases Alcohol-Associated Liver Disease Special Interest Group

Author

Im, Gene Y, Mellinger, Jessica L, Winters, Adam, Aby, Elizabeth S, Lominadze, Zurabi, Rice, John, Lucey, Michael R, Arab, Juan P, Goel, Aparna, Jophlin, Loretta L, Sherman, Courtney B, Parker, Richard, Chen, Po-Hung, Devuni, Deepika, Sidhu, Sandeep, Dunn, Winston, Szabo, Gyongyi, Singal, Ashwani K, and Shah, Vijay H

Subjects
Chronic Liver Disease and Cirrhosis, Behavioral and Social Science, Liver Disease, Health Services, Alcoholism, Alcohol Use and Health, Digestive Diseases, Substance Misuse, Clinical Research, Oral and gastrointestinal, Good Health and Well Being, Alcoholism, Attitude, Humans, Liver Diseases, Public Opinion, Surveys and Questionnaires, United States, Alcohol Use Disorder, Alcohol-Associated Liver Disease, Alcohol Pharmacotherapy, Addiction Medicine, Alcohol Survey, Clinical Sciences, Gastroenterology & Hepatology
Abstract

Background & aimsWhile abstinence-promoting behavioral and pharmacotherapies are part of the therapeutic foundation for alcohol use disorder (AUD) and alcohol-associated liver disease (ALD), these therapies, along with alcohol screening and education, are often underutilized. Our aim was to examine provider attitudes and practices for alcohol screening, treatment and education in patients with liver disease.MethodsWe conducted a survey of primarily (89%) hepatology and gastroenterology providers within (80%) and outside the United States (20%). Surveys were sent to 921 providers with 408 complete responses (44%), of whom 343 (80%) work in a tertiary liver transplant center.ResultsWhile alcohol screening rates in liver disease patients was nearly universal, less than half of providers reported practicing with integrated addiction providers, using alcohol biomarkers and screening tools. Safe alcohol use by liver disease patients was felt to exist by 40% of providers. While 60% of providers reported referring AUD patients for behavioral therapy, 71% never prescribed AUD pharmacotherapy due to low comfort (84%). Most providers (77%) reported low addiction education and 90% desired more during GI/hepatology fellowship training. Amongst prescribers, baclofen was preferred, but with gaps in pharmacotherapy knowledge. Overall, there was low adherence to the 2019 AASLD practice guidance for ALD, although higher in hepatologists and experienced providers.ConclusionsWhile our survey of hepatology and gastroenterology providers demonstrated higher rates of alcohol screening and referrals for behavioral therapy, we found low rates of prescribing AUD pharmacotherapy due to knowledge gaps from insufficient education. Further studies are needed to assess interventions to improve provider alignment with best practices for treating patients with AUD and ALD.

Published
2021

7. Increased microRNA-155 expression in the serum and peripheral monocytes in chronic HCV infection

Author

Bala Shashi, Tilahun Yaphet, Taha Odette, Alao Hawau, Kodys Karen, Catalano Donna, and Szabo Gyongyi

Subjects
Biomarker, MiR-122, MiR-155, MiR-125b, ALT, Inflammation, Medicine
Abstract

Abstract Background Hepatitis C Virus (HCV), a single stranded RNA virus, affects millions of people worldwide and leads to chronic infection characterized by chronic inflammation in the liver and in peripheral immune cells. Chronic liver inflammation leads to progressive liver damage. MicroRNAs (miRNA) regulate inflammation (miR-155, -146a and -125b) as well as hepatocyte function (miR-122). Methods Here we hypothesized that microRNAs are dysregulated in chronic HCV infection. We examined miRNAs in the circulation and in peripheral monocytes of patients with chronic HCV infection to evaluate if specific miRNA expression correlated with HCV infection. Results We found that monocytes from chronic HCV infected treatment-naïve (cHCV) but not treatment responder patients showed increased expression of miR-155, a positive regulator of TNFα, and had increased TNFα production compared to monocytes of normal controls. After LPS stimulation, miR-155 levels were higher in monocytes from cHCV patients compared to controls. MiR-125b, which has negative regulatory effects on inflammation, was decreased in cHCV monocytes compared to controls. Stimulation of normal monocytes with TLR4 and TLR8 ligands or HCV core, NS3 and NS5 recombinant proteins induced a robust increase in both miR-155 expression and TNFα production identifying potential mechanisms for in vivo induction of miR-155. Furthermore, we found increased serum miR-155 levels in HCV patients compared to controls. Serum miR-125b and miR-146a levels were also increased in HCV patients. Serum levels of miR-122 were elevated in cHCV patients and correlated with increased ALT and AST levels and serum miR-155 levels. Conclusion In conclusion, our novel data demonstrate that miR-155, a positive regulator of inflammation, is upregulated both in monocytes and in the serum of patients with chronic HCV infection. Our study suggests that HCV core, NS3, and NS5 proteins or TLR4 and TLR8 ligands can mediate increased miR-155 and TNFα production in chronic HCV infection. The positive correlation between serum miR-155 and miR-122 increase in cHCV may be an indicator of inflammation-induced hepatocyte damage.

