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Highest Rated Articles

González-Peralta RP, Kelly DA, Haber B et al for the International Pediatric Hepatitis C Therapy Group Interferon alfa-2b in combination with ribavirin for the treatment of chronic hepatitis C in children: Efficacy, safety, and pharmacokinetics. Hepatology. 2005;42:1010-1018.

Decisions about management of HCV in children should be influenced by the natural history of HCV in children and by the risks and benefits of available treatment. According to Vogt et al, (Vogt et al. N Engl J Med 1999) as many as 45% of children may clear HCV spontaneously after 20 years. In the study, nearly all children who continued to have active viral replication had normal liver tests, and those who had biopsies had normal liver histology unless comorbidities were present. Insufficient numbers of children have been treated in controlled trials.

The report by Regino et al provides evidence that HCV in children can be treated as successfully as in adults with approximately the same requirement for dose reduction and with a comparable drop-out rate as in adults. It also provides guidance about ribavirin dosing (15 mg/kg/day). The same discordance in response rate of genotype 1 compared with genotypes 2/3 is seen in children. Now we are reasonably certain about the risks and benefits of treatment as it relates to virologic clearance. Based on the benign course of HCV in children, selection of which children to treat for HCV remains to be defined.

Hisada M, Chatterjee N, Kalaylioglu Z, Battjes RJ, Goedert JJ. Hepatitis C virus load and survival among injection drug users in the United States. Hepatology. 2005;1446-1452.

Previous reports have identified risk factors associated with progression to end-stage liver (ESLD) disease in HCV. A report from Baltimore looked at a number of factors possibly associated with disease progression. In a multivariate model, risk of ESLD was higher for patients aged 38 years or older at enrollment (adjusted relative incidence, 3.67; 95% CI, 1.96-6.88) and for those who reported ingestion of more than 260 g of alcohol per week (adjusted relative incidence, 3.60; 95% CI, 1.73-7.52). Viral load was not used in the model. (Thomas DL. JAMA 2000) The authors of the current report previously reported increasing viral load with age, but no association between viral load and development of ESLD in HIV/HCV coinfected individuals. (Goedert J Infect Dis 2001) The current report indicates that risk of death from ESLD is associated with increasing viral load independent of coinfection status or alcohol intake. Unfortunately, high viral load also makes currently available HCV therapy less likely to succeed. If confirmed, these findings will require re-thinking of the way most of us approach risk/benefit analysis for the HCV-infected patient. At the very least, closer monitoring (perhaps with more frequent biopsies, or surrogate tests for fibrosis) may be needed.

Rambaldi A, Jacobs B, Iaquinto G, Gluud C. Med. Sci. Milk thistle for alcoholic and/or hepatitis B or C liver diseases — a systematic cochrane hepato-biliary group review with meta-analyses of randomized clinical trials. Am J Gastroenterol. 2005;100: 2583-2591.

Milk thistle ( Silybum marianum ) is native to the Mediterranean area and grows wild throughout Europe, North America, and Australia.
(http://www.primary.net/~gic/herb/milkt.htm ) It has been used in Europe as a remedy for liver problems for thousands of years. It continues to be used widely by patients with liver disease. As such, it occupies a prominent place in the pantheon of alternative/complementary medicine.

In 2000, under its Evidence-based Practice Program , the Agency for Healthcare Research and Quality (AHRQ) analyzed the evidence for and against the clinical efficacy of milk thistle and concluded that the value for this agent in liver disease is not clearly established.
(http://www.ahrq.gov/clinic/epcsums/milktsum.htm ). In general, interpretation of the evidence is hampered by poor study methods and/or poor quality of reporting in publications. Problems in study design include heterogeneity in etiology and extent of liver disease, small sample sizes, and variation in formulation, dosing, and duration of milk thistle therapy. Possible benefit has been shown most frequently, but not consistently, for improvement in aminotransferases, and liver function tests are overwhelmingly the most common outcome measure studied. Survival and other clinical outcome measures have been studied least often, with both positive and negative findings. Available evidence is not sufficient to suggest whether milk thistle may be more effective for some liver diseases than others or if effectiveness might be related to duration of therapy or chronicity and severity of liver disease. Regarding adverse effects, little evidence is available regarding causality, but available evidence does suggest that milk thistle is associated with few, and generally minor, adverse effects.

The current update by Rambaldi et al confirms that, 5 years later, not much has changed. Insufficient quality evidence is available to recommend milk thistle as an adjunct to management of liver disease caused by alcohol, hepatitis B, or hepatitis C.

Tugwell BD, Patel PR, Williams IT et al. Transmission of hepatitis C virus to several organ and tissue recipients from an antibody-negative donor. Annals of Internal Medicine. 2005;143:648-654.

