February 21, 2012

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By Kristen Philipkoski Feb 21, 2012 5:11 PM

In a poetic turn of virology, the scientist who discovered hepatitis C in 1989 has now also discovered a vaccine that will hopefully cure the now-incurable disease.

Not only is it poetic, it's an accomplishment that many thought was impossible. Because hepatitis C is more virulent than HIV, no one was confident a vaccine against all the various strains around the world could be developed. But Michael Houghton, the University of Alberta researcher who announced his work today at the Canada Excellence Research Chairs Summit in Vancouver, says his vaccine works against every known strain of the virus.

It could still be up to seven years before the vaccine goes through the necessary phases of clinical trials and receives FDA approval, but it's amazing news for people who thought they'd be living with hepatitis C for the rest of their lives. It also remains to be seen how much impact the vaccine will have in people who already have the disease—it will be most effective as a preventive against acquiring the disease. Hundreds of thousands of people get hepatitis C every year, and 20 to 30 per cent of them develop liver disease.

Researchers at Oxford have also made progress towards a vaccine. With news out earlier today that hepatitis C now kills more Americans than HIV, a vaccine can't come soon enough.

[Bioresearch Online]

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Does This Patient With Liver Disease Have Cirrhosis?

The Rational Clinical Examination

CLINICIAN'S CORNER

JAMA. 2012;307(8):832-842. doi: 10.1001/jama.2012.186

Jacob A. Udell, MD, MPH, FRCPC; Charlie S. Wang, MD, MSc, FRCPC; Jill Tinmouth, MD, PhD, FRCPC; J. Mark FitzGerald, MB, FRCPC; Najib T. Ayas, MD, MPH, FRCPC; David L. Simel, MD, MHS; Michael Schulzer, MD, PhD; Edwin Mak, BASc; Eric M. Yoshida, MD, MHSc, FRCPC

[+] Author Affiliations

Abstract

Context Among adult patients with liver disease, the ability to identify those most likely to have cirrhosis noninvasively is challenging.

Objective To identify simple clinical indicators that can exclude or detect cirrhosis in adults with known or suspected liver disease.

Data Sources We searched MEDLINE and EMBASE (1966 to December 2011) and reference lists from retrieved articles, previous reviews, and physical examination textbooks.

Study Selection We retained 86 studies of adequate quality that evaluated the accuracy of clinical findings for identifying histologically proven cirrhosis.

Data Extraction Two authors independently abstracted data (sensitivity, specificity, and likelihood ratios [LRs]) and assessed methodological quality. Random-effects meta-analyses were used to calculate summary LRs across studies.

Results Among the 86 studies, 19 533 patients were included in this meta-analysis, among whom 4725 had biopsy-proven cirrhosis (prevalence rate, 24%; 95% CI, 20%-28%). Many physical examination and simple laboratory tests increase the likelihood of cirrhosis, though the presence of ascites (LR, 7.2; 95% CI, 2.9-12), a platelet count <160 × 103/μL (LR, 6.3; 95% CI, 4.3-8.3), spider nevi (LR, 4.3; 95% CI 2.4-6.2), or a combination of simple laboratory tests with the Bonacini cirrhosis discriminant score >7 (LR, 9.4; 95% CI, 2.6-37) are the most frequently studied, reliable, and informative results. For lowering the likelihood of cirrhosis, the most useful findings are a Lok index <0.2 (a score created from the platelet count, serum aspartate aminotransferase and alanine aminotransferase, and prothrombin international normalized ratio; LR, 0.09; 95% CI, 0.03-0.31); a platelet count ≥160 × 103/μL (LR, 0.29; 95% CI, 0.20-0.39); or the absence of hepatomegaly (LR, 0.37; 95% CI, 0.24-0.51). The overall impression of the clinician was not as informative as the individual findings or laboratory combinations.

