718 results on '"Ghany, Marc G."'
Search Results
202. Hepatitis B cure: From discovery to regulatory approval
- Author
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Lok, Anna S., primary, Zoulim, Fabien, additional, Dusheiko, Geoffrey, additional, and Ghany, Marc G., additional
- Published
- 2017
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- View/download PDF
203. Spectrum of Liver Disease in Hepatitis B Virus (HBV) Patients Coinfected with Human Immunodeficiency Virus (HIV)
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Sterling, Richard K., primary, Wahed, Abdus, additional, Khalili, Mandana, additional, Sulkowski, Mark S., additional, Jain, Mamta, additional, Wong, David, additional, Lisker-Melman, Mauricio, additional, Ghany, Marc G., additional, Chung, Raymond T., additional, and Kleiner, David, additional
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- 2017
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- View/download PDF
204. Kinetics of Hbsag Loss in Nucleoside Analogue and Interferon Therapies
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Suarez, Daniel, primary, Ferreira, Michelle, additional, Auh, Sungyoung, additional, Calderon, Yunet, additional, Garrett, Aubrey, additional, Jortani, Saeed, additional, and Ghany, Marc G., additional
- Published
- 2017
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- View/download PDF
205. Pattern of Hepatitis B Virus (HBV) Core Antigen (HB CAG +) and Surface Antigen (HBSAG) Staining in Patients Co-Infected with Human Immunodeficiency Virus (HIV)
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Sterling, Richard K., primary, Wahed, Abdus, additional, Khalili, Mandana, additional, Sulkowski, Mark S., additional, Jain, Mamta, additional, Wong, David, additional, Lisker-Melman, Mauricio, additional, Ghany, Marc G., additional, Chung, Raymond T., additional, and Kleiner, David, additional
- Published
- 2017
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206. Characteristics of Adults in the Hepatitis B Research Network in North America Reflect Their Country of Origin and Hepatitis B Virus Genotype
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Hassan, Mohamed, MacGregor, Joan M., Luketic, Velimir A., Cooper, Stewart L., DeVole, Nata, Betts, Michael, Niu, Jianghe, Fontana, Robert J., Wong, David K., Khudyakov, Yury, Walters, Barbara, Chang, Kyong Mi, Punkova, Lili T., Cardona, Danielle, Lawlor, Sharon, Morris, Nevitt, Belle, Steven H., Zadorozny, Ella, Di Bisceglie, Adrian M., Mathisen, Terri, Minshall, Stacey, King, Debra L., Kleiner, David, Wahed, Abdus, Nagy, Rosemary A., Hofmann, Charlotte, Poerzgen, Peter, Haynes-Williams, Vanessa, Cardona-Gonzalez, Lupita, Haller, Tamara, Tran, Tram T., Cloonan, Yona, Chung, Raymond T., French, Samuel, Lisker-Melman, Mauricio, Peacock, Velma, Feld, Jordan, Danielson, Michelle, Stadheim, Linda, Barritt, A. Sidney, Olson, Emma, Do, Son, Terrault, Norah A., McKenna, Barbara, Juan, Joshua, Torrey, Keith, Smith, Paula G., Keith, James, Liu, Lucie, Perrillo, Robert, Park, Jang June, Kelley, Stephanie, Shuhart, Margaret C., Sterling, Richard K., Kowdley, Kris V., Yim, Colina, Montaner, Luis J., Carithers, Robert C., Kaza, Sravanthi, Oberhelman, Kelly, Tsai, Naoky, Pelesko, Andrew, Levine, Danielle, La, Danie, Javaid, Asad, Rodd, Cassandra, Lau, Daryl T.Y., Mooney, Jody, Janssen, Harry L.A., Lombardero, Manuel, Valiga, Mary E., Lok, Anna Suk Fong, Stoliker, Donna, Teo, Chong Gee, Heathcoate, Jenny, Li, Ruosha, Fried, Michael W., Roberts, Lewis R., Ungermann, Ashley, Lee, William M., Johnson, Geoffrey, Huddleston, Leslie, Strom, Susan, Metheny, Vikki, Lau, Ivy, Darling, Jama M., Han, Johanna, Ganova-Raeva, Lilia Milkova, Kim, W. Ray, Han, Steven Huy B., Nasser, Imad, Stahler, Alisha C., Smith, Coleman I., Afdhal, Nezam, Wang, Chia C., Khalili, Mandana, Patel, Keyur, Bass, Sheila, Ayala, Claudia, Marsh, Tiffany, Rivera, Elenita, Liang, T. Jake, Fryzek, Nancy, Ghany, Marc G., Podolskaya, Veronika, and Evon, Donna
- Abstract
Chronic hepatitis B virus (HBV) infection is an important cause of cirrhosis and hepatocellular carcinoma worldwide; populations that migrate to the US and Canada might be disproportionately affected. The Hepatitis B Research Network (HBRN) is a cooperative network of investigators from the United States and Canada, created to facilitate clinical, therapeutic, and translational research in adults and children with hepatitis B. We describe the structure of the network and baseline characteristics of adults with hepatitis B enrolled in the network.
- Published
- 2015
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207. Entecavir and Peginterferon Alfa‐2a in Adults With Hepatitis B e Antigen–Positive Immune‐Tolerant Chronic Hepatitis B Virus Infection.
- Author
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Feld, Jordan J., Terrault, Norah A., Lin, Hsing‐Hua S., Belle, Steven H., Chung, Raymond T., Tsai, Naoky, Khalili, Mandana, Perrillo, Robert, Cooper, Stewart L., Ghany, Marc G., Janssen, Harry L.A., and Lok, Anna S.
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- 2019
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- View/download PDF
208. QUEST for a cure for hepatitis C virus: the end is in sight
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Ghany, Marc G and Gara, Naveen
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- 2014
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209. Contributors
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Abad, Kashif, Abdul-Hussein, Mustafa, Adam, Rodney D., Adams, Paul C., Akst, Lee, Anderson, Kelley P., Andrès, Emmanuel, Anstead, Gregory M., Aring, Ann M., Armitage, James O., Arshi, Arash, Azar, Cecilio M., Azarbal, Amir, Bailey, Justin, Bakhutashvili, Vladimer, Balagué, Federico, Barth, Bradley E., Basello, Gina M., Bassaly, Renee, Baughn, Julie M., Beard, Sheryl, Ben-Ami, Ronen, Bencheqroun, Hassan, Bernstein, David I., Biggerstaff, Kristin Schmid, Bloomfield, Clara, Blum, William, Boateng, Stephen, Bolotin, Diana, Bonnema, Rachel A., Borenstein, David, Bragg, Dee Ann, Bragg, Scott, Bremjit, Prasheda, Brewer, Takae, Brice, Sylvia L., Brill, John, Brown, Patricia D., Brown, Patrick, Brown, Richard B., Brunsell, Susan C., Buckley, Peter F., Cadavid, Diego, Callandar, Natalie S., Caraccio, Thomas R., Carek, Peter J., Carrion, Andres F., Carvounis, Petros E., Castell, Donald O., Cayley, William E., Jr., Cerquozzi, Sonia, Cervera, Alvaro, Chaffin, Tia D., Chan, Lawrence, Chan, Miriam, Chen, Lin Yee, Chihara, Shingo, Chitlur, Meera, Chohan, Saima, Chyu, Kuang-Yuh, Cigarroa, Joaquin E., Clark, Peter E., Cleland, Paul, Cline, Matthew, Clouse, Kari R., Colenbrander, August, Commins, Ryan M., Conageski, Christine, Conly, John M., Contini, Carlo, Cormier, Allison K., Corriveau, Michael L., Cox, Bart L., Creech, Dustin A., Creo, Ana L., Cunha, Burke A., Cunha, Cheston B., Currie, Gabriel P., Curry, Amy E., Damitz, Beth A., Dattilo, Natalie C., Davaro, Raul, de Berker, David, de Leon, André, de Leon, Tate, DeCastro, Alexei, DeGeorge, Katharine C., DeLoughery, Thomas G., Dennery, Phyllis A., Dessinioti, Clio, Diamond, Michael P., Donnan, Geoffrey A., Dorsch, John N., Drevets, Douglas A., Dudley, Samuel C., Jr., Duggan, Peter R., Duggins, Maurice, Eagle, Kim, Eck, Leigh M., Egnatios, Genevieve L., Elston, Dirk M., Embil, John M., Epstein, Scott K., Evans, Patricia, Evens, Andrew M., Barry Fagan, J., Fayssoux, Kinder, Feldman, Dorianne, Fife, Terry D., Finley, David J., Fisher, William E., Fleseriu, Maria, Fletcher, Donald C., Flores, Raja, Forsberg, Sarah, Fox, Daniel P., Frank, Jennifer, Freelove, Robert S., Freeman, Ellen W., Freeman, Theodore M., Friedman, Aaron, Gaines, Melissa, Michael Gallagher, R., Ghany, Marc G., Ghazi, Muhammad Ahmad, Gibbs, Lawrence M., Gilbert, Donald L., Giusti, Robert, Gladwin, Mark T., Gluckman, Stephen J., Goddard, Andrew W., Goerl, Danae