April 25, 2013

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Virtual Press Office

Amsterdam, 25 April 2013

Amsterdam, The Netherlands, Thursday 25 April 2013: Probiotics could emerge as a treatment plan to manage hepatic encephalopathy (HE) therapy after a new study[1] announced at the International Liver Congress™ 2013 found they significantly reduced development of the notoriously difficult-to-treat disease.

The study analysed the efficacy of probiotics in preventing the development of HE in 160 cirrhotic patients over a period of approximately nine months and found significant improvements in reducing patients’ arterial ammonia levels after three months of treatment with probiotics.

Ammonia, produced by gut bacteria, is thought to be one of the main mediators of cerebral dysfunction in HE. Probiotics work by enriching the gut flora with a non-urease producing microorganisms, which decrease ammonia production.[2] Probiotics are live microorganisms (mostly bacteria) that produce a health benefit on the host when administered in adequate amounts.[3]

Twice as many patients taking a placebo developed overt HE (the study’s primary endpoint) compared to patients taking probiotics in the form of a capsule.

EASL’s Treasurer, Prof. Mauro Bernardi welcomed the findings and said they would provide a positive impact for cirrhotic patients at risk of developing HE for whom the prognosis is typically very poor.

Prof. Bernardi said: “Hepatic encephalopathy is an insidious disease that’s caused by an accumulation of toxins in the blood that are normally removed by the liver. Treatment normally involves the use of antibiotics or laxatives to suppress the production of toxic substances in the intestine but there is still a great deal of room for improvement so it will be exciting to see the results of further studies to determine if clinicians have a new form of treatment on the cards.”

Hepatic encephalopathy is a spectrum of neuropsychiatric abnormalities including personality changes, intellectual impairment and reduced levels of consciousness in patients with liver failure, after exclusion of other known brain disease.

- Ends -

Disclaimer: the data referenced in this release is based on the submitted abstract. More recent data may be presented at the International Liver Congress™ 2013.

Notes to Editors

About EASL

EASL is the leading European scientific society involved in promoting research and education in hepatology. EASL attracts the foremost hepatology experts and has an impressive track record in promoting research in liver disease, supporting wider education and promoting changes in European liver policy.

EASL’s main focus on education and research is delivered through numerous events and initiatives, including:

  • The International Liver CongressTM which is the main scientific and professional event in hepatology worldwide
  • Meetings including Monothematic and Special conferences, Post Graduate courses and other endorsed meetings that take place throughout the year
  • Clinical and Basic Schools of Hepatology, a series of events covering different aspects in the field of hepatology
  • Journal of Hepatology published monthly
  • Participation in a number of policy initiatives at European level

About The International Liver CongressTM 2013

The International Liver Congress™ 2013, the 48th annual meeting of the European Association for the study of the Liver, is being held at the RAI Convention Centre in Amsterdam from April 24 – 28, 2013. The congress annually attracts in excess of 9,000 clinicians and scientists from around the world and provides an opportunity to hear the latest research, perspectives and treatments of liver disease from principal experts in the field.

For further information on the studies, or to request an interview, please do not hesitate to contact the EASL Press Office on:

Email: easlpressoffice@cohnwolfe.com

Dimple Natali +44 7900 138 904

Courtney Lock +44 7894 386 422

References

[1] M.K Lunia, AN OPEN LABEL RANDOMISED CONTROLLED TRIAL OF PROBIOTICS FOR PRIMARY PROPHYLAXIS OF HEPATIC ENCEPHALOPATHY IN PATIENTS WITH CIRRHOSIS. Presented at the International Liver CongressTM 2013.

[2] A. Agrawal, Secondary Prophylaxis of Hepatic Encephalopathy in Cirrhosis, An Open-Label, Randomized Controlled Trial of Lactulose, Probiotics, and No Therapy. Available
http://www.medscape.com/viewarticle/767674_3 [Accessed 9/4/13].

[3] World Health Organization and Food and Agriculture Organizationof the United Nations. Health and Nutritional Properties of Probiotics in Food including Powder Milk with Live Lactic Acid Bacteria. Avahttp://www.who.int/foodsafety/publications/fs_management/en/probiotics.pdf [Accessed 9/4/13].

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ILC 2013: HEPATITIS C - NEW DAA's READY FOR PRIME TIME (Video)

ILC 2013: HEPATITIS C - EXISTING TREATMENTS (Video)

Provided by ILC Press 

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Therapy Free of Side Effects of Other HCV Drugs

By Michael Smith, North American Correspondent, MedPage Today

Published: April 25, 2013

Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco

AMSTERDAM – An investigational protease inhibitor (PI) led to viral cures in about four out of five hepatitis C virus (HCV) patients, a researcher reported here.

In a phase III study, either of two doses of faldaprevir combined with pegylated interferon and ribavirin significantly outperformed placebo, according to Peter Ferenci, MD, of the Medical University of Vienna.

But importantly, Ferenci told MedPage Today during the meeting of the European Association for the Study of the Liver, they did so without the side effects associated with earlier drugs in the class.

The efficacy results are "indeed very good," commented Mark Thursz, MD, of St. Mary's Hospital in London, who was not involved in the study but who moderated a press conference at which some details were discussed.

But the most important aspect of the results, Thursz said, is the safety profile of the drug. "This will be far better tolerated by our patients in the clinic than the earlier PIs," he told reporters.

Two protease inhibitors – telaprevir (Incivek) and boceprevir (Victrelis) – have been approved for patients with the difficult-to-treat HCV genotype 1, but they have been associated with serious and sometimes dangerous adverse events.

Both, for instance, cause significant anemia, and telaprevir has been associated with life-threatening rash that in at least two cases led to death.

But they are the only drugs so far approved that directly target HCV; the companion medications, pegylated interferon and ribavirin, are respectively an immune booster and a viral replication inhibitor.

That was the context when the industry-sponsored trial was designed, Ferenci told MedPage Today – the earlier protease inhibitors were regarded as the competitors, with interferon (given intravenously) and ribavirin alone as the standard of care.

Since then, he said, there has been a "revolution" in HCV, with a host of oral direct-acting agents under investigation and clinicians hoping that interferon and perhaps ribavirin can be banished from the clinic.

Indeed, Ferenci noted, research is underway to see if faldaprevir, in combination with other oral direct-acting HCV drugs, can be effective in the absence of interferon and possibly without interferon or ribavirin.

