October 15, 2013

A New Era is Dawning in Hepatitis C Therapy

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By George Budwell | More Articles
October 15, 2013 | Comments (0)

The standard of care for Hepatitis C (HCV) radically changed when the first direct-acting antiviral agents hit the market two years ago. Prior to their approval, the standard of care consisted of painful interferon injections 3-5 times a week for up to 48 weeks. Worse still is the fact that only about 50% of patients are even responsive to interferon, and the injections tend to make patients feel like they have the flu throughout the course of treatment.

With such a high cost compared to the potential benefits of interferon treatments, researchers have been busy looking for new oral-based therapies that are interferon-free. Direct-acting antiviral agents have been the result of this effort. Presently, there are over 20 such agents under development, with two coming up for FDA review later this month.

Gilead (NASDAQ: GILD ) is seeking approval for its much anticipated sofosbuvir on October 25th, whereas Johnson & Johnson (NYSE: JNJ ) will present its approval case for the more niche-based simeprevir a day before. Abbvie (NYSE: ABBV ) and Bristol-Meyers Squibb (NYSE: BMY ) are also expected to file New Drug Applications for their own all-oral HCV concoctions next year.

Are Sofosbuvir and Simprevir interferon-free?

The short answer is well, yes and no—or perhaps, at least not yet. While these drugs have been billed as the next generation of HCV drugs, the truth is they are more like a stepping-stone towards truly all-oral therapies that are interferon-free.

Presently, simeprevir and sofosbuvir are both seeking approval as treatments for HCV genotype 1 taken alongside interferon injections. The major advancement is that patients show dramatically improved cure rates on these particular direct-acting antiviral agents—up to 95% in clinical trials for sofosbuvir.

That said, sofosbuvir is up for approval as an interferon-free treatment for the rarer forms of HVC, namely genotypes 2 or 3. Because genotype 1 is by far the most prevalent form of the disease worldwide, however, the ultimate goal is to develop interferon-free drugs for this particular indication.

What’s the next step towards this goal?

Abbvie, Bristol-Myers Squibb, and Gilead have all been burning the midnight oil testing different combos of their various interferon-free treatments in hopes of producing such a therapy. The good news is that the results have been, well, nothing short of amazing.

The interim results of the COSMOS study testing a combo of simeprevir and sofosbuvir, for example, showed greater than 90% cure rates. Another study looking at a combo of Gilead and Bristol-Myers Squib’s drugs resulted in a 100% cure rate. While it’s unclear if these drug combos will receive explicit FDA approval due to the enormous costs associated with running such trials, doctors could use these combos off-label once the individual drugs have been approved. Based on these promising results, I expect this will be the case. 

Why are there so many companies racing to develop HCV therapies?

The long list of Big Pharma companies developing all-oral HCV is certainly impressive. Yet, it’s important to keep in mind that they are not undertaking this wildly expensive endeavor for humanitarian purposes only.

With a market size estimated at $20 billion already, there will probably be multiple all-oral based HCV therapies within the next decade, and more than one blockbuster among the group. Sofosbuvir, if approved, should see peak sales topping $6 billion. And even simprevir with its niche market as an indication for severe forms of HCV is likely going to generate sales over $600 million a year.

With both sofosbuvir and simprevir receiving Priority Review status from the FDA, it’s likely both drugs will be approved. Even so, the sheer size of the HCV market and the potential for combination treatments, suggests that front runner status won’t necessarily confer a strong competitive advantage. I expect doctors will experiment with these different drugs to find what works best in the real world. And only time will tell which of these new generation HCV therapies will get the lion’s share of the HCV market.