D., Goerl, Kyle, Gold, Mark S., Goldstein, Joshua N., Gonzales, Melissa K., González-Fernández, Marlis, Goodwin, Gregory, Gosmanov, Aidar R., Gosmanov, Niyaz, Gosmanova, Albina, Gradoni, Luigi, Graham, Timothy P., Grant-Kels, Jane M., Greenberg, Leslie A., Greene, William M., Greensher, Joseph, Gregory, David, Grevich, Sriharsha Cherukumilli, Guinan, Eva C., Gumbo, Tawanda, Hague, Melissa, Halder, Rebat M., Hall, Ronald, II, Harris, George D., Harris, Kari R., Harrison, Taylor B., Hartman, Adam L., Higuita, Nelson Iván Agudelo, Hinderliter, Stacey A., Hinshaw, Molly, Ho, Vanessa, Hockenberry, Brandon, Hohl, Raymond J., Holguin, Therese, Holstein, Sarah A., Holubar, Marisa, Homan, Gretchen, Hossani-Madani, Ahmad Reza, House, Steven A., Houssayni, Sarah, Hueston, William J., Huffstetler, Alison N., Hundahl, Scott A., Hunger, Stephen P., Hupp, Wendy S., Irwin, Gretchen M., Isenberg, Gerald A., Jackson, Alan C., Jacobson, Kurt M., Jain, Vasudha, Jaller, Jose A., James, James J., Jamieson, Katarzyna, Jarvis, James N., John, Roy M., Johnson, Lisa M., Jolissaint, Joshua S., Juckett, Gregory, Judson, Marc A., Kadhiravan, Tamilarasu, Kalia, Rachna, Kanter, Jessica, Karnad, Dilip R., Katsambas, Andreas, Katz, Ben Z., Katzman, Rebecca, Kaufer, Daniel I., Kaunitz, Andrew M., Kavanaugh, Arthur, Mark Keegan, B., Kellerman, Rick D., Kellermann, Scott, Kelly, Christina, Kemp, Stephen F., Kim, Arthur Y., Kim, Haejin, Kim, Jongoh, Kirsner, Robert S., Kodner, Charles, Kolb, Amanda, Kolla, Bhanu Prakash, Korley, Frederick K., Kovalsky, Adrienne N., Kratzke, Robert A., Kraut, Eric H., Krieger, John N., Krishnamurti, Lakshmanan, Krishnan, Kumar, Kuhlmann, Zachary, Kulkarni, Roshni, Kullo, Iftikhar J., Kumar, Seema, Kwaan, Mary R., Kyle, Robert A., Lampton, Lucius M., Lange, Richard A., Langlois, Fabienne, Larioza, Julius, Larkin, Jerome, Larrabee, David, Lau, Christine L., Lawrence-Hylland, Susan, Leikin, Jerrold B., Leikin, Scott M., Leung, Alexander K.C., LeWinter, Martin M., Li, Ming, Liebenstein, Tyler K., Lin, Albert P., Lindemann, Janet C., Linder, Jeffrey A., Lock, James, Chantel Long, M., Lyznicki, James M., Malaeb, Bahaa S., Malhotra, Uma, Malone, Michael A., Manlove, Emily, Manson, JoAnn E., Mansukhani, Meghna P., Marcocci, Claudio, Martin, Paul, Martin, Vickie, Matza, Mark A., Maxwell, Pinckney J., IV, McCall, Anthony L., McGrew, Christopher, McGuigan, Christopher C., McGuigan, Michael, Meiselman, Mick S., Melton-Meaux, Genevieve B., Mercado, Moises, Merrell, Ryan, Meyers, Steven L., Miller, Brian J., Mirza, Moben, Mishra, Kriti, Mofenson, Howard C., Mogensen, Kris M., Morales, Enrique, Morales-Arias, Jaime, Morgenthaler, Timothy I., Morison, Warwick L., Mortada, Rami, Moser, Scott E., Moss, Heather E., Mostaghimi, Ladan, Moul, Judd W., Mullen, Heidi E.K., Murphy, Michael, Mutasim, Diya F., Muthusubramanian, Arjun, Nagji, Alykhan S., Nazeef, Moniba, Neil, Tara J., Neschis, David G., Nester, Theresa, Neustadt, David H., Nguyen, Tam T., Nieves-Arriba, Lucybeth, Novac, Andrei, Novelli, Enrico M., Nye, Lauren, Obi, Andrea T., Okeson, Jeffrey P., Oliveira, Carlos R., Ong, Peck Y., Ortel, Bernhard, Overturf, Gary D., Ozgonenel, Bulent, Pacak, Karel, Padin-Rosado, Jose A., Pandolfino, John E., Paran, Yael, Pasipanodya, Jotam, Patel, Manish R., Patrick, Peter D., Patton, Simon, Paulman, Paul, Penna, Gerson O., Penna, Maria Lucia, Perkins, Allen, Peterson, Leah, Petri, William A., Jr., Petroianu, Georg A., Petronic-Rosic, Vesna, Pierach, Claus A., Pietroni, Mark, Plaza, Jose A., Pollart, Susan M., Porter, Andrew S.T., Posencheg, Michael A., Powell, Charles R., Praga, Manuel, Pusateri, Margaret, Rahko, Peter S., Vincent Rajkumar, S., Ramakrishnan, Kalyanakrishnan, Ramirez, Julio A., Rank, Matthew A., Raoult, Didier, Ravindran, Anita Devi K., Reddy, Elizabeth, Regis, Deon, Reid, Ian R., Reid, Robert L., Rennert-May, Elissa, Reveille, John D., Robinson, Malcolm K., Roche, William P., Roett, Michelle A., Rose, Peter G., Rosenthal, Richard N., Roth, Alan R., Ruha, Anne-Michelle, Rundell, Kristen, Sadovsky, Richard, Said, Adnan, Sairenji, Tomoko, Samson, Susan L., Sanchez, Carlos, Sangodkar, Sandeep, Sarode, Ravi, Terry Saunders, J., Schatz, Michael, Schiller, Lawrence R., Schoessow, Kim, Schrager, Sarina, Schroeder, Kevin, Schuller, Dan, Scripter, Cassie, Seery, Amy, Seifert, Steven A., Semel, Jeffery D., Shah, Beejal, Shah, Prediman K., Shah, Samir S., Shah, Shenil, Shammo, Jamile M., Shapiro, Eugene D., Sharara, Ala I., Sheehan, John P., Shew, Sable, Shulman, Abraham, Sievers, Karlynn, Silk, Hugh, Sinclair, Aaron, Sloane, Philip D., Smith, Zachary L., Somers, William J., Speer, Linda, Spencer, Abby L., St. Louis, Erik Kent, Stevens, Dennis L., Stephens, Todd, Stone, John H., Stratakis, Constantine A., Stulberg, Daniel, Swaroop, Prabhakar P., Takashima, Masayoshi, Takyar, Varun, Tang, Jie, Tate, Jessica, Teng, Joyce M.C., Thielman, Nathan, Thomson, Joanna, Brantley Thrasher, J., Tobin, Kenneth, Underman, Arvid E., Unruh, Mark, Uppendahl, Locke, Van Buren, George, II, van Duin, David, Van Durme, Daniel J., Vincent, Kyle, Vinh, Donald C., Viswanathan, K.N., Vyas, Jatin M., Wakefield, Thomas W., Wald, Arnold, Wald, Ellen R., Walker, Robin A., Wall, Barry M., Walling, Anne, Wang, Andrew, Wang, Ernest, Watanabe, Koji, Weber, Randal S., Weber, Ruth, Wehler, Cheryl, Weida, Jane A., Weissman, David N., Welliver, Robert C., Sr., Wester, Rebecca M., Westergaard, Ryan P., Wexler, Randell, Whitley, Brian M., Wilamowska, Katarzyna, Williams, Tracy L., Winterhoff, Boris, Wipperman, Jennifer, Wittler, Robert, Wood, Gary S., Wu, Steve W., Wyre, Hadley, Yakubov, Steven, Yang, Xinghong, Yeu, Elizabeth, Yi, Yooni, Yiannias, James A., Young, Nata, Zafereo, Mark E., and Zuckerman, Jane
- Published
- 2019
- Full Text
- View/download PDF
210. Hepatitis B Virus–Specific and Global T-Cell Dysfunction in Chronic Hepatitis B
- Author
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Park, Jang-June, primary, Wong, David K., additional, Wahed, Abdus S., additional, Lee, William M., additional, Feld, Jordan J., additional, Terrault, Norah, additional, Khalili, Mandana, additional, Sterling, Richard K., additional, Kowdley, Kris V., additional, Bzowej, Natalie, additional, Lau, Daryl T., additional, Kim, W. Ray, additional, Smith, Coleman, additional, Carithers, Robert L., additional, Torrey, Keith W., additional, Keith, James W., additional, Levine, Danielle L., additional, Traum, Daniel, additional, Ho, Suzanne, additional, Valiga, Mary E., additional, Johnson, Geoffrey S., additional, Doo, Edward, additional, Lok, Anna S.F., additional, Chang, Kyong-Mi, additional, Chung, Raymond T., additional, Roberts, Lewis R., additional, Di Bisceglie, Adrian M., additional, Lisker-Melman, Mauricio, additional, Janssen, Harry L.A., additional, Juan, Joshua, additional, Yim, Colina, additional, Heathcote, Jenny, additional, Perrillo, Robert, additional, Do, Son, additional, Han, Steven-Huy B., additional, Tran, Tram T., additional, Cooper, Stewart L., additional, Fontana, Robert J., additional, Tsai, Naoky, additional, Fried, Michael W., additional, Patel, Keyur, additional, Evon, Donna, additional, Shuhart, Margaret, additional, Wang, Chia C., additional, Ghany, Marc G., additional, Liang, T. Jake, additional, Belle, Steven, additional, Cloonan, Yona, additional, and Kleiner, David, additional
- Published
- 2016
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211. A Prospective Study of the Rate of Progression in Compensated, Histologically Advanced Chronic Hepatitis C (HEP-10-2210)
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Dienstag, Jules L., Ghany, Marc G., Morgan, Timothy R., Di Bisceglie, Adrian M., Bonkovsky, Herbert L., Kim, Hae-Young, Seeff, Leonard B., Szabo, Gyongyi, Wright, Elizabeth C., Sterling, Richard K., Everson, Gregory T., Lindsay, Karen L., Lee, William M., Lok, Anna S., Morishima, Chihiro, Stoddard, Anne M., and Everhart, James E.
