Marc G Ghany

National Institutes of Health, Maryland, United States

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Publications (125)1259.65 Total impact

  • Marc G Ghany, Naveen Gara
    Lancet. 06/2014;
  • T Jake Liang, Marc G Ghany
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    ABSTRACT: A book on hepatitis C would read like a marriage of an Orson Welles mystery and a Shakespearean play - awash in enigma, tragedy, despair, resilience, redemption, and triumph. It is only fitting that treatment of hepatitis C virus (HCV) infection stands at center stage of such a book. After the initial introduction of interferon alfa as the mainstay of therapy, the field stalled for more than 10 years. Although the introduction of ribavirin combination therapy and pegylated interferons had increased response rates, the real breakthrough came with the development of direct-acting antiviral agents (DAAs).(1) The first generation of DAAs . . .
    New England Journal of Medicine 05/2014; · 51.66 Impact Factor
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    ABSTRACT: Background Chronic delta hepatitis virus (HDV) infection rapidly progresses to cirrhosis. Treatment with peginterferon for up to 2 years is often without durable response.AimTo examine the efficacy and safety of long-term peginterferon in achieving a durable response.Methods Treatment was initiated with 180 μg/week of peginterferon alfa-2a with titration to a maximal tolerable dose, for up to 5 years. Liver biopsies and hepatic venous pressure gradients (HVPG) were evaluated at baseline, 1, 3 and 5 years. The primary endpoint was histological improvement or loss of serum HDV and HBsAg at 3 years.ResultsThirteen patients were treated for a median of 140 weeks (6–260) with an average peginterferon dose of 180 μg/week (90–270). At baseline, most had advanced disease (median Ishak fibrosis = 3) with portal hypertension (HVPG = 10.2 ± 6 mmHg). Five of 13 patients (39%) achieved the primary endpoint, with three seroconverting for HBsAg after 24, 37 and 202 weeks of treatment. Histological inflammation improved after 1 year, (median HAI: 10 vs. 7, P = 0.01) with persistence in 4/5 patients at 3 years (median HAI: 7.5). Greatest improvements occurred in the first year. Baseline bilirubin and HBsAg levels were significantly lower in virological responders than nonresponders. After 12 weeks, virological responders had a significant decline in HBsAg (1.5 log10 IU/mL, P = 0.05).Conclusion Despite increased doses and duration of therapy, treatment of chronic HDV with peginterferon remains unsatisfactory. Quantitative measures of HBsAg may be an important biomarker of early response to peginterferon therapy in chronic delta hepatitis virus infection.
    Alimentary Pharmacology & Therapeutics 05/2014; · 4.55 Impact Factor
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    ABSTRACT: Background & Aims 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. Methods The HBRN collected data on clinical characteristics of 1625 adults with chronic HBV infection who are not receiving antiviral therapy from 21 clinical centers in North America. Results Half of the subjects in the HBRN are male, and the mean age is 42 years; 72% are Asian, 15% are Black, and 11% are White, with 82% born outside of North America. The most common HBV genotype was B (39%); 745 of subjects were negative for the hepatitis B e antigen. The median serum level of HBV DNA when the study began was 3.6 log10 IU/mL; 68% of male subjects and 67% of female subjects had levels of alanine aminotransferase above the normal range. Conclusions The HBRN cohort will be used to address important clinical and therapeutic questions for North Americans infected with chronic HBV and to guide health policies on HBV prevention and management in North America.
