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Highest Rated Articles

Kamal SM, Moustafa KN, Chen J, et al. Duration of peginterferon therapy in acute hepatitis C: A randomized trial. Hepatology. 2006;43:923-931.

Kamal et al showed that high rates of sustained viral response (SVR) can be achieved with Pegylated Interferon Alpha 2b therapy in patients with acute hepatitis C virus (HCV) infection. Therapeutic regimens of 12 or 24 weeks were more effective than 8 weeks (82.4%, 91.2% and 67.6%, respectively). In patients with genotype 1, the 24-week regimen achieved 88% SVR and was superior to results for the other shorter regimens: 38% SVR for 8 weeks and 60% for 12 weeks, respectively (p<0.01 and p<0.04, respectively). Importantly, for those with a rapid viral response (RVR), no differences in outcomes were seen for the different treatment regimens (85%-88% SVR). This study may have been biased toward better results, given that patients with stronger immune response to acute hepatitis were included (high ALT values and three-fourths were symptomatic); however, treatment was delayed as patients had to have seroconverted and were screened for 8 to 12 weeks prior to starting therapy.

Leandro G, Mangia A, Hui J, Fabris P, et al. Relationship Between Steatosis, Inflammation, and Fibrosis in Chronic Hepatitis C: A Meta-Analysis of Individual Patient Data. Gastroenterology. 2006 Jun;130(6):1636-1642.

To define whether steatosis affects progression of liver disease in chronic hepatitis C infected patients, Leandro et al performed a multivariable, stepwise logistic regression analysis on individual patient data collected in 10 databases from 10 different countries (3068 patients). Steatosis was associated with HCV genotype 3, hepatic inflammation, ongoing alcohol abuse, and older age. Fibrosis was associated with hepatic inflammation, male sex, the presence of steatosis, and older age. The paper also offers an analysis by HCV genotype and by body mass index. The presence of steatosis in a genotype other than 3 has been associated with environmental factors. Even in genotype 3-infected patients, where this genotype is strongly associated with the presence of reversible steatosis, there is an association in-between steatosis and environmental factors like a high BMI and current alcohol abuse.

Data have now emerged that steatosis, either directly or indirectly via insulin resistance or steatohepatitis, negatively affects the natural history of chronic hepatitis C and the outcome of its treatment with pegylated interferon and ribavirin regimens. The health care provider should include the management of steatosis in the care of the patient with chronic hepatitis C.



Huang H, Shiffman ML, Cheung RC, et al. Identification of two gene variants associated with risk of advanced fibrosis in patients with chronic hepatitis C. Gastroenterology. 2006 Jun;130(6):1679-87. Epub 2006 Mar 6.

Huang et al studied single-nucleotide polymorphisms in two cohorts of HCV-infected patients, trying to identify any that would render these patients more or less likely to develop advanced fibrosis. Two markers in the genes DDX5 and CPT1A, and two diplotypes, including the DDX5 marker, were associated with advanced fibrosis in both cohorts. The authors offered a putative mechanism for this association is also offered: DDX5 might affect HCV RNA polymerase and NS5-dependent activation of stellate cells, and CPT1A may affect ß-oxidation and hepatocytes oxidative stress; both of these being protective functions negatively impacted by the polymorphisms.

One would hope that these discoveries and understandings will lead to timely and plausible interventions for clinical use.

Sanyal AJ, Banas C, Sargeant C, et al. Similarities and differences in outcomes of cirrhosis due to nonalcoholic steatohepatitis and hepatitis C. Hepatology. 2006 Apr;43(4):682-9.

Sanyal et al compared survival, liver synthetic failure, varices and variceal hemorrhage, ascites, encephalopathy, and HCC in 152 patients with nonalcoholic steatohepatitis (NASH) and cirrhosis who were paired with age-, sex-, and race-matched patients with HCV and cirrhosis. At baseline, the patients with NASH and cirrhosis were heavier and more frequently had hypertension, diabetes, and dyslipidemia (features of the metabolic syndrome). Those with NASH and cirrhosis were more likely to have cardiac mortality and were less likely to have ascites, HCC, or to die while having compensated liver disease.

Two important factors may have played a role in the greater morbidity and mortality outcomes of HCV-infected patients: greater lifetime alcohol consumption than patients with NASH and the fact that therapeutic regimens for HCV and cirrhosis were significant less effective in the 1990s than current therapies.