Source

Journal of Viral Hepatitis

A Meta-analysis

C. G. Tsiara, G. K. Nikolopoulos, N. L. Dimou, P. G. Bagos, G. Saroglou, E. Velonakis, A. Hatzakis

J Viral Hepat 

Abstract and Introduction

Abstract

Co-infection of human immunodeficiency virus (HIV) with hepatitis C virus (HCV) is rather common. In the era of highly active antiretroviral therapy (HAART), viral hepatitis could result in adverse outcomes in HIV+ patients. The current meta-analysis aims to evaluate the impact of HCV on immunological and virological responses after HAART initiation in HIV/HCV co-infected individuals by synthesizing the existing scientific evidence. A comprehensive search of electronic databases was performed. Eligible studies were analysed using univariate and multivariate meta-analytic methods. Totally, 21 studies involving 22533 individuals were eligible. The estimated summary difference in CD4 cell counts increase between HIV and HIV/HCV co-infected subjects after 3–12 months on HAART was 34.86 cells/mm3 [95% confidence interval (CI): 16.82–52.89]. The difference was more prominent in patients with baseline CD4 counts below 350 cells/mm3 (38.97, 95% CI: 20.00–57.93) and attenuated 2 years later (13.43, 95% CI: 0.83–26.04). The analysis of ratio measures yielded similar findings. The virological control remained unaffected by the presence of HCV (adjusted Hazard Ratio for co-infected patients vs those with HIV alone: 0.99, 95% CI: 0.91–1.07). The bivariate meta-analytic method confirmed the results of the univariate approaches. This meta-analysis supports the adverse effect of HCV on immune recovery of HIV+ patients initiating HAART, especially of those with initially impaired immunologic status. Although this effect diminishes over time, early administration of HAART in the setting of co-infection seems to be justified.

Introduction

The introduction of highly active antiretroviral therapy (HAART) led to an impressive decrease in morbidity and mortality of people infected by human immunodeficiency virus (HIV),[1, 2] but their prolonged survival allowed the emergence of co-morbidities, including infection with hepatitis C virus (HCV).

Double infection by HIV and HCV is common due to similar modes of transmission. Globally, nearly, 20 per cent of individuals with HIV have chronic hepatitis C.[3] Among HIV+ injecting drug users (IDUs), the prevalence of HCV infection ranges between 82 and 93 per cent.[4–7] HCV incidence has also increased in HIV+ male homosexuals during the last decade.[8]

Primary studies assessing the impact of HCV on HIV disease progression have yielded conflicting results.[9–12] A recent meta-analysis showed that HIV/HCV co-infection did not affect the incidence of acquired immune deficiency syndrome (AIDS) but increased overall mortality in the HAART era.[13] In terms of early HAART effectiveness, a quantitative synthesis in 2005 showed a less robust immune reconstitution in co-infected patients who initiated antiretroviral treatment.[14]

In the meantime, more relevant studies have been undertaken. The new pieces of information and the lack of a summary appraisal of virological response to HAART in the HIV/HCV setting warranted the conduct of an updated systematic review. The aim of the current meta-analysis was to combine and evaluate the accumulated scientific evidence concerning the effect of HCV on immunological and virological response in HIV-infected patients receiving HAART or combined antiretroviral treatment (c-ART) including at least 3 drugs.

Materials and Methods

Eligibility Criteria, Data Sources and Search Strategy

This meta-analysis was performed according to the MOOSE guidelines[15] and the PRISMA statement.[16] Studies of HIV+ patients were included in the analysis if: (i) they had examined the effect of HIV/HCV co-infection on immunological and/or virological response of persons receiving HAART or c-ART, (ii) they had included HAART-naïve patients at baseline and (iii) they had provided a value for CD4 T-cell counts or HIV-RNA levels difference from baseline to 3–24 months after ART initiation, or an estimate of Relative Risk (RR) for immunological and/or virological response, or sufficient data to calculate these measures. No language restrictions were imposed.

Pertinent studies were identified in Medline, Scopus and ISI Web of Science using a combination of the following terms: 'HIV', 'HCV', 'HAART', 'antiretroviral treatment', 'CD4 T', 'HIV-RNA' and 'viral load' (last search: February 2012). Titles and abstracts were screened to exclude irrelevant records. Full-text versions of the remaining articles were evaluated for eligibility. References of relevant publications and conference abstracts were also appraised to identify further studies for inclusion.