This is a case report of HCV occurring in several recipients of tissue from a single donor whose screening test for HCV was negative. The method of screening was determination of anti-HCV status. Considerable effort went into tracking down all tissue recipients, and slightly more than one-fourth were found to be HCV infected with the same HCV genotype. How could this occur? It is possible that a donor might have recently acquired HCV and had not yet developed anti-HCV. There are other reports, however, of chronic HCV viremia in the absence of measurable HCV antibodies. This is seen most often in those with chronic renal failure, but it may also occur in apparently healthy people. We have seen HCV transmitted to a renal transplant recipient by a related donor who repeatedly tested negative for anti-HCV but, as in the subject of this report, was HCV-viremic. Our recipient, unlike the patients in the current report, developed fatal fibrosing cholestatic hepatitis. This unfortunate outcome has led us to test for HCV RNA in potential donors, as recommended by the authors of this study.

American Journal of Gastroenterology
Rating	Article Title
	El-Zayadi AR, Attia M, Barakat EM. Response of hepatitis C genotype-4 naïve patients to 24 weeks of Peg-interferon-α2b/ribavirin or induction-dose interferon-a2b/ribavirin/amantadine: a non-randomized controlled study. Am J Gastroenterol. 2005;100: 2447-2452.
	Cheung RC, Currie S, Shen H et al. Chronic hepatitis C in Latinos: natural history, treatment eligibility, acceptance, and outcomes. Am J Gastroenterol. 2005;100: 2186-2193.
	Tien PC: Veterans Affairs Hepatitis C Resource Center Program: Office National Hepatitis C Program Office. Management and treatment of hepatitis C virus infection in HIV-infected adults: recommendations from the Veterans Affairs Hepatitis C Resource Center Program and National Hepatitis C Program Office. Am J Gastroenterol. 2005;100: 2338-2354.
	Jacobson IM, Gonzalez SA, Ahmed F et al. A randomized trial of pegylated interferon α-2b plus ribavirin in the retreatment of chronic hepatitis C. Am J Gastroenterol. 2005;100:2453–2462.
	Wang AY, Hickman IJ, Richards AA, Whitehead JP, Prins JB, MacDonald GA. High molecular weight adiponectin correlates with insulin sensitivity in patients with hepatitis C genotype 3, but not genotype 1 infection. Am J Gastroenterol. 2005;100: 2717-2723.
	Hand WL, Vasquez Y. Risk factors for hepatitis C on the Texas-Mexico border. Am J Gastroenterol. 2005;100:2180-2185.
	Gurguta C, Kauer C, Bergholz U, Formann E, Steindl-Munda P, Ferenci P. Tongue and skin hyperpigmentation during PEG-interferon-alpha/ribavirin therapy in dark-skinned non-Caucasian patients with chronic hepatitis C. Am J Gastroenterol. 2006;101:197-198.
Clinical Infectious Disease
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	Sherman KE, Shire NJ, Cernohous P et al. Liver injury and changes in hepatitis C Virus (HCV) RNA load associated with protease inhibitor-based antiretroviral therapy for treatment-naive HCV-HIV-coinfected patients: lopinavir-ritonavir versus nelfinavir. Clin Infect Dis. 2005;41:1186-1195.
	Kempinska A, Kwak EJ, Angel JB. Reactivation of hepatitis B infection following allogeneic bone marrow transplantation in a hepatitis B-immune patient: case report and review of the literature. Clin Infect Dis. 2005;41:1277-1282.
	Yazdanpanah Y, De Carli G, Migueres B et al. Risk factors for hepatitis C virus transmission to health care workers after occupational exposure: a European case-control study. Clin Infect Dis. 2005;41:1423-1430.
	Iorio R, Giannattasio A, Sepe A, Terracciano LM, Vecchione R, Vegnente A. Chronic hepatitis C in childhood: an 18-year experience. Clin Infect Dis. 2005;41:1431-1437.
	Macalino GE, Vlahov D, Dickinson BP, Schwartzapfel B, Rich JD. Community incidence of hepatitis B and C among reincarcerated women. Clin Infect Dis. 2005;41:998-1002.
	Overton ET, Sungkanuparph S, Powderly WG, Seyfried W, Groger RK, Aberg JA. Undetectable plasma HIV RNA load predicts success after hepatitis B vaccination in HIV-infected persons.Clin Infect Dis. 2005;41:1045-1048.
	Castrodale L, Fiore A, Schmidt T. Detection of immunoglobulin M antibody to hepatitis A virus in Alaska residents without other evidence of hepatitis. Clin Infect Dis. 2005;41:e86-e88.