Published
2012
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8. Inhibition of TLR8- and TLR4-induced Type I IFN induction by alcohol is different from its effects on inflammatory cytokine production in monocytes

Author

Kodys Karen, Bala Shashi, Pang Maoyin, Catalano Donna, and Szabo Gyongyi

Subjects
Acute, chronic, alcohol, IFNβ, IL-10, TNF alpha, Immunologic diseases. Allergy, RC581-607
Abstract

Abstract Background Prolonged alcohol consumption is a significant co-factor in the progression of chronic viral infections including hepatitis C and HIV, which are both single-stranded RNA viruses. Toll like receptor 8 (TLR8), a pattern recognition receptor expressed in monocytes, senses viral single stranded RNA as a danger signal and leads to the induction of Type I interferon (IFN) as well as the pro-inflammatory cytokine, tumor necrosis factor alpha (TNF alpha). Lipopolysaccharide (LPS), a Toll like receptor 4 (TLR4) ligand, was shown to affect inflammatory cell activation after alcohol consumption and in HIV and HCV infections. Here we hypothesized that alcohol exposure modulates TLR8- and TLR4-ligand-induced monocyte activation and affects both type I IFN and inflammatory cytokine induction. Results The TLR8 ligand, CL075, as well as the TLR4 ligand, LPS, resulted in a significant induction of TNF alpha both at the mRNA and protein levels in human monocytes. We found that both acute and prolonged alcohol treatment resulted in inhibition of type I IFN induction by either TLR8 or TLR4 ligands in human monocytes at the protein and mRNA levels. In contrast to Type I IFN production, the effects of acute and prolonged alcohol were different on inflammatory cytokine activation after TLR8 or TLR4 ligand stimulation. Acute alcohol inhibited TLR8- or TLR4-induced TNF alpha protein and mRNA induction while it augmented IL-10 production in monocytes. In contrast, prolonged alcohol treatment augmented TNF alpha without affecting IL-10 production significantly in response to either TLR8 or TLR4 ligand stimulation. Conclusions These novel results suggest first, that alcohol has a profound inhibitory effect on Type I IFN induction regardless of intracellular (TLR8) or cell surface-derived (TLR4) danger signals. Second, both acute and prolonged alcohol exposure can inhibit antiviral Type I IFN pathway activation. Third, the opposite effects of acute (inhibitory) and prolonged alcohol (augmentation) treatment on pro-inflammatory cytokine activation extend to TLR8-induced signals beyond the previously shown TLR4/LPS pathway.

Published
2011
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14. Neutrophil extracellular traps activate hepatic stellate cells and monocytes via NLRP3 sensing in alcohol-induced acceleration of MASH fibrosis

Author

Babuta, Mrigya, primary, Morel, Caroline, additional, de Carvalho Ribeiro, Marcelle, additional, Calenda, Charles, additional, Ortega-Ribera, Martí, additional, Thevkar Nagesh, Prashanth, additional, Copeland, Christopher, additional, Zhuang, Yuan, additional, Wang, Yanbo, additional, Cho, Yeonhee, additional, Joshi, Radhika, additional, Brezani, Viliam, additional, Hawryluk, Danielle, additional, Datta, Aditi Ashish, additional, Mehta, Jeeval, additional, Nasser, Imad, additional, and Szabo, Gyongyi, additional

Published
2024
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18. Alcohol-Associated Liver Disease

Author

Liu, Mengfei, Sehrawat, Tejasav S., Szabo, Gyongyi, Shah, Vijay H., Gershwin, M. Eric, editor, M. Vierling, John, editor, Tanaka, Atsushi, editor, and P. Manns, Michael, editor

Published
2020
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19. COVID-19 tissue atlases reveal SARS-CoV-2 pathology and cellular targets