Data Extraction

Data were extracted by C.T. and G.N., and discrepancies were resolved by consensus. For each eligible study, the following information, if available, was retrieved: (i) first author's name, year of publication, geographic setting and study design, (ii) diagnostic method for HCV infection, (iii) number of participants and length of follow up, (iv) patients' baseline characteristics and laboratory data, (v) mean differences (with their standard deviations) in CD4 T-cell counts and HIV-RNA levels between measurements at the time of HAART or c-ART initiation and those 3–24 months later and (vi) RRs of achieving a CD4 T-cell increase and/or a HIV-RNA reduction with the corresponding 95% confidence intervals (CIs).

Statistical Analysis

Unstandardized mean differences and their 95% CIs were analysed using fixed- and random-effects models.[17] Combined RRs were derived from the univariate random-effects method.[18] Hazard Ratios (HRs) in individual studies, if not directly provided, were computed as suggested by Perneger et al.[19] Heterogeneity tests included the Cochran's Q statistic[17] and the I-squared (I2) index.[20] The presence of publication bias was investigated by Begg's[21] and Egger's[22] tests. Potential time trends were detected in cumulative analyses.[23] Sensitivity analyses were performed through subgroup investigations or by excluding studies one at a time. A bivariate approach was also implemented to account for the potential correlation of RRs for immunological and virological response.[24]

All analyses were conducted in Stata 12 (Stata Corporation, College Station, Texas, USA). Except for heterogeneity statistics (significance was declared if P < 0.10), the results were considered significant if the corresponding P value was less than 0.05. All P values were two tailed.

Unless stated differently, only random-effects estimates are presented.

Results

Description of Eligible Studies

The literature search yielded 31 relevant studies. Ten of them were excluded because they provided insufficient data or were part of multiple publications (Fig. 1). Finally, 21 studies involving 5278 HIV/HCV co-infected patients and 17255 individuals infected by HIV alone were eligible. Among them, 10 included information on immunologic response[9, 12, 25–32] and 11 about both outcomes[33–43] (Table 1). Immunological response was measured either as CD4 T-cell count change from baseline to 3–24 months after ART initiation[9, 12, 25, 26, 28, 29, 31, 32, 35–37, 40–43] and/or as a CD4 T-cell count increase of at least 50, 75, 100, or 200 cells/mm3.[9, 12, 26, 27, 29, 30, 32–35, 38, 39] Virological response was mostly defined as decreasing plasma HIV-RNA levels below 50, 400, or 500 copies/mL or under the limit of detection.[33–42] In 7 studies, the diagnosis of HCV was made on the basis of a positive anti-HCV test and of HCV-RNA detection in plasma.[25, 27, 29, 32, 36, 42, 43] The majority of eligible studies were prospective cohorts.[9, 12, 25, 27, 30, 32–35, 37, 39, 42]

811159-fig1

Figure 1. Identification process of eligible studies.

Immunological and Virological Response

Immunological Response. There was no difference between the baseline CD4 T-cell counts of the two patient groups (P > 0.05). As presented in Table 2 and in Fig. 2, the summary difference in CD4 T-cell counts increase between HIV+ and HIV/HCV co-infected subjects in 12 studies after 3–12 months on HAART or c-ART was 34.86 cells/mm3 (95% CI: 16.82–52.89, I2 = 92.3%). This difference became bigger when the baseline CD4 T-cell counts were below 350 cells/mm3 (38.97, 95% CI: 20.00–57.93) ( Table 2 ). The results were nonsignificant (27.26, 95% CI: −2.21 to 56.72) ( Table 2 ) in the analysis of studies with dual (serologic and molecular) diagnosis of HCV. The between groups difference attenuated 2 years after ART initiation (13.43, 95% CI: 0.83–26.04, I2 = 0.0%) ( Table 2 ). The results of all subgroup analyses are presented in Table 2 .