- Subjects
Male ,Interferon-alpha ,Hepatitis C, Chronic ,Interferon alpha-2 ,Middle Aged ,Antiviral Agents ,Article ,Recombinant Proteins ,Polyethylene Glycols ,Treatment Outcome ,Disease Progression ,Humans ,Female ,Prospective Studies - Abstract
The incidence of liver disease progression among subjects with histologically advanced but compensated chronic hepatitis C is incomplete. The Hepatitis C Antiviral Long-term Treatment against Cirrhosis Trial was a randomized study of 3.5 years of maintenance peginterferon treatment on liver disease progression among patients who had not cleared virus on peginterferon and ribavirin therapy. Patients were followed subsequently off therapy. Because maintenance peginterferon treatment did not alter liver disease progression, we analyzed treated and control patients together. Among 1,050 subjects (60% advanced fibrosis, 40% cirrhosis), we determined the rate of progression to cirrhosis over 4 years and of clinical outcomes over 8 years. Among patients with fibrosis, the incidence of cirrhosis was 9.9% per year. Six hundred seventy-nine clinical outcomes occurred among 329 subjects. Initial clinical outcomes occurred more frequently among subjects with cirrhosis (7.5% per year) than subjects with fibrosis (3.3% per year) (P0.0001). Child-Turcotte-Pugh (CTP) score≥7 was the most common first outcome, followed by hepatocellular carcinoma. Following occurrence of a CTP score≥7, the rate of subsequent events increased to 12.9% per year, including a death rate of 10% per year. Age and sex did not influence outcome rates. Baseline platelet count was a strong predictor of all clinical outcomes. During the 8 years of follow-up, death or liver transplantation occurred among 12.2% of patients with advanced fibrosis and 31.5% of those with cirrhosis.Among patients with advanced hepatitis C who failed peginterferon and ribavirin therapy, the rate of liver-related outcomes, including death and liver transplantation, is high, especially once the CTP score reaches at least 7.
- Published
- 2011
212. Acute Viral Hepatitis
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Ghany, Marc G., primary and Liang, T. Jake, additional
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- 2015
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213. An Epidemiologic Investigation of a Case of Acute Hepatitis E
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Sarkar, Souvik, primary, Rivera, Elenita M., additional, Engle, Ronald E., additional, Nguyen, Hanh T., additional, Schechterly, Cathy A., additional, Alter, Harvey J., additional, Liang, T. Jake, additional, Purcell, Robert H., additional, Hoofnagle, Jay H., additional, and Ghany, Marc G., additional
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- 2015
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214. Sa1029 Retrospective Safety Analysis of Trainee-Performed Liver Biopsies at the National Institutes of Health Clinical Center - A 35-Year Experience
- Author
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Takyar, Varun, primary, Rotman, Yaron, additional, Zhao, Xiongce, additional, Ghany, Marc G., additional, Heller, Theo, additional, Doo, Edward, additional, Liang, Jake, additional, Hoofnagle, Jay, additional, and Koh, Christopher, additional
- Published
- 2015
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215. Screening for hepatitis B virus to prevent viral reactivation - who and when?
- Author
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Etzion, Ohad, primary and Ghany, Marc G., additional
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- 2015
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216. Prognostic Value of Ishak Fibrosis Stage: Findings from the HALT-C Trial
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Everhart, James E., Wright, Elizabeth C., Goodman, Zachary D., Dienstag, Jules L., Hoefs, John C., Kleiner, David E., Ghany, Marc G., Mills, A. Scott, Nash, S. Russell, Govindarajan, Sugantha, Rogers, Thomas E., Greenson, Joel K., Brunt, Elizabeth M., Bonkovsky, Herbert L., Morishima, Chihiro, and Litman, Heather J.
- Subjects
Liver Cirrhosis ,Time Factors ,Biopsy ,Humans ,Prospective Studies ,Hepatitis C, Chronic ,Prognosis ,Severity of Illness Index ,Article ,Follow-Up Studies - Abstract
Studies of the prognostic value of Ishak fibrosis stage are lacking. We used multi-year follow-up of the Hepatitis C Antiviral Long-Term Treatment Against Cirrhosis (HALT-C) Trial to determine whether individual Ishak fibrosis stages predicted clinical outcomes in patients with chronic hepatitis C. Baseline liver biopsy specimens from 1050 patients with compensated chronic hepatitis C who had failed combination peginterferon and ribavirin were reviewed by a panel of expert hepatopathologists. Fibrosis was staged with the Ishak scale (ranging from 0 = no fibrosis to 6 = cirrhosis). Biopsy fragmentation and length as well as number of portal tracts were recorded. We compared rates of prespecified clinical outcomes of hepatic decompensation and hepatocellular carcinoma across individual Ishak fibrosis stages. Of 1050 biopsy specimens, 25% were fragmented, 63% longer than 1.5 cm, 69% larger than 10 mm(2), and 75% had 10 or more portal tracts. Baseline laboratory markers of liver disease severity were worse and the frequency of esophageal varices higher with increasing Ishak stage (P0.0001). The 6-year cumulative incidence of first clinical outcome was 5.6% for stage 2, 16.1% for stage 3, 19.3% for stage 4, 37.8% for stage 5, and 49.3% for stage 6. Among nonfragmented biopsy specimens, the predictive ability of Ishak staging was enhanced; however, no association was observed between Ishak stage and outcomes for fragmented biopsy specimens because of high rates of outcomes for patients with noncirrhotic stages. Similar results were observed with liver transplantation or liver-related death as the outcome.Ishak fibrosis stage predicts clinical outcomes, need for liver transplantation, and liver-related death in patients with chronic hepatitis C. Patients with fragmented biopsy specimens with low Ishak stage may be understaged histologically.
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- 2010
217. Variants in Interferon-α Pathway Genes and Response to Pegylated-Interferon-α2a plus Ribavirin for Treatment of Chronic HCV Infection in the HALT-C Trial
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Welzel, Tania Mara, Morgan, Timothy R., Bonkovsky, Herbert L., Naishadham, Deepa, Pfeiffer, Ruth M., Wright, Elizabeth C., Hutchinson, Amy A., Crenshaw, Andrew T., Bashirova, Arman, Carrington, Mary, Dotrang, Myhanh, Sterling, Richard K., Lindsay, Karen L., Fontana, Robert J., Lee, William M., Di Bisceglie, Adrian M., Ghany, Marc G., Gretch, David R., Chanock, Stephen J., Chung, Raymond T., and O’Brien, Thomas R.
- Subjects
virus diseases ,Article - Abstract
Combination treatment with pegylated-interferon-α and ribavirin, the current recommended therapy for chronic hepatitis C virus (HCV) infection, results in a sustained virological response (SVR) in only about half of patients. Because genes involved in the interferon-α pathway may affect anti-viral responses, we analyzed the relationship between variants in these genes and SVR among participants in the HALT-C trial. Patients had advanced chronic hepatitis C and had previously failed to respond to interferon-based treatment. Participants were treated with peginterferon-α2a and ribavirin during the trial. Subjects with undetectable HCV RNA at week 72 were considered to have had an SVR. Subjects with detectable HCV RNA at week 20 were considered non-responders. We used TaqMan assays to genotype 56 polymorphisms found in 13 genes in the interferon-α pathway. This analysis compares genotypes for participants with an SVR to non-responders. The primary analysis was restricted to European American participants because a priori statistical power was low among the small number (n=131) of African American patients. We used logistic regression to control the effect of other variables that are associated with treatment response. Among 581 European American patients, SVR was associated with IFNAR1 IVS1-22G (adjusted odds ratio [aOR], 0.57; p=0.02); IFNAR2 Ex2-33C (aOR, 2.09; p=0.02); JAK1 IVS22+112T (aOR, 1.66; p=0.04); and ADAR Ex9+14A (aOR, 1.67; p=0.03). For the TYK2 -2256A promoter region variant a borderline association was present among European American participants (OR, 1.51; p=0.05) and a strong relationship among African American patients; all 10 with SVR who were genotyped for TYK2-2256 carried the A variant compared to 68/120 (57%) non-responders (p=0.006). In conclusion, genetic polymorphisms in the interferon-α pathway may affect responses to antiviral therapy of chronic hepatitis C.