    Clinical Gastroenterology and Hepatology. 01/2014;
  • Hepatology 08/2013; · 12.00 Impact Factor
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    ABSTRACT: & Aims: Infection with hepatitis B virus (HBV) can be prevented by vaccination with HBV surface (HBs) antigen, which induces HBs-specific antibodies and T cells. However, the duration of vaccine-induced protective immunity is poorly defined for healthcare workers who were vaccinated as adults. We investigated the immune mechanisms (antibody and T cell responses) of long-term protection by the HBV vaccine in 90 healthcare workers with occupational exposure to HBV, 10-28 y after vaccination. Fifty-nine of 90 health-care workers (65%) had levels of antibodies against HBs (anti-HBs) above the cut-off (>12 mIU/ml) and 30/90 (33%) had HBs-specific T cells that produced interferon (IFN)γ . Anti-HBs titers correlated with numbers of HBs-specific IFNγ-producing T cells, but not with time after vaccination. Whereas occupational exposure to HBV after vaccination did not induce antibodies to the HBV core protein (HBcore), the standard biomarker for HBV infection, CD4(+) and CD8(+) T cells against HBcore and polymerase antigens were detected. Similar numbers of HBcore- and polymerase-specific CD4(+) and CD8(+) T cells were detected in health-care workers with occupational exposure to HBV and in patients who acquired immunity via HBV infection. Most of the HBcore- and polymerase-specific T cells were CD45RO(+)CCR7(-)CD127(-) effector memory cells in exposed health-care workers and in patients with acquired immunity. In contrast, most of the vaccine-induced HBs-specific T cell cells were CD45RO(-)CCR7(-)CD127(-) and terminally differentiated. HBsAg vaccine-induced immunity protects against future infection but does not provide sterilizing immunity, as evidenced by HBcore- and polymerase-specific CD8(+) T cells in vaccinated health care workers with occupational exposure to HBV. The presence of HBcore- and HBV polymerase-specific T-cell responses is a more sensitive indicator of HBV exposure than detection of HBcore-specific antibodies.
    Gastroenterology 07/2013; · 12.82 Impact Factor
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    ABSTRACT: Background: IL28B polymorphisms are associated with spontaneous clearance of HCV infection and response to therapy. Whether IL28B genotype affects fibrosis progression or clinical outcome is unclear. Aims: To study the relationship between IL28B genotype and both histological and clinical outcomes in patients with chronic hepatitis C (CHC). Methods: Hepatic fibrosis was scored using the Ishak (0-6) scale; progression was defined as a 2-point increase in Ishak score between biopsies. Multiple logistic and Cox regressions were used to identify variables associated with fibrosis progression. Results: 1483 patients were included in a baseline cross-sectional analysis, from which 276 were eligible for a paired biopsy analysis (median time between biopsies-4 years), and 400 for a clinical outcome analysis. At baseline biopsy, patients with IL28B CC genotype had significantly higher portal inflammation (2.4 vs. 2.2) and ALT levels (133 vs. 105 U/L), p <0.05 for all. In the paired biopsy analysis, there was no difference in the frequency of fibrosis progression between patients with IL28B CC and non-CC genotypes (17% vs. 23%). In logistic regression, only higher baseline alkaline phosphatase, lower platelets and greater hepatic steatosis were associated with fibrosis progression. Patients with IL28B CC were twice as likely to develop adverse clinical outcomes compared to non-CC (32% vs. 16%), P= 0.007. Conclusions: IL28B CC genotype was associated with greater hepatic necroinflammation, higher ALT, and worse clinical outcomes in CHC patients. This suggests that IL28B CC is associated with a state of enhanced immunity that on one hand can promote viral clearance, but alternately, can increase necroinflammation and hepatic decompensation without enhancing fibrosis progression. (HEPATOLOGY 2013.).
    Hepatology 05/2013; · 12.00 Impact Factor
  • T Jake Liang, Marc G Ghany
    New England Journal of Medicine 05/2013; 368(20):1907-17. · 51.66 Impact Factor
  • Niharika R Samala, Marc G Ghany
    The Lancet Infectious Diseases 03/2013; · 19.97 Impact Factor
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    ABSTRACT: BACKGROUND: Although the short-term benefits of a sustained virological response (SVR) to interferon-based therapies of chronic hepatitis C (CHC) are well known, the long-term consequences of SVR are less clear. AIM: To assess changes in markers of disease activity and fibrosis in patients followed up to 23 years post-SVR. METHODS: The first 103 SVR patients (from 1984 to 2003) at the National Institutes of Health Clinical Center were evaluated. Serum markers before treatment and at the last visit were compared. Evaluations after 2007 included transient elastography (TE). RESULTS: Of 103 patients, three subsequently relapsed 0.7, 6.3 and 6.5 years post therapy. The remaining 100 patients (56 men, mean age 56 years) maintained SVR at final follow-up. No patients developed hepatic decompensation, but one with pre-treatment cirrhosis died 12 years post SVR of hepatocellular carcinoma. In comparison to pre-treatment values, markers improved at follow-up, including mean ALT (152-27 U/L), AST (87-24 U/L), alkaline phosphatase (78-69 U/L), IgG (1463-1113 mg/dL), platelet count (209 000-239 000/μL) and AST to platelet count ratio index (APRI: 1.31-0.33). TE was performed in 69 patients and was normal (<7.0 kPA) in 60%, moderately elevated (7.1-13.8) in 31% and cirrhotic range (>13.8) in 9%. TE and platelet counts at follow-up correlated with fibrosis on pre-treatment liver biopsy (P < 0.001). CONCLUSIONS: In 97% of patients with CHC, SVR is durable without evidence of disease progression, although some degree of hepatic fibrosis may persist and patients with pre-treatment cirrhosis are at continuing low risk for hepatocellular carcinoma.