	Marcus EL, Tur-Kaspa R. Chronic hepatitis C virus infection in older adults. Clin Infect Dis. 2005;41:1606-1612.
	Bani-Sadr F, Carrat F, Rosenthal E et al and the ANRS HC02-Ribavic Study Team. Spontaneous hepatic decompensation in patients coinfected with HIV and hepatitis C virus during interferon-ribavirin combination treatment. Clin Infect Dis. 2005;41:1806-1809.
European Journal of Gastroenterology and Hepatology
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	Foruny JR, Blazquez Javier, Moreno A. Safe use of pegylated interferon/ribavirin in hepatitis C virus cirrhotic patients with hypersplenism after partial splenic embolization. Eur J Gastroenterol Hepatol. 2005;17:1157-1164.
	Delwaide Jean, El Saouda R, Gerard C, Belaiche J, the Groupe Liegeois d'Etude des Virus Hepatotropes. Hepatitis C infection: eligibility for antiviral therapies. Eur J Gastroenterol Hepatol. 2005;17:1185-1189.
	Barrett S, Sweeney M, Crowe J. Host immune responses in hepatitis C virus clearance. Eur J Gastroenterol Hepatol. 2005;17:1089-1097.
	Gloro R, Hourmand-Ollivier I, Mosquet B et al. Fulminant hepatitis during self-medication with hydroalcoholic extract of green tea. Eur J Gastroenterol Hepatol. 2005;17:1135-1137.
	Palsson B, Verbaan H. Partial splenic embolization as pretreatment for antiviral therapy in hepatitis C virus infection. Eur J Gastroenterol Hepatol. 2005;17:1153-1155.
	Villa F, Rumi MG, Signorelli C et al. Onset of inflammatory bowel diseases during combined alpha-interferon and ribavirin therapy for chronic hepatitis C: report of two cases. Eur J Gastroenterol Hepatol. 2005;17:1243-1245.
	Schafer A, Scheurlen M, Felten M, Kraus MR. Physician-patient relationship and disclosure behaviour in chronic hepatitis C in a group of German outpatients. Eur J of Gastroenterol Hepatol. 2005;17:1387-1394.
Hepatology
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	Schofield DJ, Bartosch B, Shimizu YK et al. Human monoclonal antibodies that react with the E2 glycoprotein of hepatitis C virus and possess neutralizing activity. Hepatology. 2005;42:1055-1062.
	Grant WC, Jhaveri RR, McHutchison JG, Schulman KA, Kauf TL. Trends in health care resource use for hepatitis C virus infection in the United States. Hepatology. 2005;42:1406-1413.
	Schiano TD, Gutierrez JA , Walewski JL et al. Accelerated hepatitis C virus kinetics but similar survival rates in recipients of liver grafts from living versus deceased donors. Hepatology. 2005;42:1420-1428.
	Sansonno D, Tucci FA, De Re V et al. HCV-associated B cell clonalities in the liver do not carry the t(14;18) chromosomal translocation. Hepatology. 2005;42:1019-1027.
	Brandenburg B, Stockl L, Gutzeit C et al. A novel system for efficient gene transfer into primary human hepatocytes via cell-permeable hepatitis B virus-like particle. Hepatology. 2005;42:1300-1309.
	Youn JW, Park SH, Lavillette D et al. Sustained E2 antibody response correlates with reduced peak viremia after hepatitis C virus infection in the chimpanzee. Hepatology. 2005;42:1429-1436.
	Rice CM, You S. Treating hepatitis C: can you teach old dogs new tricks? Hepatology. 2005;42:1455-1458.
Liver Transplantation
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	Gawrieh S, Papouchado BG., Burgart LJ, Kobayashi S, Charlton MR, Gores GJ. Early hepatic stellate cell activation predicts severe hepatitis C recurrence after liver transplantation. Liver Transpl. 2005;11:1207-1213.
	Russo MW, Firpi RJ, Nelson DR, Schoonhoven R, Shrestha R, Fried MW. Early hepatic stellate cell activation is associated with advanced fibrosis after liver transplantation in recipients with hepatitis C. Liver Transpl. 2005;11:1235-1241.
	Eghtesad B, Fung JJ , Demetris AJ. Immunosuppression for liver transplantation in HCV-infected patients: mechanism-based principles. Liver Transpl. 2005;11:1343-1352.
	Mathurin P. Is alcoholic hepatitis an indication for transplantation? Current anagement and outcomes. Liver Transpl. 2005;11:S21-S24.
	Charlton M. Recurrence of hepatitis C infection: Where are we now? Liver Transpl. 2005;11:S57-S62.
	Carmiel-Haggai M, Fiel MI, Gaddipati HC. Recurrent hepatitis C after retransplantation: Factors affecting graft and patient outcome. Liver Transpl. 2005;11:1567-1573.