Conclusions For identifying cirrhosis, the presence of a variety of clinical findings or abnormalities in a combination of simple laboratory tests that reflect the underlying pathophysiology increase its likelihood. To exclude cirrhosis, combinations of normal laboratory findings are most useful

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Related article

JAMA Patient Page

Cirrhosis

Ann R. Punnoose, MD, Writer; Cassio Lynm, MA, Illustrator; Robert M. Golub, MD, Editor

JAMA. 2012;307(8):874.doi:10.1001/jama.2012.82

Cirrhosis is the end stage of any condition in which the liver progressively becomes scarred. It is diagnosed based on physical findings as well as a microscopic examination of liver tissue from a biopsy (tissue sample) or evidence from other diagnostic tests such as ultrasound. Under the microscope, cirrhosis appears as widespread bands of fibrous (made up of fibers) tissue that divide the liver into nodules (small knots or collections of tissue). Eventually, cirrhosis interferes with the function of the liver and can lead to liver failure or liver cancer. The February 22/29, 2012, issue of JAMA includes an article on diagnosing cirrhosis.

F1_medium

COMMON RISK FACTORS

  • Hepatitis B or C infection

  • Autoimmune liver diseases, which include autoimmune hepatitis, primary biliary cirrhosis, and primary sclerosing cholangitis

  • Nonalcoholic fatty liver disease, often found in obese individuals who do not drink alcohol. Although it can have a benign course, it can sometimes progress to cirrhosis.

  • Hereditary metabolic liver diseases, such as hemochromatosis (iron overload), Wilson disease (copper overload), and α1-antitrypsin deficiency (inability to make a type of protein)

  • Long-term exposure to excess amounts of alcohol can lead to inflammation in the liver, which eventually causes cirrhosis.

PHYSICAL FINDINGS

  • Because the liver does not appropriately process bile (a fluid that helps absorb digested fats) and bilirubin (a waste product), jaundice or yellowing of the skin may occur.

  • Palmar erythema (redness of the palms), spider angiomas (blood vessels that spread out in a spider shape), gynecomastia (breast enlargement in men), decreased body hair, and shrinking of the testicles may occur.

  • Patients can experience spontaneous bleeding because the liver is unable to make factors in the blood that form normal clots.

  • As cirrhosis progresses, it becomes increasingly difficult for blood to travel through the vessels in the liver. This causes increased pressure (portal hypertension) in the portal vein (the major vein in the liver). This results in the formation of esophageal varices (enlarged veins in the esophagus) that can bleed easily.

  • The liver is responsible for making several proteins, like albumin. Portal hypertension and low albumin levels cause ascites (accumulation of fluid in the abdominal space) and edema (water retention leading to swelling in dependent areas).

  • As the liver fails, it becomes unable to remove toxins from the body. This buildup can affect a person's level of awareness, called hepatic encephalopathy.

TREATMENT

  • If possible, treat the illness that led to cirrhosis to prevent progression or worsening of cirrhosis before liver failure or cancer develops.

  • Control complications that cirrhosis causes by supplementing nutrition, transfusing clotting factors to prevent bleeding, and using medications to reduce ascites, edema, and the buildup of toxins.

  • Avoid alcohol and any medications that could affect the liver.

  • When cirrhosis progresses and the complications can no longer be controlled, physicians and their patients may discuss liver transplantation.

FOR MORE INFORMATION

INFORM YOURSELF

To find this and previous JAMA Patient Pages, go to the Patient Page link on JAMA's website at www.jama.com. Many are available in English and Spanish. A Patient Page on liver transplantation was published in the January 18, 2012, issue.

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February 21, 2012 10:49 AM

MONTREAL, Feb. 21, 2012 /CNW Telbec/ - Montreal will host the first ever Canadian Symposium on the Hepatitis C Virus (HCV) on February 23 at the Hotel Hilton Bonaventure. Chaired by Dr. Naglaa Shoukry of the University of Montreal Hospital Research Centre (CRCHUM), this symposium will bring together around 200 researchers and clinicians from across Canada and around the world. The goal is to increase interactions and exchanges between researchers, healthcare professionals and community organizations to develop more effective strategies to meet the challenges of preventing and treating Hepatitis C.

CRCHUM researchers at the forefront of HCV research
CRCHUM researchers have spearheaded the development of many important discoveries in this area:

  • The effectiveness of early treatment in restoring the immune response against HCV (Drs. Naglaa Shoukry and Julie Bruneau)
  • Development of guidelines for HCV screening and treatment in injection drug users (Dr. Bruneau)
  • Clinical trials for novel HCV antiviral therapies (Drs. Bernard Willems and Marc Bilodeau)
  • Care and management of HCV infected patient post liver transplant (Dr. Denis Marleau).