    Alimentary Pharmacology & Therapeutics 03/2013; · 4.55 Impact Factor
  • Naveen Gara, Marc G Ghany
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    ABSTRACT: The treatment of chronic hepatitis C is rapidly evolving from triple therapy to regimens that do not require interferon or even ribavirin. However, pegylated interferon and ribavirin will remain the backbone of hepatitis C therapy for the time being. This review summarizes the pharmacokinetics of peginterferon and ribavirin with a particular emphasis on their side-effect profile and management. Finally, the continued role of peginterferon and ribavirin in future therapies will be discussed.
    Clinical Infectious Diseases 03/2013; · 9.37 Impact Factor
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    ABSTRACT: BACKGROUND & AIMS: Lipodystrophies are hypoleptinemic conditions characterized by fat loss, severe insulin resistance, hypertriglyceridemia, and ectopic fat accumulation. Nonalcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH) are also features of this condition. We studied the spectrum of liver disease in lipodystrophy and the effects of leptin replacement. METHODS: This was an open-label prospective study of leptin therapy in patients with inherited and acquired lipodystrophy at the National Institutes of Health. Liver biopsies were performed at baseline (N=50) and after leptin replacement (N=27). NASH activity was assessed using the NASH Clinical Research Network (CRN) scoring system. Fasting blood glucose, triglyceride, hemoglobin A(1c) and liver enzymes were measured at baseline and at the time of the final liver biopsy. RESULTS: In leptin treated patients, 86% met criteria for NASH at baseline, while only 33% had NASH after leptin replacement for 25.8 ± 3.7 months (mean ± SE, p 0.0003). There were significant improvements in steatosis grade (reduction of mean score from 1.8 to 0.9) and ballooning injury scores (from 1.2 to 0.4), with a 44.2% reduction in mean NAFLD activity score (p < 0.0001). Patients who already had fibrosis remained stable on leptin replacement. We observed significant improvement in metabolic profile, ALT and AST. In addition to NASH, four patients with acquired generalized lipodystrophy (AGL) had autoimmune hepatitis. CONCLUSIONS: The fundamental liver disease of lipodystrophy is NASH, although autoimmune hepatitis was observed in some patients with AGL. Leptin appears to be a highly effective therapy for NASH in hypoleptinemic lipodystrophic patients.
    Journal of Hepatology 02/2013; · 9.86 Impact Factor
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    ABSTRACT: OBJECTIVE: Ribavirin improves treatment response to pegylated-interferon (PEG-IFN) in chronic hepatitis C but the mechanism remains controversial. We studied correlates of response and mechanism of action of ribavirin in treatment of hepatitis C. DESIGN: 70 treatment-naive patients were randomised to 4 weeks of ribavirin (1000-1200 mg/d) or none, followed by PEG-IFNα-2a and ribavirin at standard doses and durations. Patients were also randomised to a liver biopsy 24 h before or 6 h after starting PEG-IFN. Hepatic gene expression was assessed by microarray and interferon-stimulated gene (ISG) expression quantified by nCounter platform. Temporal changes in ISG expression were assessed by qPCR in peripheral-blood mononuclear cells (PBMC) and by serum levels of IP-10. RESULTS: After 4 weeks of ribavirin monotherapy, hepatitis C virus (HCV) levels decreased by 0.5±0.5 log(10) (p=0.009 vs controls) and ALT by 33% (p<0.001). Ribavirin pretreatment, while modestly augmenting ISG induction by PEG-IFN, did not modify the virological response to subsequent PEG-IFN and ribavirin treatment. However, biochemical, but not virological, response to ribavirin monotherapy predicted response to subsequent combination treatment (rapid virological response, 71% in biochemical responders vs 22% non-responders, p=0.01; early virological response, 100% vs 68%, p=0.03; sustained virological response 83% vs 41%, p=0.053). Ribavirin monotherapy lowered serum IP-10 levels but had no effect on ISG expression in PBMC. CONCLUSIONS: Ribavirin is a weak antiviral but its clinical effect seems to be mediated by a separate, indirect mechanism, which may act to reset IFN-responsiveness in HCV-infected liver.