In the current study, investigators enrolled 652 patients with genotype 1 HCV and randomly assigned them for 24 weeks to get placebo or either 120 or 240 milligrams of faldaprevir daily. All patients also got then-standard therapy with interferon and ribavirin.

Patients with what the investigators called "early treatment success" – defined as low levels of HCV at week 4 and undetectable levels at week 8 – were eligible to stop treatment at week 24, while others got another 24 weeks of interferon and ribavirin.

In the placebo arm, 22% of patients had early treatment success, Ferenci reported, compared with 87% in the low-dose faldaprevir arm and 89% in the high-dose arm, and stopped treatment at 24 weeks.

The primary endpoint of the study was 12-week sustained virologic response (SVR12) – no detectable HCV RNA 12 weeks after the end of treatment.

The investigators found that 52% of patients in the placebo arm reached that endpoint, similar to historical results. In the low-dose faldaprevir arm, the SVR12 rate was 79%, compared with 80% in the high-dose arm (P<0.0001 for both).

The only adverse event clearly caused by the drug, Ferenci said, was an elevation in bilirubin, but that was not associated with elevated liver enzymes and had "no clinical significance."

Some patients reported rash but did not need medical attention for it, he added.

Indeed, he said, the rates of most observed adverse events, including those regarded as serious, were similar among the arms, with little difference in discontinuations owing to adverse events.

The study was supported by Boehringer Ingelheim. Ferenci reported financial links with the company and with Roche, Merck, Vertex, Idenix, Achelion, Rottapharm-Madaus, and BMS.

Thursz reported financial links with Abbott and Gilead.

Primary source: European Association for the Study of the Liver
Source reference:
Ferenci P, et al "Faldaprevir plus pegylated interferon alfa-2A and ribavirin in chronic HCV genotype-1 treatment-naïve patients: final results from STARTVERSO1, a randomised, double-blind, placebo controlled phase III trial" EASL 2013; Abstract 1416

Source

Once-Daily HCV Drug Stars in Phase III Trials

By John Gever, Deputy Managing Editor, MedPage Today

Published: April 25, 2013

Reviewed by Zalman S. Agus, MD; Emeritus Professor, Perelman School of Medicine at the University of Pennsylvania

AMSTERDAM -- Treatment-naive patients with hepatitis C virus (HCV) infection showed high viral cure rates when treated with simeprevir, an investigational once-daily oral drug, along with standard therapy, researchers said here.

Sustained 12-week virologic responses (SVR12), defined as viral loads too low to be measured, occurred in eight out of 10 patients with HCV genotype 1 receiving simeprevir in two identical, placebo-controlled phase III trials conducted in the U.S. and Europe, according to presentations at the annual meeting of the European Association for the Study of the Liver.

All patients in these trials also received standard anti-HCV treatment with pegylated interferon and ribavirin for 24 or 48 weeks. SVR12 rates in the trials' placebo groups were 50% in both cases (P<0.001 versus the simeprevir groups).

Simeprevir is an orally active, second-generation inhibitor of the HCV NS3/4A protease. Two first-generation products, boceprevir (Victrelis) and telaprevir (Incivek), were approved in 2011. Both have significant disadvantages: they must be taken three times a day, and telaprevir has been linked to life-threatening skin rashes while boceprevir can cause serious anemia.

As a result, drug firms have been working to develop HCV protease inhibitors with better safety profiles and that can be given just once a day.

Each of the phase III simeprevir studies randomized approximately 400 treatment-naive HCV patients in a 2:1 ratio to 150 mg of the drug or placebo in addition to peginterferon and ribavirin.

Both trials were designed to use "response-guided therapy," under which patients achieving viral loads of less than 25 IU/mL at week four and and below detection limits at week 12 had the peginterferon and ribavirin stopped at week 24. Those showing responses short of these standards continued on treatment through week 48.

Patients with poor responses (less than a two-log reduction in HCV viral loads by week 12 or confirmed loads of at least 25 IU/mL at weeks 24 or 36) were taken off the study.

Results of the U.S. trial, called QUEST-1, were reported by Ira Jacobson, MD, of Weill Cornell Medical College in New York City, and colleagues. Not only did simeprevir meet the study's primary endpoint of superiority over placebo in SVR12 rates, but it also was highly effective against the hard-to-treat genotype 1a form of the virus.

Additionally, it was better than placebo in patients with all three IL28B genotypes, although response rates were especially high with the drug in patients with the TT and CT forms of the gene. Responses to simeprevir were also equally good irrespective of METAVIR score, which measured liver fibrosis and inflammation.

The only subgroup for whom simeprevir was not more effective than placebo was patients with genotype 1a and the so-called Q80K polymorphism, Jacobson and colleagues indicated.

Results were closely similar in the European QUEST-2 trial, according to data reported at a press conference prior to the study's formal presentation later this week.

Adverse events in both trials were similar in number in the active-drug and placebo groups. In QUEST-2, rates of skin rash and photosensitivity were somewhat higher with simeprevir versus placebo, but those events were not increased with the drug in QUEST-1.

Conversely, anemia, neutropenia, and elevated bilirubin appeared more common with simeprevir in QUEST-1, but not in QUEST-2.

Other efficacy data from QUEST-1 were as follows:

  • Patients taken off study for poor virologic response: 7% simeprevir, 66% placebo
  • Simeprevir patients qualifying for shortened peginterferon/ribavirin treatment: 85%
  • Patients with undetectable virus at week four: 80% simeprevir, 12% placebo

Jacobson and colleagues also reported that SVR12 rates were nearly as great in patients with HCV genotype 1a as in those with the more responsive 1b genotype. However, most of the responses in the 1a patients occurred in those without the Q80K polymorphism, for whom the SVR12 rate was the same with simeprevir as with placebo.

Relatively poor simeprevir responses were also seen in patients with emergent mutations in the Ns3 protease at position 155 in genotype 1a and at position 168 in genotype 1b.

Press briefing co-moderator Mark Thursz, MD, of St. Mary's Hospital in London, commented that the data suggest that simeprevir and other second-generation products have succeeded in surpassing boceprevir and telaprevir.

"With the new protease inhibitors, [the side effect profile] seems to be better, more patients get shorter periods of treatment, and more patients get cured," he said.

A third trial of simeprevir in HCV patients previously treated with other drugs is ongoing, Jacobson and colleagues indicated.

The drug's manufacturer, the Janssen unit of Johnson & Johnson, applied last month for U.S. marketing approval of simeprevir to be given with peginterferon and ribavirin. It also has applications in the works in Japan and the European Union.