"However," notes Dr. Shoukry, "these important breakthroughs remain all too often in the laboratory and only rarely make their way into the healthcare care community."

New drugs and resistance: a debate in the scientific community
Panellists will also address the recent approval and introduction of new drugs to fight this disease. While the advent of these pharmacological developments represents a significant treatment breakthrough, it also raises issues related to drug resistance and access to these drugs by vulnerable and marginalized populations. These two themes will figure prominently in discussions at the symposium. "Our expectation is that this meeting will set the agenda for research and community outreach for the coming years," notes Shoukry.

Internationally renowned speakers
The symposium is organized by the National CIHR Research Training Program in Hepatitis C. It, which will feature speakers from throughout North America and Europe, will be held at the Hilton Bonaventure Hotel in Montreal. Topics will include a broad range of issues ranging from the virology of HCV, immunity and vaccine development against HCV to socially-based approaches to HCV prevention, psychological issues in the care of people living with hepatitis C and potential problems associated with the new treatments for HCV.

The keynote speaker at the conference is Dr. Jean-Michel Pawlotsky from the University of Paris-Est and the Henri Mondor University Hospital in Créteil, France, a leading authority on treatment of hepatitis C. "This symposium is a major first step in ensuring that basic and clinical research findings reach those who matter the most—patients," notes Dr. Shoukry.

Hepatitis C

  • The hepatitis C virus (HCV) infects 170 million individuals worldwide.
  • In Canada, approximately 240,000 people are infected
  • In Canada, there are 4,000 new infections each year.
  • The majority of HCV exposed individuals develop a life-long persistent infection that can lead to irreversible liver damage and cancer.

About the CRCHUM: www.crchum.qc.ca

About Dr Naglaa Shoukry:
http://www.chumtl.qc.ca/userfiles/Image/CENTRE_RECHERCHE/CRCHUM/Documentaions/Recherche20CRCHUM/RechercheCRCHUM_vol1no1_fr_.pdf

About the National CIHR Research Training Program in Hepatitis C: http://www.ncrtp-hepc.ca/

For further information:

Source : CRCHUM

Information:

Richard Ashby
Associate Director, Information and Development
CRCHUM
(514) 890-8000 / 14090
Richard.ashby.chum@ssss.gouv.qc.ca

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GEN0212_001_graphic_b426

Gatroenterology & Endoscopy News ISSUE: FEBRUARY 2012 | VOLUME: 63:2

Careful Patient Selection, Education Is Key for Success

by Christina Frangou

San Francisco—Soon after the FDA approved two direct-acting antiviral agents (DAAs) last spring for treating infection with hepatitis C virus (HCV), a 57-year-old black man came to see gastroenterologist Andrew Muir, MD.

The man had been diagnosed with hepatitis C in 2001. A liver biopsy one year later revealed he had stage II fibrosis. At the time, the patient declined treatment, saying the duration was too long and offered too few benefits.

But recently, he came back to Dr. Muir wanting to try a new protease inhibitor. Based on his reading, the man believed he could avoid interferon (IFN) and ribavirin (RBV), take a protease inhibitor as monotherapy for 24 weeks and expect a 75% chance of achieving a sustained virologic response (SVR).

Unfortunately, the patient’s expectations were unrealistic on all counts. The new protease inhibitor can only be given in conjunction with IFN and RBV, and the treatment duration varies. For blacks, therapy usually lasts a full 48 weeks, and in clinical trials, only 30% of black patients achieved an SVR with 28 weeks of therapy. Moreover, among black patients in the Phase III trials, SVR rates fell short of the 75% that the patient expected, and in treatment-naive blacks, only 62% receiving telaprevir and 53% on boceprevir achieved an SVR.

Educate To Encourage Adherence

Unrealistic expectations are common among patients with HCV infection who, after years of waiting for better therapies, are eager to try treatment with the new DAAs, said Dr. Muir. The DAAs on the market today are complex, with varied stoppage rules, monitoring points and some serious adverse events and drug–drug interactions.

“This is a real problem for clinicians. There’s tremendous excitement about these new therapies, but oftentimes, patients’ expectations are not in line with what these drugs can deliver,” said Dr. Muir, clinical director of hepatology at Duke University Medical Center, Durham, N.C.