Author

Delorey, Toni M., Ziegler, Carly G. K., Heimberg, Graham, Normand, Rachelly, Yang, Yiming, Segerstolpe, Åsa, Abbondanza, Domenic, Fleming, Stephen J., Subramanian, Ayshwarya, Montoro, Daniel T., Jagadeesh, Karthik A., Dey, Kushal K., Sen, Pritha, Slyper, Michal, Pita-Juárez, Yered H., Phillips, Devan, Biermann, Jana, Bloom-Ackermann, Zohar, Barkas, Nikolaos, Ganna, Andrea, Gomez, James, Melms, Johannes C., Katsyv, Igor, Normandin, Erica, Naderi, Pourya, Popov, Yury V., Raju, Siddharth S., Niezen, Sebastian, Tsai, Linus T.-Y., Siddle, Katherine J., Sud, Malika, Tran, Victoria M., Vellarikkal, Shamsudheen K., Wang, Yiping, Amir-Zilberstein, Liat, Atri, Deepak S., Beechem, Joseph, Brook, Olga R., Chen, Jonathan, Divakar, Prajan, Dorceus, Phylicia, Engreitz, Jesse M., Essene, Adam, Fitzgerald, Donna M., Fropf, Robin, Gazal, Steven, Gould, Joshua, Grzyb, John, Harvey, Tyler, Hecht, Jonathan, Hether, Tyler, Jané-Valbuena, Judit, Leney-Greene, Michael, Ma, Hui, McCabe, Cristin, McLoughlin, Daniel E., Miller, Eric M., Muus, Christoph, Niemi, Mari, Padera, Robert, Pan, Liuliu, Pant, Deepti, Pe’er, Carmel, Pfiffner-Borges, Jenna, Pinto, Christopher J., Plaisted, Jacob, Reeves, Jason, Ross, Marty, Rudy, Melissa, Rueckert, Erroll H., Siciliano, Michelle, Sturm, Alexander, Todres, Ellen, Waghray, Avinash, Warren, Sarah, Zhang, Shuting, Zollinger, Daniel R., Cosimi, Lisa, Gupta, Rajat M., Hacohen, Nir, Hibshoosh, Hanina, Hide, Winston, Price, Alkes L., Rajagopal, Jayaraj, Tata, Purushothama Rao, Riedel, Stefan, Szabo, Gyongyi, Tickle, Timothy L., Ellinor, Patrick T., Hung, Deborah, Sabeti, Pardis C., Novak, Richard, Rogers, Robert, Ingber, Donald E., Jiang, Z. Gordon, Juric, Dejan, Babadi, Mehrtash, Farhi, Samouil L., Izar, Benjamin, Stone, James R., Vlachos, Ioannis S., Solomon, Isaac H., Ashenberg, Orr, Porter, Caroline B. M., Li, Bo, Shalek, Alex K., Villani, Alexandra-Chloé, Rozenblatt-Rosen, Orit, and Regev, Aviv

Published
2021
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20. In vivo Bruton's tyrosine kinase inhibition attenuates alcohol-associated liver disease by regulating CD84-mediated granulopoiesis.

Author

Nagesh, Prashanth Thevkar, Cho, Yeonhee, Zhuang, Yuan, Babuta, Mrigya, Ortega-Ribera, Marti, Joshi, Radhika, Brezani, Veronika, Patel, Arman, Datta, Aditi Ashish, Brezani, Viliam, Hsieh, Yun-Cheng, Ramos, Adriana, Mehta, Jeeval, Copeland, Christopher, Kanata, Eleni, Jiang, Zhenghui Gordon, Vlachos, Ioannis, Asara, John, and Szabo, Gyongyi

Subjects
BRUTON tyrosine kinase, BONE marrow, RNA sequencing, GENE expression, LABORATORY mice
Abstract