Both studies were funded by Johnson & Johnson's Janssen unit.

Study authors declared that they had relationships with unspecified commercial entities that could be perceived as having a connection to the studies. Both included investigators who were Janssen employees.

Primary source: European Association for the Study of the Liver
Source reference:
Jacobson I, et al "Simeprevir (TMC435) with peginterferon/ribavirin for chronic HCV genotype-1 infection in treatment-naïve patients: results from QUEST-1, a phase III trial" EASL 2013; Abstract 1425.

Additional source: European Association for the Study of the Liver
Source reference:
Manns M, et al "Simeprevir (TMC435) with peginterferon/ribavirin for chronic HCV genotype-1 infection in treatment-naïve patients: results from QUEST-2, a phase III trial" EASL 2013; Abstract 1413.

Source

Oral Regimen Sustains Hepatitis C Viral Response to 24 Weeks

Medscape Medical News > Conference News

Daniel M. Keller, PhD

Apr 25, 2013

AMSTERDAM, the Netherlands — A regimen of 3 direct-acting antiviral drugs plus ritonavir and ribavirin produced sustained virologic response rates in more than 90% of a broad range of patients infected with hepatitis C 24 weeks after therapy, results from a new clinical trial show.

Kris Kowdley, MD, from the Liver Center of Excellence in the Digestive Disease Institute at Virginia Mason Medical Center in Seattle, Washington, presented the results here at the International Liver Congress 2013.

The randomized, open-label, multicenter phase 2b trial, known as Aviator, shows that the sustained virologic responses seen at 12 weeks with an all-oral interferon-free regimen, presented last year at the annual meeting of the American Association for the Study of the Liver Diseases by Dr. Kowdley, are sustainable.

In the Aviator trial, noncirrhotic patients with genotype 1 hepatitis C virus who were treatment-naïve or had not responded to peginterferon and ribavirin were treated with combinations of direct-acting antiviral drugs with or without ribavirin for 8, 12, or 24 weeks.

The direct-acting antiviral drugs were once-daily ABT-450r (an NS3/4A protease inhibitor boosted with ritonavir), once-daily ABT-267 (an NS5A inhibitor), and twice-daily ABT-333 (a non-nucleoside NS5B inhibitor).

The 571 patients were predominantly white, and the mean age was 48 to 53 years. The majority, 59% to 71%, had hepatitis C genotype 1a, and mean baseline viral load was 6.6 log10 hepatitis C RNA. Overall, 27% to 34% of treatment-naive patients had genotype IL28B CC, whereas only 2% to 4% of the null responders did.

Patients coinfected with HIV or hepatitis B were excluded from the study.

For the 79 treatment-naive patients who received the regimen consisting of 3 direct-acting antiviral drugs plus ribavirin for 12 weeks, 96% achieved sustained virologic response rates at 24 weeks (99% achieved this at 12 weeks).

High Response Rates

Response rates were no higher with 24 weeks of treatment than with 12 weeks of treatment. Even with only 8 weeks of treatment, 88% of patients achieved sustained virologic response rates at 24 weeks and 89% achieved this at 12 weeks.

For the null responders who received the triple-drug plus ribavirin regimen, 93% of the 45 patients who received 12 weeks of treatment achieved sustained virologic response, as did 95% of the 43 patients who received 24 weeks of treatment.

With the triple-drug plus ribavirin regimen, the achievement of sustained virologic response was similar in the treatment-naive and null-responder patients, regardless of sex, genotype (1a or 1b), host IL28B genotype, severity of liver fibrosis, or baseline RNA level.

Of the 247 patients who received the triple-drug plus ribavirin regimen for 12 or 24 weeks, 4 (1.6%) discontinued the study because of drug-related adverse effects.

Of 4 serious adverse effects noted in the analysis, 1 arthralgia was possibly related to therapy. More common adverse effects, reported in more than 10% of patients, were headache, fatigue, nausea, insomnia, and diarrhea. Of the patients with grade 3/4 laboratory abnormalities, 6 had elevated total bilirubin and 1 had elevated alanine aminotransferase, which resolved with continuation of the drugs.

Dr. Kowdley told Medscape Medical News that results from the Aviator trial highlight 2 key points. "First, prolonging the therapy for another 12 weeks does not appear to improve the sustained virologic response. Second, greater treatment exposure does not seem to increase the risk of resistance; we're not seeing a drop off or more breakthroughs, because the number of breakthroughs has remained at 0. That's a really important point."

With the triple-drug plus ribavirin regimen, which is the optimal regimen, "sustained virologic response at 24 weeks remains very durable, compared with sustained virologic response at 12 weeks. That is true in both the null responders and treatment-naive patients.... So for those patients who do end up, for whatever reason, being on 24 weeks, we can feel, I think, reasonably confident that the resistance risk is not increased," Dr. Kowdley said.

A concern all along has been the high pill burden of this all-oral regimen. Dr. Kowdley said he expects that, for upcoming trials, reformulations will combine the once-daily ABT-267, ABT-450, and ritonavir into 1 pill, while keeping the twice-daily ABT-333 and the ribavirin separate. "I would say that in the phase 3 program and going forward, the pill burden should be lower," he predicted.

The sustained virologic response for treatment-naive patients is "extremely impressive," said Mark Thursz, MD, from Imperial College in London, the United Kingdom, and secretary general of the European Association for the Study of the Liver. Similarly, for null responders, Dr. Thursz, who was not involved in the study, said he is "quite excited" by the "really high sustained virologic responses."

He remarked that, in general, the protease inhibitors in development to treat hepatitis C virus have "much cleaner profiles than the current ones that we're using," but he added that "it's not quite time to bury the interferon yet."

However, "the vital signs are not looking good for either boceprevir or telaprevir." In light of the drugs now in trials, "it's time to move on," Dr. Thursz said.

The study was supported by AbbVie. Dr. Kowdley reports receiving research support from AbbVie, Beckman Boehringer Ingelheim, Bristol-Myers Squibb, Gilead/Pharmasset, Ikaria, Intercept, Janssen, Merck, Mochida, Vertex, Scientific Consulting, and Novartis; and being on advisory boards for AbbVie, Gilead, Merck, and Vertex. Dr. Thursz has disclosed no relevant financial relationships.

International Liver Congress 2013: 48th Annual Meeting of the European Association for the Study of the Liver (EASL). Abstract 3. Presented April 25, 2013.