Jensen DM, Morgan TR, Marcellin P, et al. Early identification of HCV genotype 1 patients responding to 24 weeks peginterferon alpha-2a (40 kd)/ribavirin therapy. Hepatology. 2006;43:954-960.

In this retrospective study of the Hadzyiannis data [Ann Intern Med 2004;43:954-60], Jensen and colleagues identified predictors of early viral response (RVR) and sustained viral response (SVR) to pegylated interferon alpha 2a and ribavirin therapy in patients with chronic HCV, genotype 1, treated for 24 weeks. RVR is defined as undetectable HCV RNA at week 4 of antiviral treatment. Of 216 patients, 51 had an RVR (24%), and these were significantly more likely to achieve an SVR after 24 weeks of therapy than those with detectable HCV RNA at week 4 (88% vs 23%, respectively). Low baseline viral load (<600,000 IU/mL) and to a much lesser degree HCV subtype 1b were associated with a higher likelihood of RVR.

These results are almost identical to those obtained by Zeuzem et al (J Hepatol 2006;44:97-103). Together, these studies identify a subgroup of patients infected with genotype 1 who have low baseline viremia and rapid on treatment viral response, in whom a 24-week treatment regimen seems to be adequate and no worse than the standard 48-week treatment course, thereby offering reduction in side effects and cost.