Severe alcohol-associated hepatitis (AH) is a life-threatening form of alcohol-associated liver disease. Liver neutrophil infiltration is a hallmark of AH, yet the effects of alcohol on neutrophil functions remain elusive. Identifying therapeutic targets to reduce neutrophil-mediated liver damage is essential. Bruton's tyrosine kinase (BTK) plays an important role in neutrophil development and function; however, the role of BTK in AH is unknown. Using RNA sequencing of circulating neutrophils, we found an increase in Btk expression (P = 0.05) and phosphorylated BTK (pBTK) in patients with AH compared with healthy controls. In vitro, physiologically relevant doses of alcohol resulted in a rapid, TLR4-mediated induction of pBTK in neutrophils. In a preclinical model of AH, administration of a small-molecule BTK inhibitor (evobrutinib) or myeloid-specific Btk knockout decreased proinflammatory cytokines and attenuated neutrophil-mediated liver damage. We found that pBTK was essential for alcohol-induced bone marrow granulopoiesis and liver neutrophil infiltration. In vivo, BTK inhibition or myeloid-specific Btk knockout reduced granulopoiesis, circulating neutrophils, liver neutrophil infiltration, and liver damage in a mouse model of AH. Mechanistically, using liquid chromatography–tandem mass spectrometry, we identified CD84 as a kinase target of BTK, which is involved in granulopoiesis. In vitro, CD84 promoted alcohol-induced interleukin-1β and tumor necrosis factor–α in primary human neutrophils, which was inhibited by CD84-blocking antibody treatment. Our findings define the role of BTK and CD84 in regulating neutrophil inflammation and granulopoiesis, with potential therapeutic implications in AH. Editor's summary: Alcoholic liver disease is uniquely characterized by the hepatic infiltration of neutrophils. Nagesh et al. now show that Bruton's tyrosine kinase (BTK) is involved in this altered neutrophil homeostasis. Studying mouse models of alcohol-associated hepatitis, they found that BTK directly interacted with CD84 to promote bone marrow granulopoiesis and the inflammatory neutrophil infiltration that drives subsequent liver injury, particularly after alcohol binge. Pharmacological BTK inhibition reduced proinflammatory cytokines and attenuated neutrophil-mediated liver damage in a mouse model of alcohol-associated hepatitis. BTK activation was also found to be increased in patients with alcohol-associated hepatitis, indicating translational relevance of the identified mechanism of alcohol-induced liver injury. —Catherine Charneski [ABSTRACT FROM AUTHOR]

Published
2024
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22. Combined Insults of a MASH Diet and Alcohol Binges Activate Intercellular Communication and Neutrophil Recruitment via the NLRP3-IL-1β Axis in the Liver.

Author

Babuta, Mrigya, Nagesh, Prashanth Thevkar, Datta, Aditi Ashish, Remotti, Victoria, Zhuang, Yuan, Mehta, Jeeval, Lami, Francesca, Wang, Yanbo, and Szabo, Gyongyi

Subjects
NEUTROPHILS, LIVER, BINGE drinking, HEPATITIS, LIVER cells, LIVER regeneration, CELL communication
Abstract

Binge drinking in obese patients positively correlates with accelerated liver damage and liver-related death. However, the underlying mechanism and the effect of alcohol use on the progression of metabolic-dysfunction-associated steatotic liver disease (MASLD) remain unexplored. Here, we show that short-term feeding of a metabolic-dysfunction-associated steatohepatitis (MASH) diet plus daily acute alcohol binges for three days induce liver injury and activation of the NLRP3 inflammasome. We identify that a MASH diet plus acute alcohol binges promote liver inflammation via increased infiltration of monocyte-derived macrophages, neutrophil recruitment, and NET release in the liver. Our results suggest that both monocyte-derived macrophages and neutrophils are activated via NLRP3, while the administration of MCC950, an NLRP3 inhibitor, dampens these effects.In this study, we reveal important intercellular communication between hepatocytes and neutrophils. We discover that the MASH diet plus alcohol induces IL-1β via NLRP3 activation and that IL-1β acts on hepatocytes and promotes the production of CXCL1 and LCN2. In turn, the increase in these neutrophils recruits chemokines and causes further infiltration and activation of neutrophils in the liver. In vivo administration of the NLRP3 inhibitor, MCC950, improves the early phase of MetALD by preventing liver damage, steatosis, inflammation, and immune cells recruitment. [ABSTRACT FROM AUTHOR]

Published
2024
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24. Selonsertib for patients with bridging fibrosis or compensated cirrhosis due to NASH: Results from randomized phase III STELLAR trials