Source

Unsafe injection practices fuelling Hepatitis in India

Hetal Vyas, TNN | Apr 25, 2013, 07.55 PM IST

BANGALORE: Though little alarm has been sounded about it, Hepatitis is increasing at a worrying rate in India. Recent World Health Organization (WHO) data puts Hepatitis B cases in India at approximately 1.1 million, with 240,000 annual deaths due to complications associated with it. Similarly for Hepatitis C, the figure for India is put at 400,000 cases, with about 96,000 deaths annually of causes related to the hepatitis C infection. A large percentage of these cases are due to unsafe injection practices.

The WHO also says that unsafe practices and the overuse of injections across the globe can cause an estimated 33% of Hepatitis B virus, 42% of Hepatitis C virus and 2% of all new HIV(human immunodeficiency virus) infections every single year.

Experts said that this is definitely alarming for Indian situation where injections are administered for common symptoms like diarrhea, fever and even cough. In a year a person is given 2.9 injections on an average as per INCLEN study published in WHO's SEARO bulletin recently.

Overall, three billion injections are estimated to be administered annually in India; of which 1.89 billion were unsafe. Moreover, injections administered for curative purpose constituted 82.5% and a majority of these are unnecessary.

According to Dr. Santanu Chattopadhyay, Gastroenterologist, Founder and CEO, NationWide Primary Healthcare Services.: "Hepatitis B & C can both be contracted through the sharing of needles during drug use; via reuse of infected syringes; through blood transfusion, if the blood was not properly screened; and during a tattoo or piercing done with infected tools. In rare cases, an infected pregnant woman could spread the virus to her baby at birth. Even sharing of razors or tooth brushes with an infected person can spread the disease."

In this case, prevention is definitely better than cure. Says Dr Praveen Kumar, Medical Gastroenterologist, and Professor in Gastroenterology, Vydehi Medical College and Vydehi Mallya Hospital: "Treatment for Hepatitis is very expensive. Therefore awareness and stringent enforcement is essential to save the population. In India unsafe injection practices and the reuse of needles is a major cause of concern, so it is imperative to spread awareness among medical practitioners, patients and the public at large," he said.

The INCLEN study has found that of all the injections administered in India, 62% were found to be unsafe. They were administered incorrectly or were a threat for transmitting blood borne viruses.

Source

RTEmagicC_5dcw9v3b_94483_photo_jpg

Courtesy U.S. Dept of Veterans Affairs

Hepatitis C is rarely transmitted between long-term monogamous heterosexual partners, said Dr. Norah Terrault.

By: MICHELE G. SULLIVAN, Ob.Gyn. News Digital Network

04/25/13

The risk of sexually transmitting a chronic hepatitis C infection to a long-term monogamous heterosexual partner is very low, averaging just about 1% per year.

That risk level works out to a transmission rate of about one in every 190,000 sexual contacts, Dr. Norah Terrault and her colleagues reported in the April issue of Hepatology (2013;57:881-9).

The cross-sectional study also found that no one sexual practice – including anal intercourse or intercourse during menses – significantly increased the risk of transmission, wrote Dr. Terrault of the University of California, San Francisco. The findings can be used to provide "unambiguous and reassuring counseling messages," she and her coinvestigators noted.

The study included 500 subjects with chronic HCV infections, and their sexual partners. All couples reported longtime, monogamous relationships (median duration, 15 years); however, the relationship duration varied widely, spanning 2-52 years.

Each of the partners was interviewed separately about their sexual contacts and practices. At the time of interview, the index subjects were a median of 49 years old and the partners, a median of 48 years.

The HCV-positive subjects reported the highest incidence of past risk factors, including blood transfusions before 1992 (32%), injected illegal drugs (54%), and being stuck by a bloody sharp item in a hospital (4%). Nearly half (46%) reported having had at least 20 lifetime sexual partners, with 21% having had 50 or more.

However, partners also reported some risk factors: 11% had an early transfusion, 2% used illegal drugs, and 2% had a hospital sharps incident. Many (27%) also reported having had at least 20 sexual partners.

Among the 500 couples, 20 partners (4%) were coinfected with HCV. Of these, nine were concordantly infected, eight discordantly, and three were indeterminate.

Six of the concordant couples underwent phylogenetic typing. Three were infected with the same HCV isolate and three with different strains. The investigators estimated the time of transmission and any additional risk factor among the three couples with concordant strains.

For the first couple, with an 18-year relationship, transmission probably occurred after about 6.5 years. The female partner had a history of injected drug use, while the male had no identifiable risk factors.

The second couple had a 28-year relationship; transmission probably occurred at around 15 years, the investigators said. "The female partner had a history of injectable drug use and both partners reported more than 20 prior sexual partners, a history of sexual transmitted diseases, and a history of snorting of drugs."

For the third couple, who had been together for 10 years, transmission probably occurred at around year 6. "The male partner had a history of injectable drug use, of being stuck by a sharp bloody object while working in a hospital, and more than 20 prior sexual partners; both partners reported snorting drugs and sharing snorting equipment."

The investigators determined that these infections were probably sexually transmitted between the partners – a prevalence of about 1%. "The estimated risk per sexual contact ranged from 1/380,000 to 1/190, 000," they said.

However, they were unable to identify any behaviors that significantly increased the risk of transmission. Compared with couples without coinfection, coinfected couples were more likely to have vaginal intercourse during menses (100% vs. 66%), more likely to have anal intercourse (67% vs. 30%), and less likely to use condoms (0% vs. 30%), but none of these differences was statistically significant.

"HCV transmission by sex from chronically infected persons to their heterosexual partners in a long-term monogamous relationship likely occurs, but is a rare event," the authors concluded. "Our results provide a basis for specific counseling messages that clinicians can use with their patients... [that] support the current national recommendations that couples not change their sexual practices if they are in a monogamous heterosexual relationship."

None of the study authors reported any financial conflicts.

msullivan@frontlinemedcom.com

Source

April 25, 2013 | By John Carroll

Bristol-Myers Squibb ($BMY) just gained an inside regulatory track in the frantic race to get new interferon-free hepatitis C drugs to the FDA. The big biotech reported in its quarterly statement that the agency has provided the coveted "breakthrough" status for a combination of daclatasvir with two other direct-acting antivirals, asunaprevir, an NS3 protease inhibitor and BMS-791325, an NS5B non-nucleoside polymerase inhibitor.