- Published
- 2009
218. EVOLUTION OF HEPATIC STEATOSIS IN PATIENTS WITH ADVANCED HEPATITIS C: RESULTS FROM THE HALT-C TRIAL
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Lok, Anna S., Everhart, James E., Chung, Raymond T., Kim, Hae-Young, Everson, Gregory T., Hoefs, John C., Greenson, Joel K., Sterling, Richard K., Lindsay, Karen L., Lee, William M., Di Bisceglie, Adrian M., Bonkovsky, Herbert L., Ghany, Marc G., and Morishima, Chihiro
- Subjects
Liver Cirrhosis ,Male ,Time Factors ,Interferon-alpha ,Hepatitis C, Chronic ,Interferon alpha-2 ,Middle Aged ,Antiviral Agents ,Article ,Recombinant Proteins ,Polyethylene Glycols ,Fatty Liver ,Ribavirin ,Disease Progression ,Humans ,Female - Abstract
Hepatic steatosis is a common histologic feature in patients with chronic hepatitis C (CHC) but there are no large longitudinal studies describing the progression of steatosis in CHC. We examined changes in steatosis on serial biopsies among CHC patients participating in the Hepatitis C Antiviral Long-term Treatment against Cirrhosis (HALT-C) Trial. All 1050 patients in the trial had advanced fibrosis at baseline biopsy and were documented not to have had a sustained virological response to peginterferon and ribavirin. Most (94%) patients had genotype 1 infection. At least one protocol follow-up biopsy was read on 892 patients, and 699 had the last biopsy performed 3.5 years after randomization. At enrollment, 39% had cirrhosis and 61% had bridging fibrosis; 18%, 41%, 31%, and 10% had steatosis scores of 0, 1, 2, and 3 or 4, respectively. The mean steatosis score decreased in the follow-up biopsies in both the interferon-treated patients and controls with no effect of treatment assignment (P = 0.66). A decrease in steatosis score byor =1 point was observed in 30% of patients and was associated with both progression to cirrhosis and continued presence of cirrhosis (P = 0.02). Compared to patients without a decrease in steatosis, those with a decrease in steatosis had worse metabolic parameters at enrollment, and were more likely to have a decrease in alcohol intake, improvement in metabolic parameters, and worsening liver disease (cirrhosis, esophageal varices, and deterioration in liver function).Serial biopsies demonstrated that in patients with CHC, steatosis recedes during progression from advanced fibrosis to cirrhosis. Decreased alcohol intake and improved metabolic parameters are associated with a decline in steatosis and may modulate hepatitis C progression.
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- 2009
219. Interpretation of Positive TMA Test Results from PCR-Negative Samples Obtained after Treatment of Chronic Hepatitis C
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Morishima, Chihiro, Morgan, Timothy R., Everhart, James E., Wright, Elizabeth C., Apodaca, Minjun C., Gretch, David R., Shiffman, Mitchell L., Everson, Gregory T., Lindsay, Karen L., Lee, William M., Lok, Anna S. F., Dienstag, Jules L., Ghany, Marc G., and Curto, Teresa M.
- Subjects
Liver Cirrhosis ,Transcription, Genetic ,Gene Amplification ,Interferon-alpha ,Reproducibility of Results ,Hepacivirus ,Hepatitis C, Chronic ,Interferon alpha-2 ,Viral Load ,Antiviral Agents ,Polymerase Chain Reaction ,Article ,Recombinant Proteins ,Polyethylene Glycols ,Humans ,RNA, Viral - Abstract
The Siemens VERSANT transcription-mediated amplification (TMA) assay is extremely sensitive for the detection of hepatitis C virus (HCV) RNA in serum. Eleven of 180 subjects in the Hepatitis C Antiviral Long-term Treatment against Cirrhosis (HALT-C) Trial who achieved polymerase chain reaction (PCR)-defined sustained virological response (SVR) at week 72 also had TMA-positive results from the same blood draw; six were positive on repeat testing. We report the follow-up on these 11 patients, and the reproducibility of TMA test results from PCR-negative samples in relationship to antiviral treatment outcome. Peginterferon and ribavirin treatment was initiated in 1145 prior interferon nonresponders with advanced hepatic fibrosis. Treatment was continued for 48 weeks if patients had undetectable HCV RNA by PCR at treatment week 20. Frozen serum samples from weeks 12, 20, 24, 48, and 72 were subsequently tested by TMA. Nine of the 11 patients returned for testing (median, 30 months after the week 72 visit), and all had undetectable HCV RNA by TMA and PCR. Among 759 PCR-negative samples obtained during treatment that were tested twice by TMA, 17% overall exhibited consistently positive results, and 21% exhibited inconsistently positive results. SVR was more likely if TMA was consistently negative than if consistently or inconsistently positive. With continued treatment, patients with inconsistently positive TMA results were more likely to become TMA-negative than TMA-positive (P0.0001).In PCR-negative samples, positive TMA results may indicate the presence of low levels of HCV RNA. However, because patients with positive TMA results may achieve SVR, management decisions during therapy should not be based on a single positive TMA test result.
- Published
- 2008
220. 900 - Pattern of Hepatitis B Virus (HBV) Core Antigen (HBCAG+) and Surface Antigen (HBSAG) Staining in Patients Co-Infected with Human Immunodeficiency Virus (HIV)
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Sterling, Richard K., Wahed, Abdus, Khalili, Mandana, Sulkowski, Mark S., Jain, Mamta, Wong, David, Lisker-Melman, Mauricio, Ghany, Marc G., Chung, Raymond T., and Kleiner, David
- Published
- 2017
- Full Text
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221. 350 - Kinetics of Hbsag Loss in Nucleoside Analogue and Interferon Therapies
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Suarez, Daniel, Ferreira, Michelle, Auh, Sungyoung, Calderon, Yunet, Garrett, Aubrey, Jortani, Saeed, and Ghany, Marc G.
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- 2017
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222. 99 - Spectrum of Liver Disease in Hepatitis B Virus (HBV) Patients Coinfected with Human Immunodeficiency Virus (HIV)
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Sterling, Richard K., Wahed, Abdus, Khalili, Mandana, Sulkowski, Mark S., Jain, Mamta, Wong, David, Lisker-Melman, Mauricio, Ghany, Marc G., Chung, Raymond T., and Kleiner, David
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- 2017
- Full Text
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223. Cellular microRNA networks regulate host dependency of hepatitis C virus infection.
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Qisheng Li, Lowey, Brianna, Sodroski, Catherine, Krishnamurthy, Siddharth, Alao, Hawwa, Helen Cha, Chiu, Stephan, El-Diwany, Ramy, Ghany, Marc G., and Liang, T. Jake
- Abstract
Cellular microRNAs (miRNAs) have been shown to regulate hepatitis C virus (HCV) replication, yet a systematic interrogation of the repertoire of miRNAs impacting HCV life cycle is lacking. Here we apply integrative functional genomics strategies to elucidate global HCV–miRNA interactions. Through genome-wide miRNA mimic and hairpin inhibitor phenotypic screens, and miRNA–mRNA transcriptomics analyses, we identify three proviral and nine antiviral miRNAs that interact with HCV. These miRNAs are functionally linked to particular steps of HCV life cycle and related viral host dependencies. Further mechanistic studies demonstrate that miR-25, let-7, and miR-130 families repress essential HCV cofactors, thus restricting viral infection at multiple stages. HCV subverts the antiviral actions of these miRNAs by dampening their expression in cell culture models and HCV-infected human livers. This comprehensive HCV–miRNA interaction map provides fundamental insights into HCV-mediated pathogenesis and unveils molecular pathways linking RNA biology to viral infections. [ABSTRACT FROM AUTHOR]
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- 2017
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224. Characteristics of US-Born Versus Foreign-Born Americans of African Descent With Chronic Hepatitis B.
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Hassan, Mohamed A., Kim, W. Ray, Ruosha Li, Smith, Coleman I., Fried, Michael W., Sterling, Richard K., Ghany, Marc G., Wahed, Abdus S., Ganova-Raeva, Lilia M., Roberts, Lewis R., and Lok, Anna S. F.
- Subjects
BLACK people ,INFECTIOUS disease transmission ,RACE ,DEMOGRAPHIC characteristics ,CHRONIC hepatitis B ,GENOTYPES - Abstract
Hepatitis B virus (HBV) infection is more common in African Americans than in white Americans. We compared the epidemiologic, clinical, and virological characteristics of US-born African Americans (USAAs) to those of foreign-born African Americans (FBAAs) with chronic hepatitis B. The adult cohort study of the Hepatitis B Research Network enrolls patients with HBV infection from 21 clinical sites in the United States and Canada. A total of 237 (15%) of the adult participants with chronic HBV infection that were enrolled from January 20, 2011, to October 2, 2013, were of African descent, including 57 USAAs and 180 FBAAs (76%). Compared with FBAAs, USAAs were older and more likely to have acquired HBV through sexual exposure, to be HBeAg-positive, to have higher HBV DNA levels, and to be infected with HBV genotype A2. FBAAs from West Africa were more likely to have elevated serum alanine aminotransferase (72% vs. 50%; P < 0.01) and higher HBV DNA levels (median, 3.2 log
10 IU/mL vs. 2.8 log10 IU/mL; P = 0.03) compared with East African FBAAs. The predominant HBV genotype among West African FBAAs was E (67%), whereas genotypes A (78%) and D (16%) were common in East African FBAAs. Significant differences were found between USAAs and FBAAs, highlighting the need for tailored strategies for prevention and management of chronic HBV infection for African Americans. [ABSTRACT FROM AUTHOR]- Published
- 2017
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225. Racial Disparities in Treatment Initiation and Outcomes of Chronic Hepatitis B Virus Infection in North America.
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Khalili, Mandana, Leonard, Kelsey R., Ghany, Marc G., Hassan, Mohamed, Roberts, Lewis R., Sterling, Richard K., Belle, Steven H., and Lok, Anna S.