    Gut 02/2013; · 10.73 Impact Factor
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    Michele M. Tana, Marc G. Ghany
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    ABSTRACT: Watch a video presentation of this article Watch the interview with the author Answer questions and earn CME
    Clinical Liver Disease. 02/2013; 2(1).
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    ABSTRACT: BACKGROUND & AIMS: Liver biopsy is the standard for assessing hepatic fibrosis. Ultrasound transient elastography (TE) and the aspartate aminotransferase to platelet ratio index (APRI) are validated, non-invasive tests for identifying patients with cirrhosis. We evaluated discordance among TE, APRI, and histology diagnoses of cirrhosis. METHODS: We analyzed findings from 109 patients with chronic hepatitis C who underwent TE within 6 months of liver biopsy at the US National Institutes of Health from 2006 to 2011. Fibrosis was scored using the Ishak scale (0 to 6). APRI scores were calculated using data collected the day of the biopsy. Area under receiver operator characteristic curves for TE and APRI were calculated to distinguish patients with cirrhosis (Ishak scores of 5-6) from those without cirrhosis (Ishak scores of 0-4). The best cutoff and corresponding positive (PPV) and negative predictive values (NPV) were selected. RESULTS: Based on biopsy analysis, 18% of the patients had no fibrosis, 52% had mild fibrosis, 17% had bridging fibrosis, and 13% had cirrhosis. A TE cutoff of 13.1 kPa identified patients with cirrhosis with the highest level of accuracy (100% sensitivity, 89% specificity, 58% PPV, 100% NPV), as did an APRI cutoff value of 1.0 (79% sensitivity, 78% specificity, 34% PPV, 96% NPV). Results from TE and APRI were discordant for 28% of cases. TE identified all cases of cirrhosis and an additional 10 patients who were not found to have cirrhosis based on histology analysis; 7 of these had clinical or radiological evidence of cirrhosis, indicating that the biopsy sample was not staged correctly. CONCLUSION: TE increases the accuracies of biopsy and APRI analyses in identifying patients with cirrhosis. TE might also be used to screen patients for cirrhosis and identify those who should followed for development of hepatocellular carcinoma and varices.
    Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association 11/2012; · 5.64 Impact Factor
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    ABSTRACT: A total of 738 volunteer blood donors who were positive for anti-hepatitis C virus (HCV) were assessed for risk factors and outcomes for up to 15 years within the study and up to 54 years from the estimated onset of infection. A third-generation recombinant immunoblot assay (RIBA) was performed to distinguish true from false anti-HCV reactivity. Findings of HCV polymerase chain reaction classified subjects as having chronic HCV infection or as having recovered. Liver biopsy specimens were staged by Ishak fibrosis score and graded by histologic activity index. Of 738 anti-HCV-positive subjects, 469 (64%) had positive RIBA results, 217 (29%) had negative results, and 52 (7%) had indeterminate results. Primary independent risk factors were injection drug use (odds ratio [OR], 35.0; P < .0001), blood transfusion (OR, 9.9; P < .0001), and intranasal cocaine use, including 79 "snorters" who repeatedly denied injection drug use or blood transfusion (OR, 8.5; P < .0001). Classification and regression tree and random forest analyses confirmed these risk factors. A total of 384 RIBA-positive donors (82%) were HCV RNA positive; of these, liver biopsy specimens from 185 (48%) showed no fibrosis in 33%, mild fibrosis in 52%, bridging fibrosis in 12%, and cirrhosis in 2% a mean duration of 25 years after infection. Analysis of 63 repeat biopsy specimens showed that 8% progressed ≥2 Ishak stages over 5 years (mean progression, 0.06 Ishak stages/year). Injection drug use and blood transfusion before 1990 are dominant risk factors for HCV acquisition; intranasal cocaine use may be a surreptitious route of parenteral spread. After a mean of 25 years of HCV infection, histologic outcomes were relatively mild: 85% had no or mild fibrosis, and only 2% had cirrhosis. Nearly one-fifth spontaneously recovered.