811159-fig2

Figure 2. Univariate random-effects meta-analysis concerning the difference in CD4 T-cell increase between HIV and HIV/HCV subjects after initiation of antiretroviral treatment. Note: CI: Confidence interval.

The quantitative synthesis of HRs for increased CD4 T-cell counts (50 or 75 or 100 cells/mm3) in co-infected versus mono-infected patients after the commencement of ART yielded also significant estimates (summary adjusted HR of 8 studies: 0.82, 95% CI: 0.75–0.91) ( Table 2 ).

Virological Response. The difference in virological response was examined in 10 studies involving 13394 patients. The summary adjusted HRs for achieving undetectable viral load or HIV-RNA levels less than 50, 400 or 500 copies/mL after HAART or c-ART initiation for HIV/HCV patients compared with HIV mono-infected individuals was 0.99 (95% CI: 0.91–1.07, I2: 0.0%) ( Table 2 , Fig. 3).

811159-fig3

Figure 3. Univariate random-effects meta-analysis of adjusted Hazard Ratios for virological response in the HIV/HCV group compared with the HIV mono-infection group after initiation of antiretroviral treatment. Note: CI: Confidence interval.

Bivariate Meta-analysis. The bivariate synthesis produced similar findings. The adjusted HRs for immunological and virological responses in the HIV/HCV group compared with those patients infected with HIV alone were 0.82 (95% CI: 0.74–0.91) and 0.96 (95% CI: 0.89–1.04), respectively.

Publication Bias. In all analyses, the statistical tests of Begg and Egger supported the absence of publication bias.

Discussion

This meta-analysis of 21 studies demonstrated that HCV co-infection adversely affects early immune responses in HIV+ patients who start HAART or c-ART, especially those with baseline CD4 T-cell counts below 350 cells/mm3. This impact was less pronounced 2 years after ART initiation. The virological suppression in persons receiving potent antiretroviral therapy seems to remain unaffected by the simultaneous existence of HCV.

HIV/HCV co-infection hastens HCV-associated hepatic disease in the HAART era.[44–47] The reciprocal effect of HCV on the natural history of HIV disease is not clarified. Our meta-analysis showed the negative impact of HCV on early CD4 T-cell counts recovery in HIV+ subjects. This phenomenon has biological basis. CD4 T-cells can be infected by HCV and interactions of HIV and HCV at the cellular level could affect the immune efficacy of HAART.[48] Moreover, chronic HCV infection, in the presence of HIV, increases T-cell immune activation, which is known to limit CD4 T-cell gains.[47, 49–51] Finally, HCV has also been found to enhance CD4 T-cell apoptosis.[52] As a matter of fact, if apoptosis is partly implicated in the poorer CD4 T-cell recovery of co-infected patients, the restoration of their CD4 T-cells over time that was found in this meta-analysis dovetails with the observation that HIV replication control by HAART gradually attenuates the CD4 T-cell apoptosis rates in HIV+ patients with concomitant HCV infection.[52]

This meta-analysis showed that there was a comparable virological response to HAART in HIV+ persons regardless of HCV status. By contrast, a recent analysis of randomized clinical trials (RCTs) reported that HCV carriage was associated with altered HIV-RNA suppression in co-infected individuals.[53] This report, however, considered studies that were not designed to assess the impact of co-infection as the primary outcome of their analysis, recruited HAART-experienced patients and lacked clear description of meta-analytic techniques. Because most of the results of these trials were presented as abstracts, a new analysis of forthcoming full-text publications or of individual data would help clarify potential discrepancies between RCTs and observational research.

The meta-analysis of CD4 T-cell count change was characterized by substantial between-studies heterogeneity that predicated the conduct of subgroup analyses to explore its sources and potential impact. Previous receipt of antiretrovirals could result in heterogeneous effect estimates. Although it would be ideal to consider not only HAART- (as we did) but also ART-naïve individuals in this meta-analysis, some of the eligible studies had recruited patients with ART experience. Previous ART therapy could compromise HAART adherence, HIV load control and immunological response.[54] However, as shown in Table 2, in spite of unexpected differences in magnitude, the effect estimates were statistically significant in both cases indicating a diminished CD4 T-cell response in HIV/HCV individuals irrespective of prior ART exposure.