The combo approach is designed to stop the virus from replicating. Just days ago the company reported that the drug worked in 15 of 16 patients during a 24-week trial. Now investigators plan to settle on an ideal dose and launch a late-stage study later this year.

BMS is the latest in a long line-up of high-profile biopharma companies to land a breakthrough designation. In theory, the agency is committed to working with these companies now to expedite a path through the FDA and on to the market--possibly granting an accelerated approval ahead of a traditional pivotal study. In practice, there's still not much of a track record to demonstrate exactly what kind of advantage, if any, will be provided.

One thing, though, is certain. The roster of companies to win breakthrough status also includes Merck ($MRK), Novartis ($NVS), Johnson & Johnson ($JNJ), Vertex ($VRTX) and others--all well-established companies with a very long track record in R&D. So far, no small biotechs have made it to the list, indicating that at least initially regulators are staying in their comfort zone when it comes to who they want to work with.

The breakthrough designation also reflects a certain kind of vindication for BMS, which saw its newly acquired hep C drug 094 blow up in the clinic, killing one patient and injuring others. The company is behind Gilead ($GILD) and AbbVie ($ABBV) in this race--but it is gaining ground.

BMS has also achieved a fast-track designation for nivolumab, its PD-1 cancer drug in late-stage development. That therapy remains the company's most exciting therapy in late-stage development, according to a number of analysts who track Bristol-Myers.

- here's the release on the Q1 numbers

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SCYNEXIS Presents SCY-635 Data on HCV at International Liver Congress

SCYNEXIS_logo

April 25, 2013 11:11 AM Eastern Daylight Time

-- SCY-635 Shows Potential to Augment Current Treatments --

AMSTERDAM--(BUSINESS WIRE)--Drug discovery and development company SCYNEXIS, Inc. presented 2 studies indicating that oral treatment SCY-635 induces the production of interferon in HCV infected patients at the 48th annual meeting of the European Association for the Study of the Liver.

In an oral presentation, Dr. Koichi Watashi, Department of Virology II, National Institute of Infectious Diseases, Japan, reported results of the study, Potentiate Interferon Signaling Through Diminished PKR Phosphorylation in HCV-Infected Cells, at the Translational Research in HCV session on Thursday, April 25 from 4 to 6 p.m.

The study examined the effect of cyclophilin inhibitors on the interferon (IFN) signaling pathway using an HCV-infected cell culture system. Results of this study suggest that cyclophilin inhibitors release the negative regulation of interferon stimulated genes (ISG) and allow their translation in HCV-infected cells. This mechanism contributes to the anti-HCV activity of cyclophilin inhibitors, in addition to the direct suppression of HCV replication.

The poster presentation, entitled The Cyclophilin Inhibitor SCY-635 Restores the Innate Recognition of HCV by Peripheral Blood Mononuclear Cells (PBMC) from HCV-Infected Subjects, was presented by Peter Probst, SCYNEXIS, in the session on Hepatitis research and will be displayed from 9 a.m. to 5 p.m on Saturday, April 27.

The study evaluated the ability of SCY-635 to modulate the innate immune response to HCV of peripheral blood mononuclear cells (PBMC) from study subjects with HCV. The data suggest that SCY-635 induces production of interferon by PBMC in a portion of HCV study subjects but has no stimulatory effect on PBMC from healthy controls. It also suggests that SCY-635 may induce and maintain an adaptive anti-HCV immune response by inhibiting the HCV-induced impairment of dendritic cells.

The full abstract for the oral presentation can be found here and the abstract for the poster presentation can be viewed here.

About HCV and Therapeutic Need

The World Health Organization estimates that about 3% of the world’s population is infected with HCV and that there are more than 170 million chronic carriers who are at risk of developing liver cirrhosis and/or liver cancer. While the majority of antiviral research remains focused on viral targets such as protease and polymerase enzymes, therapies such as SCY-635 that are based on immunomodulation to counteract viral immune evasion could be of great therapeutic value.

About SCY-635

SCY-635 is a novel oral cyclophilin inhibitor in Phase 2 studies for the treatment of Hepatitis C (HCV) and in preclinical studies for the treatment of Hepatitis B (HBV). Studies to date have demonstrated that SCY-635 is unique in that it plays a dual role as a synergistic Direct Acting Antiviral (DAA) and a stimulator of the host immune system (Immune Acting Antiviral or IAA). The addition of SCY-635 to the repertoire of currently approved HCV therapies could breathe new life into the future of the immunotherapeutic options for treating HCV.

About SCYNEXIS

SCYNEXIS delivers innovative solutions to solve the toughest problems in drug discovery and development for our pharmaceutical, global health, animal health and life science partners. Our contract research services include Integrated Pharmaceutical Solutions, Discovery Research and Integrated Parasitology. We have successfully delivered preclinical and clinical drug candidates to our customers across all major therapeutic indications and have developed our own proprietary cyclophilin inhibitor programs for the treatment of a broad range of diseases, including HCV, HBV and inflammation. Founded in 2000, SCYNEXIS is located in Research Triangle Park, North Carolina. Visit www.scynexis.com.

Contacts

SCYNEXIS Media Contacts:
SCYNEXIS
Alissa Maupin, + 1-919-206-7246
Alissa.Maupin@scynexis.com
or
Media Contact:
MacDougall Biomedical Communications
Cory Tromblee, +1 781-235-3060
ctromblee@macbiocom.com

Source

Sofosbuvir: the final nail in the coffin for hepatitis C? Commentary

Download the PDF here

The Lancet Infectious Diseases May 2013

Michael P Manns a, Markus Cornberg a

In The Lancet Infectious Diseases, Eric Lawitz and colleagues1 report results from their randomised phase 2 trial, in which they showed a more than 90% cure rate of hepatitis C in patients given a combination of pegylated interferon alfa-2a (peginterferon), ribavirin, and sofosbuvir, a novel nucleoside inhibitor of the hepatitis C virus (HCV) NS5B polymerase. Among the 60 or so drugs under development for HCV, nucleoside inhibitors seem to be the most promising of the three classes of direct-acting antivirals currently in phase 3 trials (figure): NS3/4A protease inhibitors, NS5A inhibitors, and NS5B polymerase inhibitors, which can be subdivided into nucleoside inhibitors or non-nucleoside inhibitors. Nucleoside inhibitors, namely sofosbuvir, seem to be best in terms of resistance profile, activity against all virus genotypes, adverse events, and antiviral potency. And as such, the emergence of sofosbuvir is an important milestone in the fight against hepatitis C.