Author

Gadano, Adrian, Martins, Marcelo, Angus, Peter, Bate, John, Danta, Mark, George, Jacob, Hodge, Alexander, Kontorinis, Nickolas, Roberts, Stuart, Sanagapalli, Santosh, Skoien, Richard, Thompson, Alexander, Zekry, Amany, Stauber, Rudolf, Trauner, Michael, Moreno, Christophe, Reynaert, Hendrik, Verbeke, Len, Silva, Mario Reis Alvares da, Parise, Edison, Oliveira, Claudia Pinto Marques Souza de, Araujo, Roberta Chaves, Martinelli, Ana de Lourdes Candolo, Borman, Meredith, Chandok, Natasha, Elkhashab, Magdy, Fraser, Hughie, Kaita, Kelly, Ma, Mang, Marotta, Paul, Ramji, Alnoor, Tam, Edward, Yoshida, Eric, Swain, Mark, Sebastiani, Giada, Petrunia, Denis, Abergel, Armando, Anty, Rodolphe, Bourlière, Marc, Boursier, Jérôme, Bureau, Christophe, Castera, Laurent, Habersetzer, François, Hézode, Christophe, Ledinghen, Victor De, Leroy, Vincent, Loustaud-Ratti, Véronique, Mathurin, Philippe, Pol, Stanislas, Zoulim, Fabien, Hinrichsen, Holger, Ingiliz, Patrick, Lammert, Frank, Manns, Michael, Schattenberg, Jörn, Schiefke, Ingolf, Trautwein, Christian, Zeuzem, Stefan, Hui, Aric, Li, King-Kong, Wong, Vincent, Acharya, Subrat, Chowdhury, Abhijit, Duseja, Ajay, Kapoor, Dharmesh, Mukewar, Shrikant, Sarin, Shiv, Shah, Samir, Shalimar, Sood, Ajit, Tantry, BV, Ben-Ari, Ziv, Katchman, Helena, Safadi, Rifaat, Veitsman, Ella, Zuckerman, Eli, Brunetto, Maurizia, Lampertico, Pietro, Mangia, Alessandra, Akahane, Takemi, Akuta, Norio, Eguchi, Yuichiro, Fujiyama, Shigetoshi, Genda, Takuya, Hiasa, Yoichi, Ido, Akio, Ikeda, Fusao, Ikegami, Tadashi, Imajo, Kento, Itoh, Yoshito, Iwasa, Motoh, Karino, Yoshiyasu, Kato, Naoya, Kawaguchi, Takumi, Kawanaka, Miwa, Kido, Masahiro, Kobayashi, Tomoo, Kurosaki, Masayuki, Matsuzaki, Yasushi, Mita, Eiji, Mizukoshi, Eishiro, Nakahara, Takashi, Nomura, Hideyuki, Notsumata, Kazuo, Okanoue, Takeshi, Saito, Satoshi, Sakugawa, Hiroshi, Suzuki, Yoshiyuki, Takaguchi, Koichi, Takaki, Akinobu, Takashima, Tomoyuki, Tanaka, Saiyu, Tsuji, Keiji, Ueno, Yoshiyuki, Umemura, Takeji, Uto, Hirofumi, Yamashita, Nobuyuki, Yanase, Mikio, Yatsuhashi, Hiroshi, Yoneda, Masashi, Chan, Wah Kheong, Tan, Soek Siam, Garza, Laura Cisneros, Ladron De Guevara Cetina, Alma, Angeles, Rocio Guadalupe Vargas, Silva, Francisca Martinez, Van Erpecum, Karel, Orr, David, Jabłkowski, Maciej, Jaroszewicz, Jerzy, Ramos, Jose, Ahmed, Taufique, Ang, Tiing, Dan, Yock young, Goh, Boon Bee, Kaliyaperumal, Kalaiyarasi, Yip, Cherng Hann, Baik, Soon Koo, Jang, Byoung Kuk, Jun, Dae Won, Kim, Won, Kim, Hyung Joon, Kim, Ji Hoon, Lee, Kwan Sik, Lee, Chun Kyon, Lim, Young-Suk, Park, Jun Yong, Tak, Won Young, Augustin, Salvador, Perez, Salvador Benlloch, Caballeria, Juan, Luis, Jose, Panero, Calleja, Rodríguez, Jose Carrión, Garcia, Javier Crespo, Samaniego, Javier Garcia, Gibert, Pere Ginès, Prieto, Martin, Gomez, Manuel Romero, Turnes, Juan, Dufour, Jean-Francois, Moriggia, Alberto, Sheen, I-Shyan, Kao, Jia-Horng, Cheng, Pin-Nan, Huang, Jee-Fu, Yang, Sheng-Shun, Su, Wei-Wen, Chen, Chi-Yi, Chien, Rong-Nan, Lo, Gin-Ho, Chu, Chi-Jen, Wang, Horng-Yuan, Hu, Jui-Ting, Huang, Yi Wen, Agarwal, Kosh, Allison, Michael, Anstee, Quentin, Austin, Andrew, Fowell, Andrew, Ch'ng, Chin Lye, Manousou, Pinelopi, Newsome, Philip, Ryder, Stephen, Shankar, Arun, Abdelmalek, Manal, Abrams, Gary, Aguilar, Humberto, Alam, Imtiaz, Alba, Laura, Alkhouri, Naim, Allen, Alina, Aqel, Bashar, Balart, Luis, Barritt, A. Sidney, IV, Behari, Jaideep, Bennett, Michael, Bernstein, David, Bhandari, Bal