In a presentation at The Liver Meeting 2011, Dr. Muir stressed that clinicians need to take time to carefully prepare patients for DAA therapy. Physicians must have clear, detailed discussions with their patients before and throughout treatment to optimize the benefits of DAA therapy, he said.

“The major challenges are preparing patients for the rigors of therapy, checking in frequently to make decisions about the duration of treatment and managing any issues as the patient goes along,” said Dr. Muir.

When patients come into the office considering treatment with DAAs, the first step is to clarify their expectations, said Dr. Muir. Patients need to learn the reality about DAAs if they want treatment to succeed.

Dr. Muir outlines for patients the complex prescribing rules, the contraindications, the lifestyle changes and duration of treatment with DAAs. The lifestyle changes can be significant, he cautions patients. Both telaprevir and boceprevir must be taken three times a day, or once every eight hours, and always with a meal. Dr. Muir then asks if the patient still wants treatment when these things are taken into account.

“That’s no small feat. Patients must adhere to that regimen because lapses in the concentration of telaprevir and boceprevir have historically been the risk period for breakthrough variants on therapy,” said Raymond Chung, MD, chief of hepatology and vice-chief of gastroenterology at Massachusetts General Hospital, Boston. Many of Dr. Chung’s patients limit or reschedule their work hours while on DAA therapy to help with adherence.

The key to getting patients through DAA treatment successfully is to select patients carefully and prepare them assiduously, said Gary L. Davis, MD, director of general and transplant hepatology at Baylor University Medical Center, Dallas. “This means that any issues that might impact compliance, tolerance and drug access should be dealt with before treatment starts. Educating the patient is essential. Patients and their support person need to clearly understand the importance of dosing compliance, lab monitoring and treatment stopping rules/end points.”

The treatment care team then needs to remain in close contact with the patient throughout treatment to reinforce adherence and offer feedback on their process, he added. At Dr. Chung’s office at Massachusetts General Hospital, one nurse practitioner has been assigned full-time to managing patients on DAAs. She works with them on everything from managing possible reactions like rash and anemia to helping them set up a daily schedule for taking the medications.

“We have 50 to 100 patients in varying stages of DAA treatment,” said Dr. Chung. “Every one of these patients is coming in for frequent visits—weekly in the beginning—and they are very much in need of monitoring, not just for adverse events like rash but also for fatigue and their ability to carry out work.”

Begin With a Thorough History

Before patients start the new therapies, gastroenterologists and hepatologists should consider getting a liver biopsy to help guide treatment, said Dr. Muir. Physicians also should confirm a patient’s history of treatment for HCV. If patients were previously on antiviral therapies, physicians need to find out as much as they can about that experience.

“You must ask whether we can improve upon previous treatment,” said Dr. Muir. “Were there adverse events with treatments? Were there dose reductions? If so, were they appropriate? How was patient adherence to medications? Did they use alcohol?”

Based on that information, physicians should outline the likelihood of each individual patient achieving an SVR, he said. The key predictors of SVR are whether patients are treatment-naive or treatment-experienced, whether they have cirrhosis and their race. Another important issue for patients is treatment duration. Duration will vary depending on each patient’s characteristics. “It’s important to speak with every patient about their likelihood of a shorter duration of treatment,” said Dr. Muir.

The American Association for the Study of Liver Diseases recommends 48 weeks of treatment for all patients with cirrhosis, as fewer patients with cirrhosis were included in the clinical trials that led to approval of the new drugs. Among those included, virologic response levels were lower than for patients without cirrhosis. For treatment-naive patients, 46% of non-black and 29% of black patients in the boceprevir SPRINT-2 (Serine Protease Inhibitor Therapy 2) trial achieved undetectable levels of HCV by 28 weeks, making them eligible for the shortened course of treatment (Poordad F et al. N Engl J Med 2011;364:1195-1206). In the telaprevir trial, 58% of patients had an early rapid virologic response (Jacobson IM et al. N Engl J Med 2011;364:2405-2416).

Patients’ interleukin-28B (IL28B) genotype also affects the expected duration of treatment. For both boceprevir and telaprevir, patients with the IL28B CC genotype are most likely to attain an early virologic response, more likely to receive a shortened course of therapy and more likely to have an SVR, according to studies presented at last year’s annual meeting of the European Association for the Study of the Liver.