The first such milestone was the approval of interferon alfa in the early 1990s.2 The addition of ribavirin to interferon alfa in 1998 doubled response rates;3 and once weekly peginterferon was introduced in combination with ribavirin in 2001.4 In 2003, the protease inhibitor BILN 2061 (Boehringer Ingelheim, Ingelheim, Germany) provided the first proof of concept for direct-acting antivirals against HCV.5 8 years later, the protease inhibitors boceprevir and telaprevir were approved for treatment of HCV genotype-1.6, 7 Boceprevir and telaprevir improved sustained viral response rates (SVR) from about 40-44% to 68-75% in treatment-naive patients with genotype-1.6, 7

SVR means patients are cured and has been associated with prevention of hepatocellular carcinoma and even improvements in overall mortality.8 However, these protease inhibitors have several limitations: activity against genotype-1 only, dosing every 8 h, and many potentially serious drug interactions. Both protease inhibitors have to be given in combination with peginterferon plus ribavirin because monotherapy results in rapid emergence of drug-resistant variants, which explains why previous null-responders to peginterferon plus ribavirin had SVRs of only 30-40% when given triple therapy with peginterferon, ribavirin, and a NS3/4A protease inhibitor.9 Boceprevir and telaprevir add to the adverse event profile of peginterferon plus ribavirin, especially in patients with cirrhosis-namely, a doubling of anaemia.10, 11

A need for new drugs clearly exists. Ideally, novel direct-acting antivirals should fulfil the following requirements: oral administration once daily, few side-effects and drug interactions, short treatment duration, high barrier to resistance, and effectiveness against all major HCV genotypes. New drugs should also help in the development of an oral interferon-sparing regimen.12

Lawitz and colleagues' trial forms the basis for the phase 3 testing of sofosbuvir. The investigators not only showed high SVR with sofosbuvir but also the activity against HCV genotypes 1-3. No drug-resistant variants were seen with 400 mg daily sofosbuvir, and only two patients had viral relapse.1 Therefore, a daily dose of 400 mg sofosbuvir was chosen as the dose for further trials, including phase 3 trials. Sofosbuvir was safe and did not add notably to the adverse event profile of peginterferon and ribavirin. Limitations of the study were that only treatment-naive, non-cirrhotic patients were included.

Lawitz and colleagues showed that response-guided treatment for 24-48 weeks is not necessary,1 and the findings of another phase 2 study (the ATOMIC study) suggested that a treatment duration of 12 weeks' sofosbuvir in combination with peginterferon plus ribavirin is sufficient, irrespective of baseline factors such as patients' IL28B status or viral load.13 The ATOMIC trial enrolled more than 300 treatment-naive, non-cirrhotic patients with genotypes 1, 4, or 6, showing 87-89% SVR after 12 weeks or 24 weeks of sofosbuvir in combination with peginterferon plus ribavirin. Additionally, sofosbuvir has already been shown to be highly effective in protocols that do not include interferon alfa.14 12 weeks of sofosbuvir plus ribavirin resulted in 84-100% SVR in treatment-naive patients with HCV genotypes 1-3.14 However, nine of ten patients with genotype-1 who had previously not responded to peginterferon plus ribavirin had a relapse without detection of drug-resistant variants. Thus, sofosbuvir plus ribavirin might be sufficient for easy-to-treat patients but more difficult-to-treat patients might need sofosbuvir in combination with peginterferon plus ribavirin or other direct-acting antivirals. In another trial,15 sofosbuvir together with the experimental NS5A inhibitor daclatasvir (Bristol-Myers Squibb, NY, USA) showed excellent (>90%) SVR in patients with HCV genotypes 1-3.15 Sofosbuvir is now being further developed in combination with ledipasvir (formerly known as GS-5885), Gilead Science's own NS5A inhibitor-both drugs are designed as a fixed-dose combination in one tablet. Thus, sofosbuvir seems to fulfil all the aforementioned requirements for new direct-acting antivirals. The key question is, therefore, does one pill fit all?

Certainly there are some important questions to be answered before we can call sofosbuvir the final nail in the coffin for hepatitis C. How effective and safe is the drug in patients with advanced liver disease, including those with decompensated cirrhosis? Does it prevent and treat HCV recurrence after liver transplantation? How effective is it in the treatment of difficult-to-treat HCV genotypes such as genotype 3?

In February this year, Gilead Sciences announced that patients with HCV genotype-3 are more difficult to treat than previously thought.16 However, these data give hope for patients with chronic HCV infection, and, barring any unforeseen surprises, sofosbuvir should be approved by early 2014.

MPM has received financial compensation for consultancy or lecture activities from Achillion, Idenix, Vertex, Roche, Bristol-Myers Squibb, Gilead Sciences, Boehringer Ingelheim, Novartis, Merck, Janssen Pharmaceuticals, and GlaxoSmithKline, and research grants from Roche, Gilead Sciences, Novartis, Boehringer Ingelheim, Bristol-Myers Squibb, Merck, and Janssen Pharmaceuticals. MC has received financial compensation for consultancy or lecture activities from Roche, Bristol-Myers Squibb, Gilead Sciences, Novartis, Merck, and Janssen Pharmaceuticals, and research grants from Roche, Gilead Sciences, and Merck.

GILEAD'S SOFOSBUVIR FOR HEPATITIS C MEETS PRIMARY ENDPOINT IN FOURTH PIVOTAL PHASE 3 STUDY
http://www.natap.org/2013/HCV/022013_07.htm

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New Advances in The Management of Patients with Cirrhosis

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Virtual Press Office

Amsterdam, 25 April 2013

Amsterdam, The Netherlands, Thursday 25 April 2013: New data from clinical studies presented for the first time at the International Liver Congress™ 2013 provide new rationale for an old and established treatment option for portal hypertension.[1] Additionally, spleen stiffness predicts the occurrence of clinical complications, which is of paramount importance in clinical practice.[2]

In patients with cirrhosis, increasing blood pressure in the abdominal circulatory system (known as portal hypertension) leads to potentially lethal complications which might be prevented with simple medical treatment. Patients with cirrhosis and portal hypertension have increased gastrointestinal permeability which allows the movement of bacteria or bacterial components through the lining of the gut into the blood stream in a process known as bacterial translocation. Bacterial components such as lipopolysaccharide can be involved in the genesis of complications of cirrhosis.