    The Journal of Infectious Diseases 06/2012; 206(5):654-61. · 5.85 Impact Factor
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    ABSTRACT: OBJECTIVES:During the Hepatitis C Antiviral Long-term Treatment against Cirrhosis Trial, 3.5 years of maintenance peginterferon-alfa-2a therapy did not affect liver fibrosis progression or clinical outcomes among 1,050 previous interferon nonresponders with advanced fibrosis or cirrhosis. We investigated whether reduced hepatic inflammation was associated with clinical benefit in 834 patients with a baseline and follow-up biopsy 1.5 years after randomization to peginterferon or observation.METHODS:Relationships between change in hepatic inflammation (Ishak hepatic activity index, (HAI)) and serum alanine aminotransferase level, fibrosis progression and clinical outcomes after randomization, and hepatitis C virus (HCV) RNA decline before and after randomization were evaluated. Histological change was defined as a ≥2-point difference in HAI or Ishak fibrosis score between biopsies.RESULTS:Among 657 patients who received full-dose peginterferon/ribavirin "lead-in" therapy before randomization, year-1.5 HAI improvement was associated with lead-in HCV RNA suppression in both the randomized treated (P<0.0001) and control (P=0.0001) groups, even in the presence of recurrent viremia. This relationship persisted at year 3.5 in both the treated (P=0.001) and control (P=0.01) groups. Among 834 patients followed for a median of 6 years, fewer clinical outcomes occurred in patients with improved HAI at year 1.5 compared with those without such improvement in both the treated (P=0.03) and control (P=0.05) groups. Among patients with Ishak 3-4 fibrosis at baseline, those with improved HAI at year 1.5 had less fibrosis progression at year 1.5 in both the treated (P=0.0003) and control (P=0.02) groups.CONCLUSIONS:Reduced hepatic inflammation (measured 1.5 and 3.5 years after randomization) was associated with profound virological suppression during lead-in treatment with full-dose peginterferon/ribavirin and with decreased fibrosis progression and clinical outcomes, independent of randomized treatment.Am J Gastroenterol advance online publication, 12 June 2012; doi:10.1038/ajg.2012.137.
    The American Journal of Gastroenterology 06/2012; · 7.55 Impact Factor
  • Emmanuel Thomas, Marc G Ghany, T Jake Liang
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    ABSTRACT: Ribavirin has been used as an antiviral agent for several decades. Although it has activity against numerous viruses, its major use clinically has been in the treatment of respiratory syncytial virus in paediatric patients and chronic HCV infection in both children and adults. This review highlights the clinical application and mechanism of action of ribavirin and discusses the future role of ribavirin in treatment of HCV where there are intense research efforts to improve therapy.
    Antiviral chemistry & chemotherapy 05/2012; 23(1):1-12.
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    ABSTRACT: Despite appropriate immunoprophylaxis, up to 10 % of infants born to highly viremic hepatitis B virus (HBV-DNA ≥ 7 log IU/mL) mothers are infected with HBV. Use of TDF to prevent vertical transmission (VT) by such mothers has not been evaluated. To evaluate the efficacy and safety of TDF in preventing VT from highly viremic HBV-infected mothers. Data were collected retrospectively from HBV mono-infected, hepatitis B e antigen (HBeAg) positive, pregnant women between 6/2008 and 11/2010. Cases enrolled were HBV mono-infected mothers who received TDF (300 mg orally once a day) in the third trimester. Those with pregnancy complications or an abnormal fetus on sonography were excluded from use of TDF. All infants received hepatitis B immunoglobulin and vaccination at birth and subsequently. Eleven Asian mothers received TDF at the median gestational age of 29 (28-32) weeks and the median duration of TDF use before delivery was 10 (7-12) weeks. A significant reduction in serum HBV-DNA was achieved at delivery compared with baseline (mean 5.25 ± 1.79 vs. 8.87 ± 0.45 log(10) copies/mL, respectively; p < 0.01). Three had serum ALT levels more than 1.5 times the upper limit of normal and two of these normalized before delivery. The 11 infants were born with no obstetric complication or birth defects. Five infants were breastfed. All infants were hepatitis B surface antigen negative 28-36 weeks after birth. Our preliminary data suggest that TDF use in the third trimester is safe, and effectively prevents VT of HBV from high viremic HBeAg-positive mothers.