American Journal of Gastroenterology
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	Danoff A, Khan O, Wan DW, et al. Sexual dysfunction is highly prevalent among men with chronic hepatitis C virus infection and negatively impacts health-related quality of life. Am J Gastroenterol. 2006 Jun;101(6):1235-43.
	Thabut D, Le Calvez S, Thibault V, et al. Hepatitis C in 6,865 patients 65 yr or older: a severe and neglected curable disease? Am J Gastroenterol. 2006 Jun;101(6):1260-7.
	Merriman NA, Porter SB, Brensinger CM, et al. Racial difference in mortality among U.S. veterans with HCV/HIV coinfection. Am J Gastroenterol. 2006 Apr;101(4):760-7.
	Brok J, Gluud LL, Gluud C; Cochrane Hepato-Biliary Group. Ribavirin monotherapy for chronic hepatitis C infection: a Cochrane Hepato-Biliary Group systematic review and meta-analysis of randomized trials. Am J Gastroenterol. 2006 Apr;101(4):842-7.
	Fontana RJ, Sanyal AJ, Mehta S, et al. Portal hypertensive gastropathy in chronic hepatitis C patients with bridging fibrosis and compensated cirrhosis: results from the HALT-C trial. Am J Gastroenterol. 2006 May;101(5):983-92.
	Krawitt EL, Gordon SR, Grace ND et al for the New York New England Study Team. A study of low dose peginterferon alpha-2b with ribavirin for the initial treatment of chronic hepatitis C. Am J Gastroenterol. 2006 Jun;101(6):1268-73.
Annals of Internal Medicine
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	Armstrong GL, Wasley A, Simard EP et al. The Prevalence of Hepatitis C Virus Infection in the United States, 1999 through 2002. Ann Intern Med. 2006, 144(10), 705-714.
	McGuire BM, Julian BA, Bynon JS, et. al. Brief communication: Glomerulonephritis in patients with hepatitis C cirrhosis undergoing liver transplantation. Ann Intern Med. 2006 May 16;144(10):735-41.
	Spaulding AC, Weinbaum CM, Lau DT et al. A framework for management of hepatitis C in prisons. Ann Intern Med. 2006 May 16;144(10):762-9.
	Dienstag JL. Hepatitis C: a bitter harvest. Ann Intern Med. 2006. 144(10):770-771.
Clinical Infectious Disease
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	Cooper C, Al-Bedwawi S, Lee C, Garber G. Rate of infectious complications during Interferon-Based therapy for hepatitis C is not related to neutropenia. Clin Infect Dis. 2006;42:1674-1678.
	Scott JD, McMahon BJ, Bruden D et al. High rate of spontaneous negativity for hepatitis C virus RNA after establishment of chronic infection in Alaska Natives. Clin Infect Dis. 2006 Apr 1;42(7):945-52.
	Barreiro P, Martin-Carbonero L, Nunez M et al. Predictors of liver fibrosis in HIV-infected patients with chronic hepatitis C virus (HCV) infection: assessment using transient elastometry and the role of HCV genotype 3. Clin Infect Dis. 2006 Apr 1;42(7):1032-9.
	Weis N, Lindhardt BO, Kronborg G et al. Impact of hepatitis C virus coinfection on response to highly active antiretroviral therapy and outcome in HIV-infected individuals: a nationwide cohort study. Clin Infect Dis. 2006 May 15;42(10):1481-7.
	Sagnelli E, Coppola N, Pisaturo M et al. Clinical and virological improvement of hepatitis B virus-related or hepatitis C virus-related chronic hepatitis with concomitant hepatitis A virus infection. Clin Infect Dis. 2006 Jun 1;42(11):1536-43.
	McGovern BH, Wurcel A, Kim AY et al. Acute hepatitis C virus infection in incarcerated injection drug users. Clin Infect Dis. 2006 Jun 15;42(12):1663-70.
European Journal of Gastroenterology and Hepatology
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	Roche B, Samuel D. Aspects of hepatitis C virus infection relating to liver transplantation. Eur J Gastroenterol Hepatol. 2006 Apr;18(4):313-20.
	Forton D, Taylor-Robinson S, Thomas H. Central nervous system changes in hepatitis C virus infection. Eur J Gastroenterol Hepatol. 18(4):333-338, April 2006.
	Herrmann E, Zeuzem S. The kinetics of hepatitis C virus. Eur J of Gastroenterol Hepatol. 18(4):339-342, April 2006.
	Lawson A, Ryder S. Progression of hepatic fibrosis in chronic hepatitis C and the need for treatment in mild disease. Eur J Gastroenterol Hepatol. 18(4):343-347, April 2006.
	Zickmund SL, Bryce CL, Blasiole JA et al. Majority of patients with hepatitis C express physical, mental, and social difficulties with antiviral treatment. Eur J Gastroenterol Hepatol. 2006 Apr;18(4):381-8.
	Scott BB, Egner WB, on behalf of the Trent Hepatitis C Study Group. Does [alpha]1-antitrypsin phenotype PiMZ increase the risk of fibrosis in liver disease due to hepatitis C virus infection? Eur J Gastroenterol Hepatol. 18(5):521-523, May 2006.
	Cozzolongo R, Betterle C, Fabris P et al. Onset of type 1 diabetes mellitus during peginterferon [alpha]-2b plus ribavirin treatment for chronic hepatitis C. Eur J Gastroenterol Hepatol. 18(6):689-692, June 2006.
Gastroenterology
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	Berg T, von Wagner M, Nasser S et al. Extended treatment duration for hepatitis C virus type 1: comparing 48 versus 72 weeks of peginterferon-alfa-2a plus ribavirin. Gastroenterology. 2006 Apr;130(4):1086-97.