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- 2023
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226. Viral Escape Mechanisms in Hepatitis C and the Clinical Consequences of Persistent Infection
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Lemon, Stanley M., primary, Farci, Patrizia, additional, and Ghany, Marc G., additional
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227. Acute Viral Hepatitis
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Ghany, Marc G., primary and Liang, T. Jake, additional
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228. Building Bridges and Providing Transparency to the Hepatitis C Virus Drug Approval Process
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Ghany, Marc G., primary and Liang, T. Jake, additional
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- 2014
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229. Durability of Antibody Response Against Hepatitis B Virus in Healthcare Workers Vaccinated as Adults
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Gara, Naveen, primary, Abdalla, Adil, additional, Rivera, Elenita, additional, Zhao, Xiongce, additional, Werner, Jens M., additional, Liang, T. Jake, additional, Hoofnagle, Jay H., additional, Rehermann, Barbara, additional, and Ghany, Marc G., additional
- Published
- 2014
- Full Text
- View/download PDF
230. Excess mortality in patients with advanced chronic hepatitis C treated with long-term peginterferon
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Division of Gastroenterology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, From the Division of Gastroenterology and Hepatology, Saint Louis University School of Medicine, St. Louis, MO ; Department of Internal Medicine, Saint Louis University School of Medicine; 1402 South Grand Blvd., St. Louis, MO 63104, New England Research Institutes, Watertown, MA, Gastrointestinal Unit, Massachusetts General Hospital, Boston, MA ; Department of Medicine, Harvard Medical School, Boston, MA, Liver Institute of Virginia, Bon Secours Health System, Newport News, VA, Division of Digestive Diseases and Nutrition, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD ; Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, Department of Medicine, University of Connecticut Health Center, Farmington, CT ; Carolinas Medical Center,Charlotte, NC, Division of Virology, Department of Laboratory Medicine, University of Washington, Seattle, WA, Office of the Director, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, Division of Digestive and Liver Diseases, University of Texas Southwestern Medical Center, Dallas, TX, Division of Gastroenterology, University of California, Irvine, Irvine, CA ; Gastroenterology Service, VA Long Beach Healthcare System, Long Beach, CA, Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, Bisceglie, Adrian M., Stoddard, Anne M., Dienstag, Jules L., Shiffman, Mitchell L., Seeff, Leonard B., Bonkovsky, Herbert L., Morishima, Chihiro, Wright, Elizabeth C., Snow, Kristin K., Lee, William M., Fontana, Robert J., Morgan, Timothy R., Ghany, Marc G., Division of Gastroenterology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, From the Division of Gastroenterology and Hepatology, Saint Louis University School of Medicine, St. Louis, MO ; Department of Internal Medicine, Saint Louis University School of Medicine; 1402 South Grand Blvd., St. Louis, MO 63104, New England Research Institutes, Watertown, MA, Gastrointestinal Unit, Massachusetts General Hospital, Boston, MA ; Department of Medicine, Harvard Medical School, Boston, MA, Liver Institute of Virginia, Bon Secours Health System, Newport News, VA, Division of Digestive Diseases and Nutrition, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD ; Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, Department of Medicine, University of Connecticut Health Center, Farmington, CT ; Carolinas Medical Center,Charlotte, NC, Division of Virology, Department of Laboratory Medicine, University of Washington, Seattle, WA, Office of the Director, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, Division of Digestive and Liver Diseases, University of Texas Southwestern Medical Center, Dallas, TX, Division of Gastroenterology, University of California, Irvine, Irvine, CA ; Gastroenterology Service, VA Long Beach Healthcare System, Long Beach, CA, Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, Bisceglie, Adrian M., Stoddard, Anne M., Dienstag, Jules L., Shiffman, Mitchell L., Seeff, Leonard B., Bonkovsky, Herbert L., Morishima, Chihiro, Wright, Elizabeth C., Snow, Kristin K., Lee, William M., Fontana, Robert J., Morgan, Timothy R., and Ghany, Marc G.
- Abstract
Chronic hepatitis C virus infection can cause chronic liver disease, cirrhosis and liver cancer. The Hepatitis C Antiviral Long-term Treatment against Cirrhosis (HALT-C) Trial was a prospective, randomized controlled study of long-term, low-dose peginterferon therapy in patients with advanced chronic hepatitis C who failed to respond to a previous course of optimal antiviral therapy. The aim of this follow-up analysis is to describe the frequency and causes of death among this cohort of patients. Deaths occurring during and after the HALT-C Trial were reviewed by a committee of investigators to determine the cause of death and to categorize each death as liver- or nonliver-related and as related or not to complications of peginterferon. Rates of liver transplantation were also assessed. Over a median of 5.7 years, 122 deaths occurred among 1,050 randomized patients (12%), of which 76 were considered liver-related (62%) and 46 nonliver-related (38%); 74 patients (7%) underwent liver transplantation. At 7 years the cumulative mortality rate was higher in the treatment compared to the control group (20% versus 15%, P = 0.049); the primary difference in mortality was in patients in the fibrosis compared to the cirrhosis stratum (14% versus 7%, P = 0.01); comparable differences were observed when liver transplantation was included. Excess mortality, emerging after 3 years of treatment, was related largely to nonliver-related death; liver-related mortality was similar in the treatment and control groups. No specific cause of death accounted for the excess mortality and only one death was suspected to be a direct complication of peginterferon. Conclusion: Long-term maintenance peginterferon in patients with advanced chronic hepatitis C is associated with an excess overall mortality, which was primarily due to nonliver-related causes among patients with bridging fibrosis. (H EPATOLOGY 2011;)
- Published
- 2011
231. Outcome of sustained virological responders with histologically advanced chronic hepatitis C
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Division of Gastroenterology, University of Michigan Medical Center, Ann Arbor, MI, Division of Gastroenterology, University of California Irvine, Irvine, CA ; Gastroenterology Service, Veterans Affairs Long Beach Healthcare System, Long Beach, CA ; fax: 562-826-5436 ; VA Long Beach Healthcare System???11 (GI), 5901 East Seventh Street, Long Beach, CA 90822, Liver Diseases Branch, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, New England Research Institutes, Watertown, MA, Hepatology Section, Virginia Commonwealth University Medical Center, Richmond, VA, Division of Gastroenterology and Hepatology, University of Colorado at Denver and Health Sciences Center, Denver, CO, Division of Digestive and Liver Diseases, University of Texas Southwestern Medical Center, Dallas, TX, Division of Gastroenterology and Hepatology, Saint Louis University School of Medicine, St. Louis, MO, Departments of Medicine and Molecular and Structural Biology and The Liver-Biliary-Pancreatic Center, University of Connecticut Health Center, Farmington, CT, Gastrointestinal Unit, Massachusetts General Hospital, Boston, MA, and the Department of Medicine, Harvard Medical School, Boston, MA, Division of Virology, Department of Laboratory Medicine, University of Washington, Seattle, WA, Division of Gastrointestinal and Liver Diseases, Keck School of Medicine, University of Southern California, Los Angeles, CA, Morgan, Timothy R., Ghany, Marc G., Kim, Hae-Young, Snow, Kristin K., Shiffman, Mitchell L., De Santo, Jennifer L., Lee, William M., Di Bisceglie, Adrian M., Bonkovsky, Herbert L., Dienstag, Jules L., Morishima, Chihiro, Lindsay, Karen L., Lok, Anna S. F., Division of Gastroenterology, University of Michigan Medical Center, Ann Arbor, MI, Division of Gastroenterology, University of California Irvine, Irvine, CA ; Gastroenterology Service, Veterans Affairs Long Beach Healthcare System, Long Beach, CA ; fax: 562-826-5436 ; VA Long Beach Healthcare System???11 (GI), 5901 East Seventh Street, Long Beach, CA 90822, Liver Diseases Branch, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, New England Research Institutes, Watertown, MA, Hepatology Section, Virginia Commonwealth University Medical Center, Richmond, VA, Division of Gastroenterology and Hepatology, University of Colorado at Denver and Health Sciences Center, Denver, CO, Division of Digestive and Liver Diseases, University of Texas Southwestern Medical Center, Dallas, TX, Division of Gastroenterology and Hepatology, Saint Louis University School of Medicine, St. Louis, MO, Departments of Medicine and Molecular and Structural Biology and The Liver-Biliary-Pancreatic Center, University of Connecticut Health Center, Farmington, CT, Gastrointestinal Unit, Massachusetts General Hospital, Boston, MA, and the Department of Medicine, Harvard Medical School, Boston, MA, Division of Virology, Department of Laboratory Medicine, University of Washington, Seattle, WA, Division of Gastrointestinal and Liver Diseases, Keck School of Medicine, University of Southern California, Los Angeles, CA, Morgan, Timothy R., Ghany, Marc G., Kim, Hae-Young, Snow, Kristin K., Shiffman, Mitchell L., De Santo, Jennifer L., Lee, William M., Di Bisceglie, Adrian M., Bonkovsky, Herbert L., Dienstag, Jules L., Morishima, Chihiro, Lindsay, Karen L., and Lok, Anna S. F.