Follow Through: Monitor for Response, Resistance, Reactions, Interactions

When the new HCV drugs were first approved, physicians’ offices reported some trouble getting approval from third-party payers for the full course of treatment, said Dr. Chung. His office had to provide documentation of successful early virologic response to get the go-ahead from payers to approve continuation of treatment with a protease inhibitor.

“You can imagine that if any gaps occur in the virologic tests or their reporting, this could lead to interruption of protease inhibitor therapy. It’s been a real challenge,” he said.

Experts recommend following patients very carefully over the course of treatment, monitoring any virologic breakthroughs or adverse reactions to the medications, particularly rash and anemia. Dr. Chung sees patients after the first, second and fourth week of therapy, and every four weeks thereafter if patients are having an uneventful course. Treatment monitoring is essential to prevent unwarranted continuation of treatment in patients when a breakthrough has occurred, he said.

“That would signal the emergence of resistant variants. Upon discovery, it would be paramount to discontinue the entire regimen to prevent selection of additional resistance mutations,” he said.

Equally important is the need to monitor patients closely for adverse reactions and drug–drug interactions. As IFN and RBV remain the backbone of this HCV regimen, the same contraindications exist as with standard dual therapy: decompensated cirrhosis, renal insufficiency, advanced cardiac/pulmonary disease, active depression, severe mental illness, anemia/neutropenia/thrombocytopenia and noncompliance.

Additionally, there are important drug–drug interactions with boceprevir and telaprevir. Both DAAs inhibit the CYP3A4/5 enzyme. Drugs metabolized by CYP3A4/5 may have increased effect in the presence of boceprevir or telaprevir. The DAAs themselves are metabolized by this cytochrome. As a result, other drugs that induce or inhibit CYP3A4/5 could affect HCV levels.

“Planning is key to deal with drug–drug interactions,” said Dr. Muir. It’s very important to do a risk–benefit analysis of treatment with boceprevir and telaprevir, taking into account patients’ comorbidities, he added.

It is important to review all drugs that the patient is taking, including over-the-counter and herbal medications. Check with the patient’s primary care provider, cardiologist and psychiatrist about medication use, Dr. Muir said. “It’s a good time to revisit the need for all medications. Ask if the antidepressant can be changed, the blood pressure medicines. Can the patient hold their statin for 12 weeks?” he said.

Women taking oral contraceptives should be advised to try other methods of contraception, such as an intrauterine device or barrier methods. Additionally, pregnant women should not take either drug, as both are considered pregnancy category X, meaning the risks “clearly outweigh potential benefits,” according to the FDA.

Anemia and rashes are the two most common adverse events associated with the new therapies. Experts suggest physicians be proactive about managing both.

Before a patient starts therapy, do a pretreatment evaluation for anemia and consider the impact on comorbidities, such as cardiac and pulmonary disorders. Weigh the benefits of reducing the dose versus increasing or starting erythropoietin.

For rashes, patients should be proactive by moisturizing twice a day, limiting sun exposure and wearing loose-fitting clothing. Dr. Chung recommends including a dermatologist on the treatment team.

Keep an Eye on the ‘Holy Grail of Therapy’

One other important element that needs to be taken into account when considering patients for DAA therapy is whether patients should wait for something else to be approved, said Dr. Chung. Recent results from Phase II studies of second-generation DAAs suggest that some combination of these could be approved in the next three years (see “New Polymerase Inhibitor Could Become Cornerstone of Interferon-free HCV Treatment Regimen,” by Christina Frangou. Gastroenterology & Endoscopy News 2012;63[2]:16 and “Second Study of New Hep C Drug Is Promising for Difficult-to-Treat HCV Genotype 1 Patients,” by Christina Frangou. Gastroenterology & Endoscopy News 2012;63[2]:17-19). These therapies omit IFN from the treatment regimen and can generally be taken orally once a day, with or without food.

“That’s something critical to consider. With all the complexities of therapy—the issues of tolerability, adherence, drug–drug interactions, quality of life—there’s another equally important set of events going on, and that’s the emerging data on all-oral, interferon-free treatments,” said Dr. Chung. “It’s clear that the promise of interferon-sparing therapy is very real. For all of us, that would be the holy grail of therapy.”