The first study evaluated the effects of a non-selective beta-blocker (NSBB) on gastrointestinal permeability and bacterial translocation in patients with cirrhosis with high levels of portal hypertension.1 Patients with severe portal hypertension (HVPG* ≥20mmHg) had increased markers of gastrointestinal permeability and bacterial translocation compared to patients with lower levels of portal hypertension (HVPG<20mmHg). Treatment with NSBB significantly reduced HVPG, improved gastrointestinal permeability and decreased bacterial translocation (LPS-binding protein (LBP) -16% p=0.018; IL-6 -41% p< 0.0001) levels.

Patients who were found to have the highest levels of gastrointestinal permeability were also found to be at most risk of bleeding from oesophageal varices; a complication of cirrhosis which carries a high risk of mortality.

These findings provide a new rationale for the use of non-selective beta-blockers in patients with cirrhosis. EASL’s Treasurer Prof. Mauro Bernardi commented on the data: “The movement of bacteria from the gut and into the bloodstream is extremely serious and potentially fatal in patients with cirrhosis often leading to complications or death. Beta-blockers have been successfully used in a number of conditions and as a standard treatment to control blood pressure in other disease areas. In cirrhosis, they have been used for decades for primary and secondary prophylaxis of bleeding from oesophageal varices. The results of this study show that besides improving portal hypertension, as it was thought up to now, their beneficial effects are also due to their ability to reduce bacterial translocation which may widen the indications for the use of these drugs in this setting.”

In the diagnostic landscape, promising data to support the validity of non-invasive techniques were also presented at the congress. HVPG, an invasive measurement technique currently considered as the best predictor to identify progression to severe scarring of the liver and disrupted essential body functions (clinical decompensation), was compared to techniques such as the evaluation of spleen stiffness (SS) combined with the MELD** score.2

The study showed that in compensated (early) patients with cirrhosis both the SS (p<0.0001) and the MELD (p=0.016) score provided an accurate prediction of clinical decompensation, and their combination in a new score had a predicting power even superior to that of HVPG.

Prof. Mauro Bernardi added, “HVPG is an invasive technique, which can often be discomforting for patients, is only performed in specialised centres and needs experienced operators to be fully reliable. While further studies will be required, if non-invasive techniques continue to present accurate predictions, they would be welcomed in the overall management of compensated patients with cirrhosis.”

Disclaimer: the data referenced in this release is based on the submitted abstract. More recent data may be presented at the International Liver Congress™ 2013.

-Ends-

Notes to Editors

*HVPG or hepatic venous pressure gradient is the most widely used parameter for assessing portal hypertension

**MELD is a scoring system for assessing the severity of chronic liver disease

Compensated cirrhosis, where the body still functions fairly well despite scarring of the liver, is strongly associated with the development of portal hypertension.

Notes to Editors

About EASL

EASL is the leading European scientific society involved in promoting research and education in hepatology. EASL attracts the foremost hepatology experts and has an impressive track record in promoting research in liver disease, supporting wider education and promoting changes in European liver policy.

  • EASL’s main focus on education and research is delivered through numerous events and initiatives, including:
  • The International Liver CongressTM which is the main scientific and professional event in hepatology worldwide
  • Meetings including Monothematic and Special conferences, Post Graduate courses and other endorsed meetings that take place throughout the year
  • Clinical and Basic Schools of Hepatology, a series of events covering different aspects in the field of hepatology
  • Journal of Hepatology published monthly
  • Participation in a number of policy initiatives at European level

About The International Liver CongressTM 2013

The International Liver Congress™ 2013, the 48th annual meeting of the European Association for the study of the Liver, is being held at the RAI Convention Centre in Amsterdam from April 24 – 28, 2013. The congress annually attracts in excess of 9000 clinicians and scientists from around the world and provides an opportunity to hear the latest research, perspectives and treatments of liver disease from principal experts in the field.

For further information on the studies, or to request an interview, please do not hesitate to contact the EASL Press Office on:

Email: easlpressoffice@cohnwolfe.com

Dimple Natali +44 7900 138 904

Courtney Lock +44 7894 386 422

References

[1] Reiberger, T et al, IMPROVEMENT OF INTESTINAL PERMEABILITY AND REDUCING BACTERIAL TRANSLOCATION BY BETABLOCKER TREATMENT IS ASSOCIATED WITH A LOWER RISK OF VARICEAL BLEEDING. Abstract presented at the International Liver CongressTM 2013.

2 Colecchia, A et al, SPLEEN AND LIVER STIFFNESS MEASUREMENT CAN PREDICT CLINICAL COMPLICATIONS IN COMPENSATED CIRRHOTIC PATIENTS: A PROSPECTIVE STUDY

Abstract presented at the International Liver CongressTM 2013.

Source

Novel Therapeutic Approches to Cure Chronic HBV Infection

banner_ilc2013_easl_eu

Virtual Press Office

Amsterdam, 25 April 2013

Amsterdam, The Netherlands, Thursday 25 April 2013: Exciting new data presented today at the International Liver Congress™ 2013 include results from early in vitro and in vivo studies targeting covalently closed circular DNA (cccDNA), which may form the basis of a cure for chronic hepatitis B virus (HBV) infection.

HBV cccDNA is organized into mini-chromosomes within the nucleus of infected cells by histone and non-histone proteins. Despite the availability of efficient therapies against HBV, long-term persistence of cccDNA necessitates life-long treatments to suppress the virus. The following three experimental studies demonstrate effective HBV-cccDNA targeting/depletion using novel therapeutic approaches which offer the potential of a cure.

Liver regeneration induces strong reduction of viral replication and cccDNA levels, but not complete cccDNA eradication; without antiviral treatment, de novo HBV infection can be re-established

Key findings of research[1] in HBV-infected human hepatocytes using the uPA/SCID chimeric mouse system show that liver regeneration induces strong reduction of viral replication and cccDNA levels, with rapid formation of cccDNA-free hepatocytes. However, because complete cccDNA eradication is not achieved, in the absence of antiviral treatment, de novo HBV infection could be re-established in quiescent (non-dividing) human hepatocytes. This suggests that induction of hepatocyte turn-over together with antiviral drugs inducing viral suppression, such as nucleoside analogues and IFN, or blocking cell entry, may accelerate the clearance of the viral minichromosome.

Targeting epigenetic control of nuclear cccDNA minichromosome to suppress HBV transcription and replication may form basis for other therapeutic approaches to curing chronic HBV infection.