	Pal S, Sullivan DG, Kim S et al. Productive replication of hepatitis C virus in perihepatic lymph nodes in vivo: implications of HCV lymphotropism. Gastroenterology. 2006 Apr;130(4):1107-16.
	Mirandola S, Realdon S, Iqbal J et al. Liver microsomal triglyceride transfer protein is involved in hepatitis C liver steatosis. Gastroenterology. 2006 Jun;130(6):1661-9. Epub 2006 Mar 6.
	Furutani T, Hino K, Okuda M, et al. Hepatic iron overload induces hepatocellular carcinoma in transgenic mice expressing the hepatitis C virus polyprotein. Gastroenterology. 2006 Jun;130(7):2087-98.
	Paradis V, Asselah T, Dargere D et al. Serum proteome to predict virologic response in patients with hepatitis C treated by pegylated interferon plus ribavirin. Gastroenterology. 2006 Jun;130(7):2189-97.
Hepatology
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	Kamal SM, Turner B, He Q et al. Progression of fibrosis in hepatitis C with and without schistosomiasis: correlation with serum markers of fibrosis. Hepatology. 2006 Apr;43(4):771-9.
	Perumalswami P, Kleiner DE, Lutchman G et al. Steatosis and progression of fibrosis in untreated patients with chronic hepatitis C infection. Hepatology. 2006;43:780-787.
	Sangiovanni A, Prati GM, Fasani P et al. The natural history of compensated cirrhosis due to hepatitis C virus: A 17-year cohort study of 214 patients. Hepatology. 2006 Jun;43(6):1303-10.
	Volkmann X, Cornberg M, Wedemeyer H et al. Caspase activation is required for antiviral treatment response in chronic hepatitis C virus infection. Hepatology. 2006 Jun;43(6):1311-6.
	Paeshuyse J, Kaul A, De Clercq E et al. The non-immunosuppressive cyclosporin DEBIO-025 is a potent inhibitor of hepatitis C virus replication in vitro. Hepatology. 2006 Apr;43(4):761-70.
	Wilson LE, Torbenson M, Astemborski J et al. Progression of liver fibrosis among injection drug users with chronic hepatitis C. Hepatology. 2006 Apr;43(4):788-95.
	Duong FH, Christen V, Filipowicz M, Heim MH. S-Adenosylmethionine and betaine correct hepatitis C virus induced inhibition of interferon signaling in vitro. Hepatology. 2006 Apr;43(4):796-806.
	Strickland GT. Liver disease in Egypt: Hepatitis C superseded schistosomiasis as a result of iatrogenic and biological factors. Hepatology. 2006;43:915-922.
	von Hahn T, Lindenbach BD, Boullier A et al. Oxidized low-density lipoprotein inhibits hepatitis C virus cell entry in human hepatoma cells. Hepatology. 2006;43:932-942.
	Talal AH, Ribeiro RM, Powers KA, Grace M. Pharmacodynamics of PEG-IFN alpha differentiate HIV/HCV coinfected sustained virological responders from nonresponders. Hepatology. 2006;43:943-953.
	Lanford RE, Guerra B, Lee H, Chavez D, Brasky KM, Bigger CB. Genomic response to interferon-alpha in chimpanzees: Implications of rapid downregulation for hepatitis C kinetics. Hepatology. 2006;43:961-972.
	Callender GG, Rosen HR, Roszkowski JJ et al. Identification of a hepatitis C virus-reactive T cell receptor that does not require CD8 for target cell recognition. Hepatology. 2006;43:973-981.
	Kuiken C, Mizokami M, Deleage G et al. Hepatitis C databases, principles and utility to researchers. Hepatology. 2006;43:1157-1165.
	Charlton MR, Pockros PJ, Harrison SA. Impact of obesity on treatment of chronic hepatitis C. Hepatology. 2006 Jun;43(6):1177-86.
	Fang X, Zeisel MB, Wilpert J et. al. Host cell responses induced by hepatitis C virus binding. Hepatology. 2006 Jun;43(6):1326-36.
	Saadoun D, Asselah T, Resche-Rigon M et al. Cryoglobulinemia is associated with steatosis and fibrosis in chronic hepatitis C. Hepatology. 2006 Jun;43(6):1337-45.
	Strnad P, Lienau TC, Tao GZ et al. Keratin variants associate with progression of fibrosis during chronic hepatitis C infection. Hepatology. 2006 Jun;43(6):1354-63.
	Frick DN. Step-by-step progress toward understanding the hepatitis C virus RNA helicase. Hepatology. 2006 Jun;43(6):1392-5.
	Shiina M, Rehermann B. Hepatitis C vaccines: Inducing and challenging memory T cells. Hepatology. 2006 Jun;43(6):1395-8.
Journal Acquired Immune Deficiency Syndrome
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	Fishbein DA, Lo Y, Netski D, Thomas DL, Klein RS. Predictors of hepatitis C virus RNA levels in a prospective cohort study of drug users. J Acquir Immune Defic Syndr. 2006 Apr 1;41(4):471-6.
	Gonzalez SA, Liu RC, Edlin BR, Jacobson IM, Talal AH. HIV/Hepatitis C Virus-Coinfected Patients With Normal Alanine Aminotransferase Levels. J Acquir Immune Defic Syndr. 2006 Apr 15;41(15):582-589.
Liver Transplantation
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	Guo L, Orrego M, Rodriguez-Luna H, Balan V et al. Living donor liver transplantation for hepatitis C-related cirrhosis: no difference in histological recurrence when compared to deceased donor liver transplantation recipients. Liver Transpl. 2006 Apr;12(4):560-5.
	Langrehr JM, Puhl G, Bahra M et al. Influence of donor/recipient HLA-matching on outcome and recurrence of hepatitis C after liver transplantation. Liver Transpl. 2006 Apr;12(4):644-51.