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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/advagg_css\/css__ce2QY63WIanKyr8eSq7eavr1XQRRmFD6ZSmwpyJi8lM__zXwFqpqmxrZOXXcd_TpBQpjuELbmIP9wBR5UuTDWAO4__YJWWMMdfCJuAFm5cUEp88OsodhO3ZA-2lzRfoBsSlk4.css\u0022 media=\u0022all\u0022 \/\u003E\n\u003Clink rel=\u0027stylesheet\u0027 type=\u0027text\/css\u0027 href=\u0027\/sites\/all\/modules\/contrib\/panels\/plugins\/layouts\/onecol\/onecol.css\u0027 \/\u003E\u003C\/head\u003E\u003Cbody\u003E\u003Cdiv class=\u0022panels-ajax-tab-panel panels-ajax-tab-panel-sageoa-tab-art\u0022\u003E\u003Cdiv class=\u0022panel-display panel-1col clearfix\u0022 \u003E\n  \u003Cdiv class=\u0022panel-panel panel-col\u0022\u003E\n    \u003Cdiv\u003E\u003Cdiv class=\u0022panel-pane pane-highwire-markup\u0022 \u003E\n  \n      \n  \n  \u003Cdiv class=\u0022pane-content\u0022\u003E\n    \u003Cdiv class=\u0022highwire-markup\u0022\u003E\u003Cdiv xmlns=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022 id=\u0022content-block-markup\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\n            \u003Cp id=\u0022p-1\u0022\u003ENew research about the treatment of hepatitis C is discussed in this article. Specific topics include sofosbuvir-based therapy, new Interferon- and ribavirin-free therapies, as well as the use of alpha-fetoprotein to predict hepatocellular carcinoma.\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003EViral Infections\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003ELiver Conditions\u003C\/li\u003E\u003C\/ul\u003E\u003Cul class=\u0022kwd-group clinical-trial\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003EHepatology\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EViral Infections\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003ELiver Conditions\u003C\/li\u003E\u003C\/ul\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-1\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ESOFOSBUVIR-BASED THERAPY FOR HEPATITIS C VIRUS\u003C\/h2\u003E\n         \u003Cp id=\u0022p-2\u0022\u003EK. Rajender Reddy, MD, University of Pennsylvania, Philadelphia, Pennsylvania, USA, discussed sofosbuvir (SOF)-based therapy for hepatitis C virus (HCV)-infected patients. Direct-acting anti-HCV compounds are categorized concerning activity. Inhibitors of nonstructural (NS) protein 5A include dalatasvir, ledipasvir, and ABT-267. Polymerase inhibitors (ie, non-nucleoside [NUC] NS5 and NUC NS5B inhibitors) include SOF, mericitabine, ALS-2200, ABT-333, ABT-072, VX-222, BMS-731225, deleobuvir, setrobuvir, and filibuvir. NS3 protease inhibitors include ABT-450 in combination with ritonavir, MK-5172, asunaprevir, danoprevir, sovaprevir, simeprevir, faldaprevir, baceprevir, and telaprevir.\u003C\/p\u003E\n         \u003Cp id=\u0022p-3\u0022\u003EThe effectiveness of a 12-week SOF plus ribavirin (RBV) regimen in treatment-na\u00efve patients infected with HCV genotype 1 has been chronicled [Gane EJ et al. \u003Cem\u003EN Engl J Med.\u003C\/em\u003E 2013]. High sustained virologic response at 24 weeks (SVR24) rates were also obtained using the 12-week regimen in the absence of pegylated interferon (PEG) and with varying durations of interferon treatment. SOF monotherapy was not as effective.\u003C\/p\u003E\n         \u003Cp id=\u0022p-4\u0022\u003EThe open-label NEUTRINO trial [NCT1641640] examined SOF plus PEG\/RBV in genotype 1, 4, and 6 patients. High SVR12 rates in all genotypes in cirrhotic and noncirrhotic black and nonblack patients were evident [Lawitz et al. \u003Cem\u003EN Engl J Med.