In the infected liver cell the rate of replication of HBV is regulated by the acetylation or methylation of histone proteins which surround the cccDNA minichromosome – so called epigenetic regulation. In a separate innovative study[2], the suppression of HBV transcription and replication by small molecules that target the epigenetic control of nuclear cccDNA minichromosome was investigated. The different classes of small molecules studied included: Class I, II and III histone deacetylase inhibitors (HDACi); p300 and PCAF histone acetyltransferases (HAT) inhibitors; hSirt1 activators; JMJD3 histone demethylase inhibitors.

The combined inhibition of p300 and PCAF HATs resulted in an evident reduction of HBV replication which mirrored the decrease of pgRNA transcription. The hSirt1/2 activator MC2791 and the JMJD3 inhibitor MC3119, albeit with different efficiency, inhibited both HBV replication and cccDNA transcription. Results represent a proof of concept that activation of hSirt1 and Ezh2 (through the inhibition of its functional antagonist JMJD3) by small molecules can induce an active epigenetic suppression of HBV cccDNA minichromosome similar to that observed with IFNα, and lead to persistent cccDNA silencing.

Lymphtoxin beta receptor (LTbR) agonisation represents basis for novel alternative therapeutic approach to curing chronic HBV infection

The final study[3] demonstrated that stimulating the lymphtoxin beta receptor (LTbR) provides an effective, long lasting and non-cytopathic mechanism for achieving effective HBV-cccDNA depletion in infected hepatocytes. Cell culture models including HBV-infected HepaRG cells and primary human hepatocytes were used to test the effect of antibodies stimulating human LTbR (BS1 or CBE11). Results show that a strong and dose-dependent anti-HBV effect was achieved by activation of the LTbR. All HBV replication markers were decreased with this treatment, including cccDNA in cells where HBV infection was already established.

Hepatitis B is the most prevalent cause of chronic viral hepatitis and a major global health problem. Prof. Fabien Zoulim, EASL Educational Councillor commented on the exciting new data: “In chronic hepatitis B infection, the viral genome forms a stable minichromosome - the covalently closed circular DNA (cccDNA) - which can persist throughout the lifespan of the hepatocyte.”

“Current treatments focus on suppression of HBV and discovery of compounds directly targeting cccDNA has been one of the major challenges to curing HBV infection; but these preliminary data show novel therapeutic approaches can be applied to successfully target cccDNA with the long-term aspiration of finding a cure” added Prof. Fabien Zoulim.

Disclaimer: the data referenced in this release is based on the submitted abstract. More recent data may be presented at the International Liver Congress™ 2013.

-Ends-

Notes to Editors

About EASL

EASL is the leading European scientific society involved in promoting research and education in hepatology. EASL attracts the foremost hepatology experts and has an impressive track record in promoting research in liver disease, supporting wider education and promoting changes in European liver policy.

EASL’s main focus on education and research is delivered through numerous events and initiatives, including:

  • The International Liver CongressTM which is the main scientific and professional event in hepatology worldwide
  • Meetings including Monothematic and Special conferences, Post Graduate courses and other endorsed meetings that take place throughout the year
  • Clinical and Basic Schools of Hepatology, a series of events covering different aspects in the field of hepatology
  • Journal of Hepatology published monthly
  • Participation in a number of policy initiatives at European level

About The International Liver CongressTM 2013

The International Liver Congress™ 2013, the 48th annual meeting of the European Association for the study of the Liver, is being held at the RAI Convention Centre in Amsterdam from April 24 – 28, 2013. The congress annually attracts in excess of 9000 clinicians and scientists from around the world and provides an opportunity to hear the latest research, perspectives and treatments of liver disease from principal experts in the field.

For further information on the studies, or to request an interview, please do not hesitate to contact the EASL Press Office on:

Email: easlpressoffice@cohnwolfe.com

Dimple Natali +44 7900 138 904

Courtney Lock +44 7894 386 422

References

[1] Allweiss L et al, PROLIFERATION OF HEPATITIS B VIRUS INFECTED HUMAN HEPATOCYTES INDUCES SUPPRESSION OF VIRAL REPLICATION AND RAPID CCCDNA DECREASE IN HUMANIZED MICE. Presented at the International Liver Congress™ 2013.

[2] Palumbo GA et al, SUPPRESSION OF HEPATITIS B VIRUS (HBV) TRANSCRIPTION AND REPLICATION BY SMALL MOLECULES THAT TARGET THE EPIGENETIC CONTROL OF NUCLEAR CCCDNA MINICHROMOSOME. Presented at the International Liver Congress™ 2013.

[3] Lucifora J et al, LYMPHOTOXIN BETA RECEPTOR ACTIVATION LEADS TO DEGRADATION OF HBV CCCDNA FROM INFECTED HEPATOCYTES. Presented at the International Liver Congress™ 2013.

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A new survey by hepatitiscnews.com has found that almost two thirds of people living with hepatitis C have experienced discrimination and stigma in their daily lives due to their condition.

(PRWEB) April 25, 2013

The survey, carried out by online community hepatitisCnews.com, also uncovered low awareness levels of the virus, with four out of ten respondents admitting that they had never heard of hepatitis C until their diagnosis.

While 87% of those taking part in the survey shared their diagnosis with family and friends, over 70% said that people they told had little understanding of how the virus is transmitted.

One respondent commented: “Education and open discussion is needed within the media, much as there has been with mental illness and depression.”

Almost eight out of 10 respondents feel there is not enough help or support for people living with hepatitis C.

Often referred to as a silent disease, as in many cases it does not result in any symptoms, hepatitis C is most commonly transmitted through contact with an infected person’s blood. The hepatitis C virus can cause serious liver damage and, if left untreated, can result in scarring of the liver, cancer or even death. According to the World Health Organization, an estimated 150 million people worldwide are living with the virus.

Dr Matthew Foxton, consultant hepatologist at Chelsea and Westminster Hospital and King’s College Hospital says: “While it is encouraging that there is an increased openness about hepatitis C, there are still many misconceptions as to how it is transmitted. Greater awareness and understanding about hepatitis C will not only reduce the stigma experienced by so many people but also reduce the risk of transmission.”

The survey was carried out on hepatitiscnews.com, an online community and news resource for people living with hepatitis C. The site features tips on living well with hepatitis C, details of resources and support groups worldwide, expert advice and regular updates on hepatitis C and liver disease.

For further information, visit http://www.hepatitiscnews.com.

ENDS

Contact Tudor Reilly Health
Christine Lydon at Tudor Reilly
Tel: +44 (0) 20 7034 3200

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