Raj, Bonacini, Maurizio, Borg, Brian, Brown, Kimberly, Bzowej, Natalie, Caldwell, Stephen, Chami, Tawfik, Coates, Allan, Cueli, Adolfo, Davis, Mitchell, deLemos, Andrew, Desai, Archita, Dunn, Winston, Ferreira, Nelson, Fine, Michael, Firpi-Morell, Roberto, Freedland, Curtis, Freilich, Bradley, Fuchs, Michael, Galambos, Michael, Gallegos-Orozco, Juan, Galler, Greg, Ghali, Maged, Ghalib, Reem, Gill, Satinder, Gillis, Marcum, Gilroy, Richard, Gordon, Stuart, Gunn, Nadege, Halegoua-DeMarzio, Dina, Hassan, Mohamed, Hassanein, Tarek, Herring, Robert, Jr., Hong, John, Huang, Jonathan, Kabler, Heidi, Kayali, Zeid, Knapple, Whitfield, Kolli, Geetha, Kowdley, Kris, Krause, Richard, Lawitz, Eric, Lidofsky, Steven, Lim, Joseph, Lipkis, Donald, Loomba, Rohit, Mahgoub, Amar, Malespin, Miguel, Manch, Richard, Mannis, Steven, Manos, Paul, McDonald, Thomas, McKenzie, Mark, Mena, Edward, Merriman, Raphael, Moehlen, Martin William, Montgomery, Richard, Murphy, Robert, Natarajan, Yamini, Neff, Guy, Noureddin, Mazen, Ortiz-Lasanta, Grisell, Pagadala, Mangesh, Patel, Keyur, Patton, Heather, Peyton, Adam, Pimstone, Neville, Poulos, John, Pound, David, Pyrsopoulos, Nikolaos, Rafiq, Nila, Ravendhran, Natarajan, Ravinuthala, Ravi, Reddy, K. Rajendar, Reindollar, Robert, Reynolds, Justin, Rinella, Mary, Rizvi, Syed, Rockey, Don, Rodriguez-Perez, Federico, Ruane, Peter, Rubin, Raymond, Ryan, Michael, Saeian, Kia, Sanyal, Arun, Sarkar, Souvik, Scanga, Andrew, Schiff, Eugene, Schmidt, Warren, Schneider, Jeffrey, Sepe, Thomas, Shah, Dhiren, Shaikh, Obaid, Shankar, Uday, Sheikh, Aasim, Sheikh, Muhammad, Sherman, Kenneth, Shiffman, Mitchell, Siddique, Asma, Smith, Matthew, Suarez, Rosa, Talal, Andrew, Te, Helen, Tekola, Bezawit, Tetri, Brent, Thuluvath, Paul, Toro, Doris, Torres, Dawn, Trinh, Huy, Trotter, James, Vento, Angel, Vierling, John, Vuppalanchi, Raj, Waters, Michael, Weisberg, Ilan, Wieland, Amanda, Williams, Alonzo, Younes, Ziad, Adams, Leon, Harding, Damian, Hodge, Alex, Kontorinis, Nick, Strasser, Simone, Thompson, Alex, Horsmans, Yves, Steenkiste, Christophe Van, Bailey, Robert, Giard, Jeanne-Marie, Montano-Loza, Aldo, Puglia, Marco, Tsoi, Keith, Larrey, Dominique, Nguyen-Khac, Eric, Ratziu, Vlad, Spengler, Ulrich, Wiegand, Johannes, Hui, Aric Josun, Acharya, Subrat Kumar, Sarin, Shiv Kumar, Tantry, Vishwanath, Braun, Marius, Hazzan, Rawi, Lurie, Yoav, Colombo, Massimo, Fujii, Hideki, Hashimoto, Etsuko, Kato, Masaki, Ogawa, Koji, Takehara, Tetsuo, Tokushige, Katsutoshi, Garza, Laura Esthela Cisneros, Ladrón De Guevara, Alma Laura, Schultz, Michael, Janczewska, Ewa, Toro, Doris H., Jeong, Sook-Hyang, Kim, Yoon Jun, Lee, Jin-Woo, Ang, Tiing Leong, Bee, George Goh Boon, Benlloch, Salvador, Caballería, Juan, Calleja, José Luis, Rodríguez, Jose A. Carrión, Crespo, Javier, Diago, Moises, Fernandez-Rodriguez, Conrado, García-Samaniego, Javier, Ginès, Pere, Romero, Manuel, Dufour, Jean-François, Alazawi, William, Ch'ng, Chin-Lye, Forton, Daniel, Priest, Matthew, Sheridan, David, Ankoma-Sey, Victor, Balakrishnan, Maya, Bambha, Kiran, Barritt, A. Sidney, Bhandari, Bal, Brandman, Danielle, Chang, Charissa, Corey, Kathleen, Feldman, Michael, Gholam, Pierre, Goff, John, Marzio, Dina Halegoua-De, Harrison, Stephen, Hellstern, Paul, Jr., Herring, Robert, Iyer, Rajalakshmi, Jakiche, Antoine, Kohli, Anita, Krok, Karen, Kugelmas, Marcelo, Kumar, Sonal, Lai, Michelle, Mahmoud, Mitchell, Mantry, Parvez, Marsano, Luis, Nguyen, Tuan, Park, James, Patton, Heather M., Pockros, Paul, Reddy, Rajender, Rodriguez, Miguel, Sarles, Harry, Satapathy, Sanjaya, Sedghi, Shahriar, Shah, Nikunj, Sheikh, Muhammad Yasin, Sigal, Samuel, Stanca, Carmen, Steinbook, Michael, Szabo, Gyongyi, Terrault, Norah, Tong, Myron, Victor, David, Zervos, Xaralambos, Harrison, Stephen A., Wong, Vincent Wai-Sun, Caldwell, Stephen H., Shiffman, Mitchell L., Camargo, Marianne, Li, Georgia, Kersey, Kathryn, Jia, Catherine, Zhu, Yanni, Djedjos, C. Stephen, Subramanian, G. Mani, Myers, Robert P., Anstee, Quentin M., Romero-Gomez, Manuel, Goodman, Zachary, Lawitz, Eric J., and Younossi, Zobair