It is important to diagnose HCV infection based on HCV-RNA detection to avoid misclassification of HCV antibody positive patients who are HCV aviremic.[55] To explore the effect of potential misclassification, the meta-analysis of CD4 T-cell increase was performed separately by method of HCV diagnosis. The subanalyses showed that the results ceased being statistically significant in studies that adopted both serological and molecular testing. Although this could be a chance finding, it certainly calls for more accurate and consistent across studies definition of HCV infection.

The negative effect of co-infection on immunological response to HAART was observed only in patients with baseline CD4 T-cell counts below 350 cells/mm3. This finding supports the current European Guidelines for Antiretroviral Treatment,[56] which recommend immediate ART administration in HIV/HCV co-infected patients when CD4 T-cell counts drop below 500 cells/mm3. It should be noted, however, that this meta-analysis included a limited number of studies that had involved patients with initial CD4 counts above 350 cells/mm3. Future research needs to address this stratifying always immunological response by baseline CD4 T-cell counts.

The differences in CD4 T-cell recovery could be attributed to unmeasured confounding effects. For instance, the rates of HCV infection are extremely high among IDUs and previous research has shown that CD4 T-cell recovery is compromised in drug injectors compared with other groups,[57] although this finding was not corroborated in other studies.[58, 59] It seems, however, that the immunological response of IDUs to ART could be influenced by many factors that result in poor adherence to the prescribed regimen including their potential incarceration, their participation in substitution programmes, their current injection status, the presence of psychiatric conditions or the provision of psychological support.[60–63] The optimal way to elucidate the confounding effect of HIV risk groups in CD4 T-cell increase is to compare HIV mono-infected and HIV/HCV co-infected individuals by HIV risk group. Unfortunately, many of the eligible studies in this meta-analysis lacked the necessary information to perform this type of subgroup investigations.

The current work updates a previous synthesis[14] using thirteen more reports, performing many subgroup analyses, and implementing some new meta-analytic methods. It indicates a delayed immunological response in HIV/HCV co-infected patients receiving potent combinations of antiretrovirals, especially among those with CD4 T-cell counts below 350 cells/mm3. The delayed recovery of CD4 T-cells during the first year of HAART could increase the risk of toxicities or non-AIDS events. However, the clinical significance of the blunted CD4 T-cell response in the first months of HAART therapy is not fully elucidated yet and future prospective studies should explore its short-term and long-term consequences.

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  60. Mehta SH, Lucas G, Astemborski J, Kirk GD, Vlahov D, Galai N. Early immunologic and virologic responses to highly active antiretroviral therapy and subsequent disease progression among HIVinfected injection drug users. AIDSCare 2007; 19: 637–645.

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  62. Ortego C, Huedo-Medina TB, Llorca J et al. Adherence to highly active antiretroviral therapy (HAART): a meta-analysis. AIDS Behav 2011; 15: 1381–1396.

  63. Malta M, Strathdee SA, Magnanini MM, Bastos FI. Adherence to antiretroviral therapy for human immunodeficiency virus/acquired immune deficiency syndrome among drug users: a systematic review. Addiction 2008; 103: 1242–1257.

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CDC: Supplement Linked to Hepatitis, Liver Failure

Medscape Medical News

Larry Hand
Oct 15, 2013

People using a supplement for weight loss or muscle building may be susceptible to acute hepatitis and liver failure, the Centers for Disease Control and Prevention (CDC) has warned. The agency published the warning and clinician recommendations October 11 in its Morbidity and Mortality Weekly Report.

Sarah Y. Park, MD, from the Epidemic Intelligence Service, CDC, Atlanta, Georgia, and colleagues analyzed cases of severe acute hepatitis and fulminant liver failure reported by the Hawaii Department of Health (HDOH). The first 7 previously healthy individuals presented to HDOH between May and September, reporting they had used the supplement OxyELITE Pro (USPlabs) before illness onset.