Dr. Chung currently recommends that all patients with HCV infection who have advanced-stage disease, regardless of whether they are treatment-naive or experienced, should be considered for boceprevir or telaprevir, provided the benefits outweigh the risks. Patients who can reasonably defer treatment because of early-stage disease or who cannot tolerate IFN may be able to wait for investigational therapies to be approved. These patients also may be eligible for investigational studies, which are ongoing.


Dr. Muir disclosed that he is on advisory committees or review panels for Merck & Co., and Vertex Pharmaceuticals; is a consultant for Inhibitex, Merck & Co., and Vertex Pharmaceuticals; and receives grant/research support from Abbott Laboratories, Anadys, Bristol-Myers Squibb, Gilead, Medtronic, Merck & Co., Pfizer, Roche, Santaris, Scynexis and Vertex Pharmaceuticals. Dr. Chung receives grant/research support from Gilead, Merck & Co., Pfizer and Romark. Dr. Davis is a consultant for Vertex Pharmaceuticals and receives grant/research support from Abbott Laboratories, Boehringer Ingelheim, Bristol-Myers Squibb, Genentech, Gilead, Novartis, Pharmasset, Tibotec and Vertex Pharmaceuticals.

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Hepatitis C Bigger Killer than HIV

31272

By Michael Smith, North American Correspondent, MedPage Today

Published: February 20, 2012

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

More Americans now die from hepatitis C infection than from HIV, researchers from the Centers for Disease Control and Prevention reported.

The rate of HIV deaths has been falling while the rate for hepatitis C has been rising and the two curves crossed each other in 2007, according to Kathleen Ly, MPH, and colleagues.

In that year, they wrote in the Feb. 21 issue of Annals of Internal Medicine, 12,734 deaths were blamed on HIV, compared with 15,106 attributed to hepatitis C.

The analysis, based on death certificates from 1999 through 2007, also showed that the death rate for hepatitis B has been falling slightly, although it was the underlying or contributing cause of 1,815 deaths in 2007.

The figures probably represent "only a fraction of a larger burden of morbidity and mortality from viral hepatitis," Ly and colleagues argued, noting that chronic hepatitis infection -- both B and C -- is most prevalent among people born from 1945 through 1965.

Most of those with the disease do not know they are infected and they are now reaching the age where they are at risk for hepatitis-related diseases and death, they noted.

Indeed, in 2007, 73.4% of hepatitis C-related deaths were among people ages 45 through 64, while 59.4% of hepatitis B-related deaths occurred in that age group, they found.

Ly and colleagues cautioned that someone other than the primary physician often completes death certificates, so that they may not be completely accurate. But the effect of that bias, they noted, should be roughly the same over time and so should not affect the trends.

Also, they noted, viral hepatitis was often not detected and thus not reported as a cause of death.

The findings come at a time when the treatment picture for hepatitis C is changing rapidly, as a range of new direct-acting agents is approved and comes to the clinic.

Before 1990, HCV infection had only a 10% cure rate with early interferon monotherapy. In 2011, HCV-specific protease inhibitors combined with pegylated interferon and ribavirin, achieved close to 70% sustained virologic response rates for patients with genotype 1 infections.

Within five years, it may be possible to achieve 90% cure rates using combinations of the new agents, according to Harvey Alter, MD, and Jake Liang, MD, both of the National Institutes of Health in Bethesda, Md.

"What is currently lacking in this optimistic perspective is a national 'find-and-treat' policy" to reduce the burden of the disease, they argued in an accompanying editorial.

Preventing the long-term consequences of hepatitis C – liver disease and cancer – "is now achievable if our collective will can evolve as rapidly as our pharmacologic skill."

One possible step forward would be a change in screening policy for hepatitis C, according to David Rein, PhD, of the social science research organization NORC at the University of Chicago in Atlanta, and colleagues.

Currently, the CDC recommends antibody screening for people with such risk factors or indicators as a history of injection-drug use or elevated alanine aminotransferase levels.

But one-time screening and then treating people based on birth cohort – specifically those born from 1945 through 1965 – would be cost-effective, Rein and colleagues argued in a companion study in the journal.

Their analysis showed that birth-cohort screening identified an extra 808,580 cases of chronic infection, compared with the status quo, at a cost of $2,874 per case.

Depending on the form of subsequent treatment, the screening would prevent between 82,300 and 121,000 deaths, with an incremental cost-effectiveness ratio per quality-adjusted life year gained ranged from $15,700 to $35,700, Rein and colleagues calculated.