Published
2020
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26. Randomized-controlled trial of anakinra plus zinc vs. prednisone for severe alcohol-associated hepatitis

Author

Gawrieh, Samer, primary, Dasarathy, Srinivasan, additional, Tu, Wanzhu, additional, Kamath, Patrick S., additional, Chalasani, Naga P., additional, McClain, Craig J., additional, Bataller, Ramon, additional, Szabo, Gyongyi, additional, Tang, Qing, additional, Radaeva, Svetlana, additional, Barton, Bruce, additional, Nagy, Laura E., additional, Shah, Vijay H., additional, Sanyal, Arun J., additional, and Mitchell, Mack C., additional

Published
2024
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29. Standard Definitions and Common Data Elements for Clinical Trials in Patients With Alcoholic Hepatitis: Recommendation From the NIAAA Alcoholic Hepatitis Consortia

Author

Crabb, David W, Bataller, Ramon, Chalasani, Naga P, Kamath, Patrick S, Lucey, Michael, Mathurin, Philippe, McClain, Craig, McCullough, Arthur, Mitchell, Mack C, Morgan, Timothy R, Nagy, Laura, Radaeva, Svetlana, Sanyal, Arun, Shah, Vijay, and Szabo, Gyongyi

Subjects
Clinical Trials as Topic/classification/*standards, Consensus, Endpoint Determination, Hepatitis, Alcoholic/classification/*diagnosis/mortality/therapy, Humans, Research Design/*standards, Risk Factors, Severity of Illness Index, Terminology as Topic, Time Factors, Treatment Outcome
Abstract