- Abstract
Retrospective studies suggest that subjects with chronic hepatitis C and advanced fibrosis who achieve a sustained virological response (SVR) have a lower risk of hepatic decompensation and hepatocellular carcinoma (HCC). In this prospective analysis, we compared the rate of death from any cause or liver transplantation, and of liver-related morbidity and mortality, after antiviral therapy among patients who achieved SVR, virologic nonresponders (NR), and those with initial viral clearance but subsequent breakthrough or relapse (BT/R) in the HALT-C (Hepatitis C Antiviral Long-Term Treatment Against Cirrhosis) Trial. Laboratory and/or clinical outcome data were available for 140 of the 180 patients who achieved SVR. Patients with nonresponse (NR; n = 309) or who experienced breakthrough or relapse (BT/R; n = 77) were evaluated every 3 months for 3.5 years and then every 6 months thereafter. Outcomes included death, liver-related death, liver transplantation, decompensated liver disease, and HCC. Median follow-up for the SVR, BT/R, and NR groups of patients was 86, 85, and 79 months, respectively. At 7.5 years, the adjusted cumulative rate of death/liver transplantation and of liver-related morbidity/mortality in the SVR group (2.2% and 2.7%, respectively) was significantly lower than that of the NR group (21.3% and 27.2%, P < 0.001 for both) but not the BT/R group (4.4% and 8.7%). The adjusted hazard ratio (HR) for time to death/liver transplantation (HR = 0.17, 95% confidence interval [CI] = 0.06-0.46) or development of liver-related morbidity/mortality (HR = 0.15, 95% CI = 0.06-0.38) or HCC (HR = 0.19, 95% CI = 0.04-0.80) was significant for SVR compared to NR. Laboratory tests related to liver disease severity improved following SVR. Conclusion: Patients with advanced chronic hepatitis C who achieved SVR had a marked reduction in death/liver transplantation, and in liver-related morbidity/mortality, although they remain at risk for HCC. (H EPATOLOGY 2010;)
- Published
- 2010
232. Variants in interferon-alpha pathway genes and response to pegylated interferon-Alpha2a plus ribavirin for treatment of chronic hepatitis C virus infection in the hepatitis C antiviral long-term treatment against cirrhosis trial
- Author
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Division of Gastroenterology, University of Michigan Medical Center, Ann Arbor, MI, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, Division of Gastroenterology, University of California - Irvine, Irvine, CA, and Gastroenterology Service, VA Long Beach Healthcare System, Long Beach, CA, Departments of Medicine and The Liver-Biliary-Pancreatic Center, University of Connecticut Health Center, Farmington, CT, and Carolinas Medical Center, Charlotte, NC, New England Research Institutes, Watertown, MA, Office of the Director, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, Core Genotyping Facility, NCI/Division of Cancer Epidemiology and Genetics, Advanced Technology Program, SAIC-Frederick Inc., NCI-Frederick, Frederick, MD, Department of Medicine, Johns Hopkins University, Baltimore, MD, Cancer and Inflammation Program, Laboratory of Experimental Immunology, SAIC-Frederick Inc., NCI-Frederick Inc., Frederick, MD, Computer Sciences Corp., Rockville, MD, Hepatology Section, Virginia Commonwealth University Medical Center, Richmond, VA, Division of Gastrointestinal and Liver Diseases, Keck School of Medicine, University of Southern California, Los Angeles, CA, Division of Digestive and Liver Diseases, University of Texas Southwestern Medical Center, Dallas, TX, Division of Gastroenterology and Hepatology, Saint Louis University School of Medicine, St. Louis, MO, Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, Virology Division, Department of Laboratory Medicine, University of Washington, Seattle, WA, Gastrointestinal Unit, Medical Services, Massachusetts General Hospital, and the Department of Medicine, Harvard Medical School, Boston, MA, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD ; fax: 301-480-1917. ; 6120 Executive Boulevard, Room 6111, MSC 7246, Rockville, MD 20892, Welzel, Tania Mara, Morgan, Timothy R., Bonkovsky, Herbert L., Naishadham, Deepa, Pfeiffer, Ruth M., Wright, Elizabeth C., Hutchinson, Amy A., Crenshaw, Andrew T., Bashirova, Arman, Carrington, Mary, Dotrang, Myhanh, Sterling, Richard K., Lindsay, Karen L., Fontana, Robert J., Lee, William M., Di Bisceglie, Adrian M., Ghany, Marc G., Gretch, David R., Chanock, Stephen J., Chung, Raymond T., O'Brien, Thomas R., Division of Gastroenterology, University of Michigan Medical Center, Ann Arbor, MI, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, Division of Gastroenterology, University of California - Irvine, Irvine, CA, and Gastroenterology Service, VA Long Beach Healthcare System, Long Beach, CA, Departments of Medicine and The Liver-Biliary-Pancreatic Center, University of Connecticut Health Center, Farmington, CT, and Carolinas Medical Center, Charlotte, NC, New England Research Institutes, Watertown, MA, Office of the Director, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, Core Genotyping Facility, NCI/Division of Cancer Epidemiology and Genetics, Advanced Technology Program, SAIC-Frederick Inc., NCI-Frederick, Frederick, MD, Department of Medicine, Johns Hopkins University, Baltimore, MD, Cancer and Inflammation Program, Laboratory of Experimental Immunology, SAIC-Frederick Inc., NCI-Frederick Inc., Frederick, MD, Computer Sciences Corp., Rockville, MD, Hepatology Section, Virginia Commonwealth University Medical Center, Richmond, VA, Division of Gastrointestinal and Liver Diseases, Keck School of Medicine, University of Southern California, Los Angeles, CA, Division of Digestive and Liver Diseases, University of Texas Southwestern Medical Center, Dallas, TX, Division of Gastroenterology and Hepatology, Saint Louis University School of Medicine, St. Louis, MO, Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, Virology Division, Department of Laboratory Medicine, University of Washington, Seattle, WA, Gastrointestinal Unit, Medical Services, Massachusetts General Hospital, and the Department of Medicine, Harvard Medical School, Boston, MA, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD ; fax: 301-480-1917. ; 6120 Executive Boulevard, Room 6111, MSC 7246, Rockville, MD 20892, Welzel, Tania Mara, Morgan, Timothy R., Bonkovsky, Herbert L., Naishadham, Deepa, Pfeiffer, Ruth M., Wright, Elizabeth C., Hutchinson, Amy A., Crenshaw, Andrew T., Bashirova, Arman, Carrington, Mary, Dotrang, Myhanh, Sterling, Richard K., Lindsay, Karen L., Fontana, Robert J., Lee, William M., Di Bisceglie, Adrian M., Ghany, Marc G., Gretch, David R., Chanock, Stephen J., Chung, Raymond T., and O'Brien, Thomas R.
- Abstract
Combination treatment with pegylated-interferon-alpha (PEG IFN-??) and ribavirin, the current recommended therapy for chronic hepatitis C virus (HCV) infection, results in a sustained virological response (SVR) in only about half of patients. Because genes involved in the interferon-alpha pathway may affect antiviral responses, we analyzed the relationship between variants in these genes and SVR among participants in the Hepatitis C Antiviral Long-Term treatment Against Cirrhosis (HALT-C) trial. Patients had advanced chronic hepatitis C that had previously failed to respond to interferon-based treatment. Participants were treated with peginterferon-??2a and ribavirin during the trial. Subjects with undetectable HCV RNA at week 72 were considered to have had an SVR. Subjects with detectable HCV RNA at week 20 were considered nonresponders. We used TaqMan assays to genotype 56 polymorphisms found in 13 genes in the interferon-alpha pathway. This analysis compares genotypes for participants with an SVR to nonresponders. The primary analysis was restricted to European American participants because a priori statistical power was low among the small number (n = 131) of African American patients. We used logistic regression to control the effect of other variables that are associated with treatment response. Among 581 European American patients, SVR was associated with IFNAR1 IVS1-22G (adjusted odds ratio, 0.57; P = 0.02); IFNAR2 Ex2-33C (adjusted odds ratio, 2.09; P = 0.02); JAK1 IVS22+112T (adjusted odds ratio, 1.66; P = 0.04); and ADAR Ex9+14A (adjusted odds ratio, 1.67; P = 0.03). For the TYK2 -2256A promoter region variant, a borderline association was present among European American participants (OR, 1.51; P = 0.05) and a strong relationship among African American patients; all 10 with SVR who were genotyped for TYK2 -2256 carried the A variant compared with 68 of 120 (57%) nonresponders ( P = 0.006). Conclusion: Genetic polymorphisms in the interferon-?? pathway may
- Published
- 2009
233. Interpretation of positive transcription-mediated amplification test results from polymerase chain reaction???negative samples obtained after treatment of chronic hepatitis C
- Author
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Division of Gastroenterology, University of Michigan Medical Center, Ann Arbor, MI, Virology Division, Department of Laboratory Medicine, University of Washington, Seattle, WA ; fax: 206-744-9858. ; Department of Laboratory Medicine, University of Washington, Box 359690, Seattle, WA 98104, Division of Gastroenterology, University of California???Irvine, Irvine, CA, and Gastroenterology Service, VA Long Beach Healthcare System, Long Beach, CA, Division of Digestive Diseases and Nutrition, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, Office of the Director, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, Virology Division, Department of Laboratory Medicine, University of Washington, Seattle, WA, Hepatology Section, Virginia Commonwealth University Medical Center, Richmond, VA, Section of Hepatology, Division of Gastroenterology and Hepatology, University of Colorado School of Medicine, Denver, CO, Division of Gastrointestinal and Liver Diseases, Keck School of Medicine, University of Southern California, Los Angeles, CA, Division of Digestive and Liver Diseases, University of Texas Southwestern Medical Center, Dallas, TX, Gastrointestinal Unit (Medical Services), Massachusetts General Hospital and the Department of Medicine, Harvard Medical School, Boston, MA, Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, New England Research Institutes, Watertown, MA, Morishima, Chihiro, Morgan, Timothy R., Everhart, James E., Wright, Elizabeth C., Apodaca, Minjun C., Gretch, David R., Shiffman, Mitchell L., Everson, Gregory T., Lindsay, Karen L., Lee, William M., Lok, Anna S. F., Dienstag, Jules L., Ghany, Marc G., Curto, Teresa M., Division of Gastroenterology, University of Michigan Medical Center, Ann Arbor, MI, Virology Division, Department of Laboratory Medicine, University of Washington, Seattle, WA ; fax: 206-744-9858. ; Department of Laboratory Medicine, University of Washington, Box 359690, Seattle, WA 98104, Division of Gastroenterology, University of California???Irvine, Irvine, CA, and Gastroenterology Service, VA Long Beach Healthcare System, Long Beach, CA, Division of Digestive Diseases and Nutrition, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, Office of the Director, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, Virology Division, Department of Laboratory Medicine, University of Washington, Seattle, WA, Hepatology Section, Virginia Commonwealth University Medical Center, Richmond, VA, Section of Hepatology, Division of Gastroenterology and Hepatology, University of Colorado School of Medicine, Denver, CO, Division of Gastrointestinal and Liver Diseases, Keck School of Medicine, University of Southern California, Los Angeles, CA, Division of Digestive and Liver Diseases, University of Texas Southwestern Medical Center, Dallas, TX, Gastrointestinal Unit (Medical Services), Massachusetts General Hospital and the Department of Medicine, Harvard Medical School, Boston, MA, Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, New England Research Institutes, Watertown, MA, Morishima, Chihiro, Morgan, Timothy R., Everhart, James E., Wright, Elizabeth C., Apodaca, Minjun C., Gretch, David R., Shiffman, Mitchell L., Everson, Gregory T., Lindsay, Karen L., Lee, William M., Lok, Anna S. F., Dienstag, Jules L., Ghany, Marc G., and Curto, Teresa M.