The CDC, HDOH, and US Food and Drug Administration launched a public health investigation after a September 9 HDOH report. Investigators conducted patient interviews and medical records reviews and collected supplement samples for analysis.

Responding to a public health alert in Hawaii, clinicians reported 45 more possible cases. Investigators determined that 29 of them were real cases, with patients (48% men, 52% women) ranging in age from 16 to 66 years. Dates of illness onset ranged from May 10 to October 3.

Of the 29 patients, 24 reported using the supplement during the 60 days before illness onset, with 12 of them using that supplement solely and 12 using that supplement and at least 1 additional supplement.

The symptoms most often reported include loss of appetite, light-colored stool, dark urine, and jaundice. Of 10 patients who had liver biopsy data available, 7 "had histology consistent with hepatitis from drug/toxic injury, with findings including hepatocellular necrosis and cholestasis," the investigators write. Eleven patients were hospitalized for 1 to 7 days, 1 patient died, and 2 patients had liver transplants.

The investigators expanded their efforts nationally, including surveying poison center data and disseminating information through organ transplant programs, and identified 4 additional cases outside Hawaii. The investigation continues, along with US Food and Drug Administration product testing.

"While the investigation is ongoing and these data are preliminary, clinical data, laboratory tests, and histopathology of liver biopsy specimens collected thus far suggest drug- or herb-induced hepatotoxicity," the investigators write.

Specific Recommendations for Clinicians and Consumers

The CDC has 3 specific recommendations for clinicians: when evaluating patients with acute hepatitis, ask about dietary supplements use, report relevant patients to the local or state health department, and discuss patient management options with a medical or clinical toxicologist by calling their local poison center at 800-222-1222.

For consumers, the CDC advises, "Persons who use dietary supplements for weight loss or muscle gain should do so with caution and under a medical provider's close supervision."

Morb Mortal Wkly Rep. 2013;62:817-819. Full text

Source

Also See: OxyElite Pro: Health Advisory - Acute Hepatitis Illness Cases Linked To Product Use

J Infect Dis. (2013) doi: 10.1093/infdis/jit541 First published online: October 14, 2013

Koji Hara, Maria M. Rivera, Christopher Koh, Mary DeMino, Sandra Page, Pothu Raju Nagabhyru, Barbara Rehermann, T. Jake Liang, Jay H. Hoofnagle and Theo Heller

+ Author Affiliations

Translational Hepatology Unit Liver Diseases Branch, National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK), National Institutes of Health (NIH)

Address Correspondence to: Theo Heller, MD, Liver Diseases Branch/NIDDK/NIH, Building 10, room 9B16, 10 Center Drive MSC 1800, Bethesda MD 20892-1800, Phone: 301 496 1721, Fax: 301 402 0491, Email: Theller@nih.gov

Abstract

Background. A sustained virological response (SVR) is the major endpoint of therapy of chronic HCV infection. Late relapse is rare and poorly characterized. Three of 103 SVR patients treated at the National Institutes of Health had late relapse. We evaluated HCV RNA sequences in serum and liver tissue to distinguish relapse from reinfection

Methods. Per patient, 10 to 22 clones of amplified 5'UTR were evaluated in pretreatment and relapse sera, and SVR liver biopsies. Genotypes and sequence diversity were evaluated. Four patients who relapsed prior to SVR were compared as early relapsers.

Results. Serum HCV RNA for the first 24 weeks post-therapy in all late relapsers were repeatedly negative, but became positive at 8, 75 and 78 months post SVR. Reinfection risk factors were absent in 2 of 3 patients. In all early and late relapsers, apart from minor variations, the original HCV sequence was present before treatment and after relapse. All late relapser liver biopsies were HCV RNA positive at SVR, with near-identical sequence to other time points.

