Kagawa, Tatehiro

Keeffe, Emmet B.

Yu, Ming-Lung

Hepatitis Research and Treatment

English

PubMed

Tatehiro Kagawa

Emmet B. Keeffe

Ming-Lung Yu

Crossref

Hindawi Publishing CorporationHepatitis Research and TreatmentVolume 2010, Article ID 275274, 2 pagesdoi:10.1155/2010/275274EditorialPegylated Interferon and Ribavirin Treatment forHepatitis C Virus InfectionTatehiro Kagawa,1 Emmet B. Keeffe,2 and Ming-Lung Yu31 Department of Gastroenterology, Tokai University School of Medicine, 143 Shimokasuya, Isehara 259-1193, Japan2 Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University Medical Center,Palo Alto, CA 94304-1509, USA3 Department of Internal Medicine, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung Medical University Hospital,Kaohsiung Medical University, Kaohsiung 801, TaiwanCorrespondence should be addressed to Tatehiro Kagawa, kagawa@is.icc.u-tokai.ac.jpReceived 25 November 2010; Accepted 25 November 2010Copyright © 2010 Tatehiro Kagawa et al. This is an open access article distributed under the Creative Commons AttributionLicense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properlycited.We are pleased to serve as editors of this special issue. Wewere gratified by the excellent response to the call for papersand the high quality of the eleven manuscripts that wereultimately accepted for this special issue.This issue begins, as is appropriate, with a historicalperspective by R. M. Friedman and S. Contente from theUniformed Services University of the Health Sciences ontreatment of chronic hepatitis C with interferon, followedby a paper by C.-H. Chen and M.-L. Yu from KaohsiungMedical University tracing the evolution of interferon-basedtherapy, including the addition of ribavirin and pegylationof interferon. Both of these papers provide an interestingcapsule of where we began with the initial recognition ofthe antiviral activity of interferon in 1957, followed by theevolution interferon-based therapy of chronic hepatitis Cwith the addition of ribavirin in the mid-1990s and thedemonstration of the superiority of pegylated interferon(peginterferon) plus ribavirin in the early 2000s. The sus-tained virologic response (SVR) rate increased from 8%–9%with interferon monotherapy to 30% in genotype 1 patientswith the addition of ribavirin, and then to 40%–50% withthe transition to peginterferon plus ribavirin. As noted inseveral papers in this special issue, we are on the thresholdof increasing the SVR rate in 2011 up to 65%–75% withthe addition of a protease inhibitor to the standard of carewith peginterferon plus ribavirin. Thus, advances in thetreatment of chronic hepatitis C continue to march forward,with SVR rates increasing from less than 10%with interferonmonotherapy to close to 75% in the very near future withtriple therapy using a protease inhibitor. What is remarkableis that this progress has all taken place within the past 20years. In the next paper, T. Kagawa and E. Keeﬀe reviewthe recent literature evaluating the long-term outcomesof antiviral therapy in patients with chronic hepatitis Cthat convincingly demonstrate the impact of interferon-based treatment of chronic hepatitis C. The published datashows slowed disease progression in patients who achieve anSVR, including improved inflammation and fibrosis scoreson follow-up biopsy, reduced incidence of hepatocellularcarcinoma, and prolonged life expectancy with reduced liver-related deaths. Thus, the progress in treatment over the past20 years is paying dividends to our patients.The prediction of response to interferon-based therapy isan important issue for patients considering embarking on acourse of therapy, and providers of care continue to improvetheir ability to predict success in individual patients by takinginto account baseline host (age, race, gender, histology (stageof fibrosis and presence or absence of steatosis), body weight,insulin resistance, and IL28B genotype) and viral factors(genotype and HCV RNA level). A number of papers inthis special issue address predictors of viral response. N.Izumi et al. provide a thorough and scholarly review ofthe various factors that predict an SVR and their relativeimportance. R. Cubillas et al. from Southwestern MedicalCenter in Dallas elegantly demonstrate that tumor necrosisfactor receptor 1 is upregulated in dendritic cells in patientswith chronic hepatitis C who respond to therapy. Althoughnot clinically available, R. Kubota et al. demonstrate that2 Hepatitis Research and Treatmenterythrocyte ribavirin levels can predict which patients aremore likely to achieve an early virologic response after 12weeks of treatment.A number of miscellaneous papers in this special issueaddress the treatment of chronic hepatitis C in a numberof special populations. M. Numata et al. from severalJapanese medical centers treated 122 patients with genotype1 infection and demonstrated by multivariate analysis thatadherence to peginterferon and ribavirin was the onlypredictor of SVR. The rate of SVR fell sharply when exposureto peginterferon was less than 80% and also decreased in astepwise fashion when ribavirin exposure was 60%–80% andless than 60% compared with greater than 80%. D. F. Meyeret al. from several New York medical centers report that dailyhigh-dose consensus interferon (24 µg) plus weight-basedribavirin was not successful in genotype 1 nonresponders toprior therapy and was associated with substantial side eﬀects.Y. Y. Hwang and R. H. S. Liang from Queen Mary Hospital inHong Kong review antiviral therapy in hematologic patientsand point out that the published literature demonstratesthat HCV RNA levels increase during chemotherapy andimmunosuppression and that there is a risk of reboundimmunity against hepatitis C with liver injury after dis-continuation of immunosuppression. They recommend thatclose monitoring during chemotherapy is appropriate andthat antiviral therapy with peginterferon and ribavirinshould be deferred until complete of chemotherapy andrecovery of immunity. H. Weclawiak et al. focus on themanagement of chronic hepatitis C during hemodialysisand reinforce the recommendation to treat during dialysis,as there is a high rate of SVR that eliminates recurrenceof HCV infection after kidney transplantation. They alsoreinforce the standard recommendation not to treat chronichepatitis C after kidney transplantation because of the highrisk of acute allograft rejection. Finally, Y. Sugawara et al.from the University of Tokyo provide a thorough reviewof the controversies and challenges in the management ofrecurrent chronic hepatitis C after liver transplantation.Although there is no general consensus on who, when andhow to treat, the overall SVR rate is 25%–45% with standardpeginterferon plus ribavirin, in spite of a high prevalenceof intolerability. The newer antiviral therapies in 2011 maybring greater success in the management of patients withposttransplant recurrent HCV infection.The editors are confident that the readers will enjoyreading this special issue and the diverse topics that areexpertly reviewed.Tatehiro KagawaEmmet B. 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Pegylated Interferon and Ribavirin Treatment for Hepatitis C Virus Infection

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Pegylated Interferon and Ribavirin Treatment for Hepatitis C Virus Infection

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