- Abstract
The Siemens VERSANT?? transcription-mediated amplification (TMA) assay is extremely sensitive for the detection of hepatitis C virus (HCV) RNA in serum. Eleven of 180 subjects in the Hepatitis C Antiviral Long-term Treatment against Cirrhosis (HALT-C) Trial who achieved polymerase chain reaction (PCR)-defined sustained virological response (SVR) at week 72 also had TMA-positive results from the same blood draw; six were positive on repeat testing. We report the follow-up on these 11 patients, and the reproducibility of TMA test results from PCR-negative samples in relationship to antiviral treatment outcome. Peginterferon and ribavirin treatment was initiated in 1145 prior interferon nonresponders with advanced hepatic fibrosis. Treatment was continued for 48 weeks if patients had undetectable HCV RNA by PCR at treatment week 20. Frozen serum samples from weeks 12, 20, 24, 48, and 72 were subsequently tested by TMA. Nine of the 11 patients returned for testing (median, 30 months after the week 72 visit), and all had undetectable HCV RNA by TMA and PCR. Among 759 PCR-negative samples obtained during treatment that were tested twice by TMA, 17% overall exhibited consistently positive results, and 21% exhibited inconsistently positive results. SVR was more likely if TMA was consistently negative than if consistently or inconsistently positive. With continued treatment, patients with inconsistently positive TMA results were more likely to become TMA-negative than TMA-positive ( P < 0.0001). Conclusion: In PCR-negative samples, positive TMA results may indicate the presence of low levels of HCV RNA. However, because patients with positive TMA results may achieve SVR, management decisions during therapy should not be based on a single positive TMA test result. (H EPATOLOGY 2008.)
- Published
- 2008
234. Hepatitis E: The nonendemic perspective
- Author
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Samala, Niharika, primary and Ghany, Marc G., additional
- Published
- 2013
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235. The Hepatitis B Vaccine Protects Re-Exposed Health Care Workers, But Does Not Provide Sterilizing Immunity
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Werner, Jens M., primary, Abdalla, Adil, additional, Gara, Naveen, additional, Ghany, Marc G., additional, and Rehermann, Barbara, additional
- Published
- 2013
- Full Text
- View/download PDF
236. Association of IL28B genotype with fibrosis progression and clinical outcomes in patients with chronic hepatitis C: A longitudinal analysis
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Noureddin, Mazen, primary, Wright, Elizabeth C., additional, Alter, Harvey J., additional, Clark, Shauna, additional, Thomas, Emmanuel, additional, Chen, Richard, additional, Zhao, Xiongce, additional, Conry-Cantilena, Cathy, additional, Kleiner, David E., additional, Liang, T. Jake, additional, and Ghany, Marc G., additional
- Published
- 2013
- Full Text
- View/download PDF
237. The liver diseases of lipodystrophy: The long-term effect of leptin treatment
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Safar Zadeh, Elika, primary, Lungu, Andreea O., additional, Cochran, Elaine K., additional, Brown, Rebecca J., additional, Ghany, Marc G., additional, Heller, Theo, additional, Kleiner, David E., additional, and Gorden, Phillip, additional
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- 2013
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238. Acute hepatitis C: to treat or not to treat
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Samala, Niharika R, primary and Ghany, Marc G, additional
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- 2013
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239. Current and Future Therapies for Hepatitis C Virus Infection
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Liang, T. Jake, primary and Ghany, Marc G., additional
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- 2013
- Full Text
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240. Spontaneous Mutations in the HBV Genome and their Clinical Implications
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Mansourian, Pejman G., primary, Ghany, Marc G., additional, and Thomas, Emmanuel, additional
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- 2013
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241. Discordance Among Transient Elastography, Aspartate Aminotransferase to Platelet Ratio Index, and Histologic Assessments of Liver Fibrosis in Patients With Chronic Hepatitis C
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Gara, Naveen, primary, Zhao, Xiongce, additional, Kleiner, David E., additional, Liang, T. Jake, additional, Hoofnagle, Jay H., additional, and Ghany, Marc G., additional
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- 2013
- Full Text
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242. Effect of ribavirin on viral kinetics and liver gene expression in chronic hepatitis C
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Rotman, Yaron, primary, Noureddin, Mazen, additional, Feld, Jordan J, additional, Guedj, Jeremie, additional, Witthaus, Michael, additional, Han, Hwalih, additional, Park, Yoon J, additional, Park, Su-Hyung, additional, Heller, Theo, additional, Ghany, Marc G, additional, Doo, Edward, additional, Koh, Christopher, additional, Abdalla, Adil, additional, Gara, Naveen, additional, Sarkar, Souvik, additional, Thomas, Emmanuel, additional, Ahlenstiel, Golo, additional, Edlich, Birgit, additional, Titerence, Rachel, additional, Hogdal, Leah, additional, Rehermann, Barbara, additional, Dahari, Harel, additional, Perelson, Alan S, additional, Hoofnagle, Jay H, additional, and Liang, T Jake, additional
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- 2013
- Full Text
- View/download PDF
243. Hepatitis B virus treatment: Management of antiviral drug resistance
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Tana, Michele M., primary and Ghany, Marc G., additional
- Published
- 2013
- Full Text
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244. Antiviral drug-resistant HBV: Standardization of nomenclature and assays and recommendations for management
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Division of Gastroenterology, University of Michigan, Ann Arbor, MI ; fax: 734-936-7392 ; Division of Gastroenterology, University of Michigan Health System, 3912 Taubman Center, Ann Arbor, MI 48109-0362, INSERM, U271; Universit?? Lyon I; Hospices Civils de Lyon, Lyon, France, Victorian Infectious Diseases Reference Laboratory, North Melbourne, Victoria, Australia, Liver Diseases Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, French National Reference Center for Viral Hepatitis B, C and delta, Department of Virology and INSERM U841, Hopital Henri Mondor, Universite Paris 12, Creteil, France, Liver Research Unit, Chang Gung University and Memorial Hospital, Taipei, Taiwan, Department of Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan, Theoretical Biology and Biophysics Group (T-10), Los Alamos National Laboratory, Los Alamos, NM, Lok, Anna S., Zoulim, Fabien, Locarnini, Stephen, Bartholomeusz, Angeline, Ghany, Marc G., Pawlotsky, Jean-Michel, Liaw, Yun-Fan, Mizokami, Masashi, Kuiken, Carla, Division of Gastroenterology, University of Michigan, Ann Arbor, MI ; fax: 734-936-7392 ; Division of Gastroenterology, University of Michigan Health System, 3912 Taubman Center, Ann Arbor, MI 48109-0362, INSERM, U271; Universit?? Lyon I; Hospices Civils de Lyon, Lyon, France, Victorian Infectious Diseases Reference Laboratory, North Melbourne, Victoria, Australia, Liver Diseases Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, French National Reference Center for Viral Hepatitis B, C and delta, Department of Virology and INSERM U841, Hopital Henri Mondor, Universite Paris 12, Creteil, France, Liver Research Unit, Chang Gung University and Memorial Hospital, Taipei, Taiwan, Department of Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan, Theoretical Biology and Biophysics Group (T-10), Los Alamos National Laboratory, Los Alamos, NM, Lok, Anna S., Zoulim, Fabien, Locarnini, Stephen, Bartholomeusz, Angeline, Ghany, Marc G., Pawlotsky, Jean-Michel, Liaw, Yun-Fan, Mizokami, Masashi, and Kuiken, Carla
- Abstract
Substantial advances have been made in the treatment of chronic hepatitis B in the past decade. Approved treatments for chronic hepatitis B include 2 formulations of interferon and 4 nucleos(t)ide analogues (NAs). Sustained viral suppression is rarely achieved after withdrawal of a 48-week course of NA therapy, necessitating long, and in many cases, indefinite treatment with increasing risk of development of drug resistance. Antiviral resistance and poor adherence are the most important factors in treatment failure of hepatitis B. Thus, there is a need to standardize nomenclature relating to hepatitis B antiviral resistance, and to define genotypic, phenotypic, and clinical resistance to NA therapy. (H EPATOLOGY 2007;46:254???265.)