\u003C\/em\u003E 2013]. SOF was also effective in the POSITRON trial [\u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT01542788\u0026amp;atom=%2Fspmdc%2F14%2F48%2F26.atom\u0022\u003ENCT01542788\u003C\/a\u003E] for HCV genotype 2 cirrhotic and noncirrhotic patients refractory to other treatments; the response (SVR12) was less pronounced for genotype 3 [Jacobson IM et al. \u003Cem\u003EN Engl J Med.\u003C\/em\u003E 2013]. Treatment of prior relapsers or nonresponders with a 12- or 16-week regimen involving SOF plus RBV in the FUSION trial [\u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT01604850\u0026amp;atom=%2Fspmdc%2F14%2F48%2F26.atom\u0022\u003ENCT01604850\u003C\/a\u003E] was also more effective in genotype 2 noncirrhotic patients, especially with longer treatment [Jacobson IM et al. \u003Cem\u003EN Engl J Med.\u003C\/em\u003E 2013]. The FISSION trial [\u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT01497366\u0026amp;atom=%2Fspmdc%2F14%2F48%2F26.atom\u0022\u003ENCT01497366\u003C\/a\u003E] documented a markedly better response to 12 weeks of SOF plus RBV versus PEG plus RBV in noncirrhotic, treatment-na\u00efve, genotype 2 patients. SVR12 displayed by their cirrhotic counterparts, and cirrhotic and noncirrhotic patients infected with HCV genotype 3, was relatively poor [Lawitz et al. \u003Cem\u003EN Engl J Med.\u003C\/em\u003E 2013].\u003C\/p\u003E\n         \u003Cp id=\u0022p-5\u0022\u003EIn the VALENCE trial [\u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT01682720\u0026amp;atom=%2Fspmdc%2F14%2F48%2F26.atom\u0022\u003ENCT01682720\u003C\/a\u003E], SOF plus RBV was offered for 12 or 24 weeks. The extended treatment produced high SVR12 rates in HCV genotype 2 or 3 treatment-na\u00efve and treatment-experienced cirrhotic and noncirrhotic patients [Zeuzem S et al. \u003Cem\u003EN Engl J Med.\u003C\/em\u003E 2014].\u003C\/p\u003E\n         \u003Cp id=\u0022p-6\u0022\u003EION-1 [\u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT01701401\u0026amp;atom=%2Fspmdc%2F14%2F48%2F26.atom\u0022\u003ENCT01701401\u003C\/a\u003E] and ION-2 [NTC01768286] chronicled the efficacy of 12- or 24-week treatment with a PEG- and RBV-free regimen (SOF + ledipasvir) in HCV genotype 1-infected cirrhotic and noncirrhotic, treatment-na\u00efve and treatment-experienced patients, including patients who failed prior therapy [Afdhal N et al. \u003Cem\u003EN Engl J Med.\u003C\/em\u003E 2014a, 2014b]. A shorter duration (8-week) may be effective [Kowdley KV et al. \u003Cem\u003EN Engl J Med.\u003C\/em\u003E 2014], with even shorter treatment requiring the addition of a third direct-acting antiviral agent [Gane EJ. \u003Cem\u003EGastroenterol\u003C\/em\u003E. 2014].\u003C\/p\u003E\n         \u003Cp id=\u0022p-7\u0022\u003EThe collective findings point to the availability of various treatment options, with the selected platform treatment depending on a number of factors.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-2\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ENEW INTERFERON- AND RIBAVIRIN-FREE THERAPIES FOR HEPATITIS C VIRUS INFECTION\u003C\/h2\u003E\n         \u003Cp id=\u0022p-8\u0022\u003EGregory Everson, MD, University of Colorado, Denver, Colorado, USA, discussed possible HCV therapies that do not involve PEG and RBV. These focus on the 3 aforementioned targets of HCV replication\u2014NS5A, NUC\/non-NUC NS5B, and NS3 protease [Gane EJ, Agarwal K. \u003Cem\u003EAm J Transplant\u003C\/em\u003E. 2014].\u003C\/p\u003E\n         \u003Cp id=\u0022p-9\u0022\u003EAn approach that may be very effective in HCV control uses a combination of ABT450 (protease inhibitor), ritonavir (enhances ABT450 action), ombitasvir (NS5a inhibitor), dasabuvir (non-NUC protease inhibitor) \u00b1 RBV. Six phase 3 trials have examined this combination.