Heavy drinkers are at risk for a spectrum of histologic alcohol-related liver injury: steatosis, alcoholic steatohepatitis (ASH), alcohol-related fibrosis, and cirrhosis. Alcoholic hepatitis (AH), the clinical entity associated with severe ASH, has high short-term mortality. The standard-of-care therapy, prednisolone, has limited efficacy and many side effects; no other treatment has consistently shown survival benefit. The National Institute on Alcohol Abuse and Alcoholism (NIAAA)-funded Alcoholic Hepatitis Consortia carry out translational research on pathophysiologic mechanisms, genetic and environmental risk factors, phase II clinical trials, and development of biomarkers. The consortia members were convened by the National Institutes of Health to address diagnostic criteria and practical issues related to clinical AH research, and to develop a set of common data elements to harmonize ongoing and future trials. This was accomplished through 3 face-to-face meetings of the investigators and representatives of the National Institutes of Health, and subsequent electronic communications over the course of 6 months. Evidence for the recommendations was based on published trials and observational data from several of the consortia members. A draft manuscript was iteratively reviewed by members of the consortia. The goal was to reach agreements on recommendations and definitions that could facilitate trial design, and simultaneously be tested by research groups pooling their data. The recommendations made here are specifically directed to achieve better uniformity in clinical trials, rather than serving as clinical practice guidelines.

Published
2016

37. Dysregulated meta-organismal metabolism of aromatic amino acids in alcohol-associated liver disease

Author

Mrdjen, Marko, primary, Huang, Emily, additional, Pathak, Vai, additional, Bellar, Annette, additional, Welch, Nicole, additional, Dasarathy, Jaividhya, additional, Streem, David, additional, McClain, Craig J., additional, Mitchell, Mack, additional, Radaeva, Svetlana, additional, Barton, Bruce, additional, Szabo, Gyongyi, additional, Dasarathy, Srinivasan, additional, Wang, Zeneng, additional, Hazen, Stanley L., additional, Brown, J. Mark, additional, and Nagy, Laura E., additional

Published
2023
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38. Bile acid-induced IRF3 phosphorylation mediates cell death, inflammatory responses and fibrosis in cholestasis-induced liver and kidney injury via regulation of ZBP1

Author

Zhuang, Yuan, primary, Ortega-Ribera, Martí, additional, Thevkar Nagesh, Prashanth, additional, Joshi, Radhika, additional, Huang, Huihui, additional, Wang, Yanbo, additional, Zivny, Adam, additional, Mehta, Jeeval, additional, Parikh, Samir M., additional, and Szabo, Gyongyi, additional

Published
2023
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42. HCV, Alcohol, and the Liver

Author

Bukong, Terence N., Saha, Banishree, Szabo, Gyongyi, Miyamura, Tatsuo, editor, Lemon, Stanley M., editor, Walker, Christopher M., editor, and Wakita, Takaji, editor

Published
2016
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46. Alcohol and HCV: Implications for Liver Cancer

Author

Szabo, Gyongyi, Saha, Banishree, Bukong, Terence N., Cohen, Irun R., Series editor, Lajtha, N.S. Abel, Series editor, Paoletti, Rodolfo, Series editor, Lambris, John D., Series editor, Vasiliou, Vasilis, editor, Zakhari, Samir, editor, Seitz, Helmut K., editor, and Hoek, Jan B., editor

Published
2015
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48. Safety, Pharmacokinetics, and Efficacy Signals of Larsucosterol (DUR-928) in Alcohol-Associated Hepatitis

Author

Hassanein, Tarek, primary, McClain, Craig J., additional, Vatsalya, Vatsalya, additional, Stein, Lance L., additional, Flamm, Steven L., additional, Martin, Paul, additional, Cave, Matthew C., additional, Mitchell, Mack, additional, Barton, Bruce, additional, Nagy, Laura, additional, Szabo, Gyongyi, additional, McCullough, Arthur, additional, Dasarathy, Srinivasin, additional, Shah, Jaymin, additional, Blevins, Christina, additional, Scott, Deborah, additional, Krebs, William, additional, Brown, James E., additional, and Lin, WeiQi, additional

Published
2023
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49. Alcohol-induced extracellular asc specks perpetuate liver inflammation and damage in alcoholic hepatitis even after alcohol cessation

Author

de Carvalho Ribeiro, Marcelle, primary, Iracheta-Vellve, Arvin, additional, Babuta, Mrigya, additional, Calenda, Charles D., additional, Copeland, Christopher, additional, Zhuang, Yuan, additional, Lowe, Patrick P., additional, Hawryluk, Danielle, additional, Catalano, Donna, additional, Cho, Yeonhee, additional, Barton, Bruce, additional, Dasarathy, Srinivasan, additional, McClain, Craig, additional, McCullough, Arthur, additional, Mitchell, Mack, additional, Nagy, Laura E., additional, Radaeva, Svetlana, additional, Lien, Egil, additional, Golenbock, Douglas T., additional, and Szabo, Gyongyi, additional

Published
2023
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