    Digestive Diseases and Sciences 04/2012; 57(9):2423-9. · 2.26 Impact Factor
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    ABSTRACT: Adefovir and tenofovir are nucleotide analogues used as long-term therapy of chronic hepatitis B. Side effects are few, but prolonged and high-dose therapy has been associated with proximal renal tubular dysfunction (RTD). To assess the incidence of RTD during long-term nucleotide therapy of chronic hepatitis B. A total of 51 patients being treated at the Clinical Center, National Institutes of Health were studied. Diagnosis of RTD required de novo appearance of at least three of five features: hypophosphataemia, hypouricaemia, serum creatinine elevation, proteinuria or glucosuria. Among 51 patients treated for 1-10 (mean 7.4) years with adefovir (n = 42), tenofovir (n = 4) or adefovir followed by tenofovir (n = 5), 7 (14%) developed RTD. Time to onset ranged from 22 to 94 (mean 49) months with an estimated 10-year cumulative rate of 15%. All seven had low urinary percent maximal tubular reabsorption of phosphate (<82%). Patients with RTD were older (58 vs. 44 years; P = 0.01) and had lower baseline glomerular filtration rates (82 vs. 97 cc/min; P = 0.08) compared to those without; but did not differ in other features. Six patients with RTD were switched to entecavir, all subsequently had improvements in serum phosphate (2.0-3.0 mg/dL), creatinine (1.6-1.1 mg/dL), uric acid (2.7-3.8 mg/dL) and proteinuria. Renal tubular dysfunction develops in 15% of patients treated with adefovir or tenofovir for 2-9 years and is partially reversible with change to other antivirals. Monitoring for serum phosphate, creatinine and urinalysis is prudent during long-term adefovir and tenofovir therapy.
    Alimentary Pharmacology & Therapeutics 04/2012; 35(11):1317-25. · 4.55 Impact Factor

Publication Stats

6k Citations
1,259.65 Total Impact Points

Institutions

  • 2000–2014
    • National Institutes of Health
      • • Branch of Liver Diseases Branch (LDB)
      • • National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
      • • Branch of Digestive Diseases (DDB)
      Maryland, United States
  • 1998–2014
    • The National Institute of Diabetes and Digestive and Kidney Diseases
      Maryland, United States
  • 2011
    • Massachusetts General Hospital
      • Department of Medicine
      Boston, MA, United States
  • 2005–2011
    • Washington University in St. Louis
      • Division of Gastroenterology
      Saint Louis, MO, United States
  • 2010
    • New England Research Institutes
      Watertown, Massachusetts, United States
  • 2005–2010
    • University of Michigan
      • Department of Internal Medicine
      Ann Arbor, MI, United States
  • 2004–2009
    • Virginia Commonwealth University
      • Division of Gastroenterology, Hepatology and Nutrition
      Richmond, Virginia, United States
    • University of Texas Southwestern Medical Center
      • Division of Digestive and Liver Diseases
      Dallas, TX, United States
  • 2008
    • University of Southern California
      • Division of Gastrointestinal and Liver Diseases
      Los Angeles, CA, United States
  • 2006–2007
    • UConn Health Center
      • Department of Medicine
      Farmington, CT, United States
    • University of Colorado
      • Division of Gastroenterology and Hepatology
      Denver, CO, United States
    • University of Washington Seattle
      • Department of Laboratory Medicine
      Seattle, WA, United States
  • 1996–2005
    • Tulane University
      • Section of Gastroenterology
      New Orleans, LA, United States
  • 2003
    • University of Texas Medical Branch at Galveston
      • Department of Internal Medicine
      Galveston, TX, United States