\u003C\/p\u003E\n         \u003Cp id=\u0022p-10\u0022\u003EIn noncirrhotic patients, the regimen including RBV produced high SVR12 rates in HCV genotype 1-infected, treatment-na\u00efve [SAPPHIRE I; NCT0716585] or treatment-experienced patients, of whom nearly half were prior nonresponders [SAPPHIRE II; \u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT01715415\u0026amp;atom=%2Fspmdc%2F14%2F48%2F26.atom\u0022\u003ENCT01715415\u003C\/a\u003E; Feld JJ et al. \u003Cem\u003EN Engl J Med.\u003C\/em\u003E 2014a, 2014b]. SVR12 was unaffected by factors that diminish response to interferon-based treatment.\u003C\/p\u003E\n         \u003Cp id=\u0022p-11\u0022\u003ERBV may not be necessary for an anti-HCV effect in noncirrhotic patients, based on results of high SVR12 from the 12-week use of the RBV-free regimen in HCV genotype 1b-infected, treatment-experienced or treatment-na\u00efve patients in the PEARL II [\u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT01674725\u0026amp;atom=%2Fspmdc%2F14%2F48%2F26.atom\u0022\u003ENCT01674725\u003C\/a\u003E] and PEARL III [\u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT01767116\u0026amp;atom=%2Fspmdc%2F14%2F48%2F26.atom\u0022\u003ENCT01767116\u003C\/a\u003E] trials, respectively, and HCV genotype 1a-infected, treatment-na\u00efve patients in the PEARL IV trial [\u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT01833533\u0026amp;atom=%2Fspmdc%2F14%2F48%2F26.atom\u0022\u003ENCT01833533\u003C\/a\u003E; Andreone P et al. \u003Cem\u003EGastroenterol\u003C\/em\u003E. 2014; Ferenci P et al. \u003Cem\u003EN Engl J Med.\u003C\/em\u003E 2014]. RBV may be needed for optimal anti-HCV effect in genotype 1a patients.\u003C\/p\u003E\n         \u003Cp id=\u0022p-12\u0022\u003EThe influence of cirrhosis was examined in the TURQUOISE II trial [\u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT01704755\u0026amp;atom=%2Fspmdc%2F14%2F48%2F26.atom\u0022\u003ENCT01704755\u003C\/a\u003E]. The 12- and 24-week regimen included RBV. High SVR12 rates were evident, with prior nonresponders benefiting most from the longer treatment duration [Poordad F et al. \u003Cem\u003EN Engl J Med.\u003C\/em\u003E 2014].\u003C\/p\u003E\n         \u003Cp id=\u0022p-13\u0022\u003EAnother potentially efficacious regimen uses the protease inhibitor asunaprevir + NS5a protein inhibitor daclatasvir plus non-NUC polymerase inhibitor BMS-791325. Evaluation of fixed doses in HCV genotype 1a and 1b, cirrhotic, and noncirrhotic [Everson GT et al. \u003Cem\u003EGastroenterol\u003C\/em\u003E. 2014] patients demonstrated high SVR12, particularly for genotype 1a. Findings of the HALLMARK-DUEL trial [\u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT01581203\u0026amp;atom=%2Fspmdc%2F14%2F48%2F26.atom\u0022\u003ENCT01581203\u003C\/a\u003E] indicate that the asunaprevir plus daclatasvir combination may also be useful [Manns M et al. \u003Cem\u003ELancet\u003C\/em\u003E 2014].\u003C\/p\u003E\n         \u003Cp id=\u0022p-14\u0022\u003EThe as-yet unpublished C-WORTHY trial of the protease inhibitor MK-5172 and the NS5a protein inhibitor MK-8742 demonstrated high SVR12 rates for HCV noncirrhotic patients with or without RBV and for HCV\/HIV coinfected patients in the RBV-containing regimen, with similar patterns evident for patients with cirrhosis and prior nonresponders.\u003C\/p\u003E\n         \u003Cp id=\u0022p-15\u0022\u003EThese treatments are expensive. However, the costs of not treating chronic HCV infection are considerable.