- Published
- 2007
245. Modeling hepatic fibrosis in African American and Caucasian American patients with chronic hepatitis C virus infection
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Department of Internal Medicine, University of Michigan, Ann Arbor, MI ; fax: 734-936-7392 ; 3912 Taubman Center, Ann Arbor, MI 48109-0362, National Cancer Institute, Bethesda, MD, University of Pittsburgh, Pittsburgh, PA, University of California San Francisco, San Francisco, CA, Beth Israel Deaconess Medical Center, Boston, MA, University of Miami, Miami, FL, National Institutes of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, Fontana, Robert J., Kleiner, David E., Bilonick, Richard, Terrault, Norah, Afdhal, Nezam, Belle, Steven H., Jeffers, Lennox J., Ramcharran, Darmendra, Ghany, Marc G., Hoofnagle, Jay H., Department of Internal Medicine, University of Michigan, Ann Arbor, MI ; fax: 734-936-7392 ; 3912 Taubman Center, Ann Arbor, MI 48109-0362, National Cancer Institute, Bethesda, MD, University of Pittsburgh, Pittsburgh, PA, University of California San Francisco, San Francisco, CA, Beth Israel Deaconess Medical Center, Boston, MA, University of Miami, Miami, FL, National Institutes of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, Fontana, Robert J., Kleiner, David E., Bilonick, Richard, Terrault, Norah, Afdhal, Nezam, Belle, Steven H., Jeffers, Lennox J., Ramcharran, Darmendra, Ghany, Marc G., and Hoofnagle, Jay H.
- Abstract
Assessment of histological stage is an integral part of disease management in patients infected with the hepatitis C virus (HCV). The aim of this study was to develop a model incorporating objective clinical and laboratory parameters to estimate the probability of severe fibrosis ( i.e. , Ishak fibrosis ??? 3) in previously untreated African American (AA) and Caucasian American (CA) patients with HCV genotype 1. The Ishak fibrosis scores of 205 CA and 194 AA patients enrolled in the Viral Resistance to Antiviral Therapy of Chronic Hepatitis C study (Virahep-C) were modeled using simple and multiple logistic regression. The model was then validated in an independent cohort of 461 previously untreated patients with HCV. The distribution of fibrosis scores was similar in the AA and CA patients as was the proportion of patients with severe fibrosis (35% vs. 39%, P = .47). After accounting for the number of portal areas in the biopsy, patient age, serum aspartate aminotransferase, alkaline phosphatase, and platelet count were independently associated with severe fibrosis in the overall cohort, and the relationship with fibrosis was similar in both the AA and CA subgroups. The area under the receiver operating characteristic curve (AUROC) of the Virahep-C model (0.837) was significantly better than in other published models ( P = .0003). The AUROC of the Virahep-C model was 0.851 in the validation population. In conclusion , a model consisting of widely available clinical and laboratory features predicted severe hepatic fibrosis equally well in AA and CA patients with HCV genotype 1 and was superior to other published models. The excellent performance of the Virahep-C model in an external validation cohort suggests the findings are replicable and potentially generalizable. (H EPATOLOGY 2006;44:925???935.)
- Published
- 2007
246. Hepatitis E Virus Does Not Contribute to Hepatic Decompensation Among Patients With Advanced Chronic Hepatitis C.
- Author
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Samala, Niharika, Wright, Elizabeth C., Buckler, A. Gretchen, Vargas, Vanessa, Shetty, Kirti, Reddy, K. Rajender, Lucey, Michael R., Alter, Harvey J., Hoofnagle, Jay H., and Ghany, Marc G.
- Abstract
Background & Aims Hepatitis E (HEV) can cause acute-on-chronic liver failure in persons with pre-existing liver disease. We investigated whether HEV infection contributes to hepatic decompensation in patients with previously stable, advanced chronic hepatitis C. Methods We performed a case–control study using stored serum samples from subjects enrolled in the randomized phase of the Hepatitis C Antiviral Long-Term Treatment Against Cirrhosis Trial (n = 1050; mean age, 51 y; 70% male; 40% with cirrhosis at baseline). Cases were subjects who developed hepatic decompensation within a 24-week period. Controls (3 per case) were subjects without hepatic decompensation matched for fibrosis stage and followed up for a similar period. A serum sample obtained within 6 months after the decompensation event in cases and the same follow-up period in controls were tested for anti-HEV IgG. Subjects with a positive result had a baseline sample similarly tested for anti-HEV IgG. We measured levels of anti-HEV IgM and HEV RNA in blood samples from incident cases. Results Of the 1050 subjects analyzed, 314 (30%) experienced a clinical event. Of the 314 subjects who experienced decompensation as defined, 89 (28%) were tested for anti-HEV, along with 267 controls (without decompensation). Similar proportions of cases and controls tested positive for anti-HEV (22.5% and 20.6%, respectively; P = .70). Ten incident HEV infections were identified—4 in cases (4.5%) and 6 in controls (2.2%) ( P = .28). HEV RNA was not detected in blood samples from the 10 incident infections. Only 2 of the 4 incident infections among cases were related temporally to the decompensation event. Conclusions HEV does not appear to be a significant cause of hepatic decompensation among persons with previously stable, advanced chronic hepatitis C in the United States. [ABSTRACT FROM AUTHOR]
- Published
- 2016
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247. Letter: systematic review with meta‐analysis on the impact of functional cure on clinical outcomes in patients with chronic hepatitis B—authors' reply.
- Author
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Vittal, Anusha, Sharma, Disha, Hu, Alvin, Majeed, Nehna A., Auh, Sungyoung, and Ghany, Marc G.
- Subjects
CHRONIC hepatitis B ,TREATMENT effectiveness - Abstract
LINKED CONTENT: This article is linked to Vittal et al papers. To view these articles, visit https://doi.org/10.1111/apt.16659 and https://doi.org/10.1111/apt.16758 [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
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248. Effect of human immunodeficiency virus infection on hepatitis C virus infection in hemophiliacs
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From the Section of Gastroenterology and Hepatology, and Hematology and Oncology, Department of Medicine, Tulane University School of Medicine, New Orleans, Louisiana; Chiron Corporation, Emeryville, California; Division of Gastroenterology, University of Michigan Medical Center, 3912 Taubman Center, Box 0362, 48109, Ann Arbor, Michigan, From the Section of Gastroenterology and Hepatology, and Hematology and Oncology, Department of Medicine, Tulane University School of Medicine, New Orleans, Louisiana; Chiron Corporation, Emeryville, California, Ann Arbor, Sanchez-Pescador, R., Leissinger, C., Lagier, R., Lok, A.S.F., Ghany, Marc G., From the Section of Gastroenterology and Hepatology, and Hematology and Oncology, Department of Medicine, Tulane University School of Medicine, New Orleans, Louisiana; Chiron Corporation, Emeryville, California; Division of Gastroenterology, University of Michigan Medical Center, 3912 Taubman Center, Box 0362, 48109, Ann Arbor, Michigan, From the Section of Gastroenterology and Hepatology, and Hematology and Oncology, Department of Medicine, Tulane University School of Medicine, New Orleans, Louisiana; Chiron Corporation, Emeryville, California, Ann Arbor, Sanchez-Pescador, R., Leissinger, C., Lagier, R., Lok, A.S.F., and Ghany, Marc G.
- Abstract
Chronic liver disease due to hepatitis C virus (HCV) infection is a major problem in hemophiliacs. Recent reports suggested that hemophiliacs coinfected with hepatitis C virus and human immunodeficiency virus (HIV) have an increased incidence of liver failure but the mechanism of accelerated liver injury is not clear. We tested plasma from 100 hemophiliacs for anti-HCV by second generation ELISA, anti-HIV by EIA, and HCV RNA and HIV RNA by branched DNA and polymerase chain reaction assays to determine if hemophiliacs coinfected with HCV and HIV have higher HCV RNA levels and more active liver disease. Seventy-nine (79%) patients were anti-HCV positive, of whom 85% were HCV RNA positive. None of the anti-HCV-negative patients had detectable HCV RNA in plasma. Forty-two (42%) patients were anti-HIV positive, of whom 47% had detectable HIV RNA. All the anti-HIV-positive patients were also anti-HCV positive. The prevalence of both anti-HCV and anti-HIV increased significantly with age. There was no difference in HCV RNA levels between anti-HIV-positive and anti-HIV-negative patients (mean: 21??4 vs 18??5 Meq/ml), although HCV RNA levels were significantly higher in anti-HIV-positive patients with CD4 counts<200/mm 3 (P =0.008). There was an inverse correlation between HCV RNA levels and CD4 counts but no correlation was found between HCV RNA and serum aminotransferase levels. We found a high prevalence of HCV and HIV coinfection in our hemophiliacs. Hepatitis C virus replication appears to be increased in patients with severe immunodeficiency secondary to progressive HIV infection. However, there was no correlation between HCV RNA and serum ALT level, suggesting that HCV is not directly cytopathic.
- Published
- 2006
249. Reduction in Hepatic Inflammation Is Associated With Less Fibrosis Progression and Fewer Clinical Outcomes in Advanced Hepatitis C
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Morishima, Chihiro, primary, Shiffman, Mitchell L, additional, Dienstag, Jules L, additional, Lindsay, Karen L, additional, Szabo, Gyongyi, additional, Everson, Gregory T, additional, Lok, Anna S, additional, Di Bisceglie, Adrian M, additional, Ghany, Marc G, additional, Naishadham, Deepa, additional, Morgan, Timothy R, additional, and Wright, Elizabeth C, additional
- Published
- 2012
- Full Text
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250. The Application and Mechanism of Action of Ribavirin in Therapy of Hepatitis C
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Thomas, Emmanuel, primary, Ghany, Marc G, additional, and Liang, T Jake, additional
- Published
- 2012
- Full Text
- View/download PDF
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