Conclusion. Sequence comparisons suggest that reappearance of HCV RNA years after an SVR can be from relapse of the initial viral infection rather than reinfection from a different virus.

Received June 7, 2013.
Revision received July 9, 2013.
Accepted July 17, 2013.

Published by Oxford University Press on behalf of the Infectious Diseases Society of America 2013.

Source

Dig Liver Dis. 2013 Oct 9. pii: S1590-8658(13)00422-2. doi: 10.1016/j.dld.2013.08.137. [Epub ahead of print]

Deuffic-Burban S, Mathurin P, Rosa I, Bouvier AM, Cannesson A, Mourad A, Canva V, Louvet A, Deltenre P, Boleslawski E, Truant S, Pruvot FR, Dharancy S.

Inserm U995, University of Lille Nord de France, Lille, France; Inserm ATIP-AVENIR, Denis Diderot University, Paris, France.

Abstract

BACKGROUND: In light of the impact of emerging hepatitis C virus treatments on morbidity and mortality, we sought to determine whether candidates for liver transplantation for hepatocellular carcinoma and decompensated cirrhosis will decrease sufficiently to match liver grafts for hepatitis C virus-infected patients.

AIMS: Using a Markov model, we quantified future liver graft needs for hepatitis C virus-induced diseases and estimated the impact of current and emerging treatments.

METHODS: We simulated progression of yearly-hepatitis-C-virus-infected cohorts from the beginning of the epidemic and calculated 2013-2022 candidates for liver transplantation up until 2022 without and with therapies. We compared these estimated numbers to projected trends in liver grafts for hepatitis C virus.

RESULTS: Overall, current treatment would avoid transplantation of 4425 (4183-4684) potential candidates during the period 2013-2022. It would enable an 88% and 42% reduction in the gap between liver transplantation activity and candidates for hepatocellular carcinoma and decompensated cirrhosis, respectively. Emerging hepatitis C virus treatments would allow adequacy in transplant activities for hepatocellular carcinoma. However, they would not lead to adequacy in decompensated cirrhosis from 2013 to 2022. Results were robust to sensitivity analysis.

CONCLUSION: Our study indicates that patients will benefit from public health policies regarding hepatitis C virus screening and therapeutic access to new emerging treatments.

Copyright © 2013 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.

KEYWORDS: Direct-acting antiviral agents, HCV epidemic, Liver graft allocation, Markov model, Multi-organ procurement

PMID: 24119483 [PubMed - as supplied by publisher]

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PRNewswire

Washington, DC - Walter E. Washington Convention Center
November 1 - 5, 2013

ALEXANDRIA, Va., Oct. 15, 2013 /PRNewswire/ -- The Liver Meeting® is the premier Annual Meeting in the science and practice of hepatology, including the latest findings on new drugs, novel treatments, and the results from pilot and multicenter studies.

Approximately 10 percent of Americans have some form of liver disease, but fortunately, the research community has made great strides in recent years in developing new treatments for patients. 

At this year's meeting, 2306 abstracts addressing these issues that will be presented, including 270 abstracts that will be presented in oral sessions. Those abstracts are available to members of the press at our website (www.aasld.org).

Washington, DC:  November 1 – 5, 2013

  • Poster Presentations:    November 2 – 5
  • Oral Presentations:       November 3 – 5 

An AASLD President's press conference highlighting key abstracts and issues presented at The Liver Meeting® is scheduled for Saturday, November 2 at 4:00 pm.

The following two programs will highlight the latest in viral hepatitis treatment:

  • The HCV Symposium will discuss the integration of new therapies for the treatment of chronic hepatitis
  • The Hepatitis Debrief will provide a synthesis of new data on the treatment of viral hepatitis presented at The Liver Meeting®

Founded in 1950, AASLD is the leading organization of scientists and healthcare professionals committed to preventing and curing liver disease. AASLD has grown into an international society responsible for all aspects of hepatology, and our annual meeting attracts more than 9,500 physicians, surgeons, researchers, and allied health professionals from around the world.