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-3\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EPREDICTING DEVELOPMENT OF HEPATOCELLULAR CARCINOMA IN HCV-INFECTED PATIENTS\u003C\/h2\u003E\n         \u003Cp id=\u0022p-16\u0022\u003EJames Trotter, MD, Baylor University Medical Center, Waco, Texas, USA, discussed the use of alpha-fetoprotein (AFP) to predict hepatocellular carcinoma (HCC).\u003C\/p\u003E\n         \u003Cp id=\u0022p-17\u0022\u003EAFP is a serum protein that fulfills much of the functions of albumin in the fetal and postnatal period. It is elevated during hepatic proliferation in development, regeneration, and malignancy. Although easy to measure in blood, AFP is not produced by 25% to 30% of HCCs, producing a substantial false-negative rate. Moreover, AFP can be elevated in cases of hepatitis and cirrhosis, producing false-positive results.\u003C\/p\u003E\n         \u003Cp id=\u0022p-18\u0022\u003EEfforts to find better predictive models of HCC have focused on the analysis of data points from the electronic medical records of thousands of patients to generate predictive models using common lab tests, including aspartate aminotransferase, alanine aminotransferase (ALT), alkaline phosphatise, bilirubin, prothrombin, and platelets. The data mining, which is easier and less expensive to do than actual studies, is based on known associations of advanced age and more severe\/longer duration of liver disease with HCC, and the lack of association of ALT with elevated AFP.\u003C\/p\u003E\n         \u003Cp id=\u0022p-19\u0022\u003EThe Department of Veterans Affairs database was examined to identify patients with HCV infection. Patients (n = 11 721; median age 52.0 years, 98.1% male, and, limiting generalization of the findings, only 39% non-Hispanic white patients) treated from 1998 to 2005 had antibody to HCV, detectable HCV RNA, cirrhosis, and \u2265 1 measurement of serum AFP after HCV diagnosis. The total number of AFP tests was 35 494. By 2005, 987 (8.4%) of the patients had developed HCC. The median follow-up was 3.5 years.\u003C\/p\u003E\n         \u003Cp id=\u0022p-20\u0022\u003EAFP level, ALT, platelet count, and age were linked with increased frequency of HCC. The probability of HCC was three times higher for normal vs high ALT. The risk of HCC was increased as platelet count decreased; low platelet number was indicative of more severe and prolonged liver disease and worse portal hypertension. Finally, HCC risk increased with age.\u003C\/p\u003E\n         \u003Cp id=\u0022p-21\u0022\u003EThe findings offer the possibility that data from common lab tests can be used to compute a score that is predictive of HCC risk. The real-life implications of the level of risk (eg, 10% vs 30%) remain to be clarified.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2014 MD Conference Express\u00ae\u003C\/li\u003E\u003C\/ul\u003E\u003Cspan class=\u0022highwire-journal-article-marker-end\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Cspan id=\u0022related-urls\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Ca href=\u0022http:\/\/mdc.sagepub.com\/content\/14\/48\/26.abstract\u0022 class=\u0022hw-link hw-link-article-abstract\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView Summary\u003C\/a\u003E\u003C\/div\u003E  \u003C\/div\u003E\n\n  \n  \u003C\/div\u003E\n\u003C\/div\u003E\n  \u003C\/div\u003E\n\u003C\/div\u003E\n\u003C\/div\u003E\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_openurl.js?nzog0d\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}