Please contact AASLD at 703-299-9766 for information about the above presentations, or to receive any additional information about The Liver Meeting® – or visit our website at www.aasld.org.  

Please visit our website to register as press for the meeting, or contact Ann Haran at aharan@aasld.org with any questions.

This release was issued through The Xpress Press News Service, merging e-mail and satellite distribution technologies to reach business analysts and media outlets worldwide. For more information, visit http://www.XpressPress.com.

SOURCE American Association for the Study of Liver Diseases (AASLD)

RELATED LINKS
http://www.aasld.org

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Video: Hep C TV Monthly Roundup

Hep C TV - October 2013
 
 

Published on Oct 11, 2013

A monthly round-up of all things hep C! Taking a look at recent developments in hep C treatments, celebrities who live with the virus and the latest contributions from our community here at Hepatitis C News.

Please visit their website: Hepatitis C News

Image credits:
Last.fm
Qype
Washington Post
Outsourcing Pharma
Elsevier
Pedestrian.TV
Coachella 2013 images
Vibe.com
abc.net

Video credits:
16x9 OnGlobal
WWE Hall of Fame
Aioria Andrei
Nolan Fans

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PRESS RELEASE
Oct. 14, 2013, 2:16 p.m. EDT

PR-Logo-Newswire

Achillion Pharmaceuticals, Inc. Sued by Investors After Stock Drops 58% on Announcement that Clinical Hold of Drug Sovaprevir Will Continue

SAN DIEGO and NEW HAVEN, Conn., Oct. 14, 2013 /PRNewswire via COMTEX/ -- Shareholder rights law firm Robbins Arroyo LLP announces that an investor of Achillion Pharmaceuticals, Inc. has filed a federal securities fraud class action complaint in the U.S. District Court, District of Connecticut. The complaint alleges that the company and certain of its officers violated the Securities and Exchange Act of 1934 between April 21, 2012 and September 27, 2013 (the "Class Period").

Learn more about our investigation on our Shareholder Rights Blog: http://www.robbinsarroyo.com/shareholders-rights-blog/achillion-pharmaceuticals-inc/

Achillion Accused of Misleading Investors Regarding Viability of Sovaprevir

Shares of Achillion fell $4.22 per share, or more than 58%, on September 27, 2013, after the company disclosed that the U.S. Food and Drug Administration ("FDA") continued its clinical hold on sovaprevir, its premier investigative drug for the treatment of hepatitis. This steep decline comes just two months after Achillion experienced an initial 25% decline per share on the announcement that the FDA instituted the clinical hold on July 1, 2013.

According to the complaint, defendants made false and/or misleading statements and failed to disclose material adverse facts about the company's business, operations, and prospects, including the safety and suitability of sovaprevir. Defendants failed to inform investors that sovaprevir did not interact well with other drugs commonly administered to treat hepatitis and/or HIV, and misled investors to believe that even though patients in the company's clinical trials for sovaprevir had elevations in liver enzymes, that these liver enzymes elevations were transient and returned to baseline values and were attributable to non-drug-related factors.

If you invested in Achillion and would like to discuss your shareholder rights please contact attorney Darnell R. Donahue at (800) 350-6003, DDonahue@robbinsarroyo.com, or via the shareholder information form on the firm's website.

Robbins Arroyo LLP is a nationally recognized leader in securities litigation and shareholder rights law. The firm represents individual and institutional investors in shareholder derivative and securities class action lawsuits, and has helped its clients realize more than $1 billion of value for themselves and the companies in which they have invested. For more information, please go to http://www.robbinsarroyo.com.

Attorney Advertising. Past results do not guarantee a similar outcome.

Contact: Darnell R. Donahue Robbins Arroyo LLPDDonahue@robbinsarroyo.com  (619) 525-3990 or Toll Free (800) 350-6003 www.robbinsarroyo.com

SOURCE Robbins Arroyo LLP

Copyright (C) 2013 PR Newswire. All rights reserved

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