The analysis of hepatitis C burden was supported by the CDC. The authors are employees of the agency.

The analysis of birth-cohort screening was supported by the CDC. Rein did not report any financial links with industry. Several authors are employees of the CDC.

The journal said the editorial authors made no disclosures.

Primary source: Annals of Internal Medicine
Source reference:
Ly KN, et al "The increasing burden of mortality from viral hepatitis in the United States between 1999 and 2007" Ann Intern Med 2012; 156: 271-278.

Additional source: Annals of Internal Medicine
Source reference:
Rein DB, et al "The cost-effectiveness of birth-cohort screening for hepatitis C antibody in U.S. primary care settings" Ann Intern Med 2012; 156: 263-270.

Additional source: Annals of Internal Medicine
Source reference:
Alter HJ, Liang TJ "Hepatitis C: The end of the beginning and possibly the beginning of the end" Ann Intern Med 2012; 156: 317-319.

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Also See:

  1. Boomers' Drug Use Pushes Hepatitis Deaths Past HIV, Study Finds
  2. Hepatitis C Now Killing More Americans than HIV

WATERTOWN, Mass., Feb. 21, 2012 /PRNewswire/ -- Enanta Pharmaceuticals, Inc., a research and development company dedicated to creating best-in-class small molecule drugs in the infectious disease field, announced today that it has entered into an exclusive collaboration and license agreement with Novartis for the worldwide development, manufacture and commercialization of its lead development candidate, EDP-239, from its NS5A hepatitis C virus (HCV) inhibitor program. Enanta has received IND approval for EDP-239 from the FDA.

NS5A, a clinically validated target, is a non-structural viral protein that is essential to viral replication. Research efforts have shown that targeting NS5A gives rise to profound antiviral activity, and as a result, this protein has emerged as an important target for antiviral drug development. Enanta's NS5A program and intellectual property estate in the HCV field were derived from its internal drug discovery efforts. EDP-239, Enanta's lead candidate targeting NS5A was most recently recognized on Windhover's list of the "Top Most Interesting Infectious Disease Projects to Watch".

Under the terms of the agreement, Enanta will receive an upfront payment of $34 million and is eligible to receive up to $406 million if certain clinical, regulatory, and commercial milestones are met. Enanta is also eligible to receive tiered double-digit royalties on worldwide sales of products, and retains co-detail rights in the United States. Novartis will be responsible for all costs associated with the development, manufacture and commercialization of EDP-239 and will fund Enanta's drug discovery efforts on certain additional compounds targeting NS5A.

"Novartis is a recognized leader in the field of HCV, and access to its global expertise combined with our shared vision for commercializing HCV therapies will support the successful development and commercialization of products targeting NS5A," said Jay R. Luly, PhD, President & CEO, Enanta Pharmaceuticals. "We believe EDP-239 has great potential as a potent ingredient in combination drug therapy, and our preclinical studies have demonstrated high potency against multiple genotypes of the virus, excellent safety profile and a preclinical pharmacokinetic profile amenable to once-a-day dosing in humans."

About the Hepatitis C Virus
Hepatitis C is a liver disease affecting over 170 million people worldwide. The virus is spread through direct contact with the blood of an infected person. Hepatitis C increases a person's risk of developing chronic liver disease, cirrhosis, liver cancer and death. Liver disease associated with HCV infection is growing rapidly, and there is an acute need for new therapies that are safer and more effective. Specifically targeted antiviral therapies for HCV, such as NS3/4a protease and NS5A inhibitors, may have the potential to increase the proportion of patients in whom the virus can be eradicated.

About Enanta
Enanta Pharmaceuticals is a research and development company that uses its novel chemistry approach and drug discovery capabilities to create best in class small molecule drugs in the infectious disease field. Enanta is developing novel protease, NS5A, nucleoside(tide) polymerase, and cyclophilin-based inhibitors targeted against the Hepatitis C virus (HCV). Additionally, the Company has created a new class of antibiotics, called Bicyclolides, which overcomes bacterial resistance. Antibacterial focus areas include overcoming resistance to superbugs, treating respiratory tract infections, and developing intravenous and oral treatments for hospital and community MRSA infections. Enanta is a privately held company headquartered in Watertown, Mass. Enanta's news releases and other information are available on the company's web site at www.enanta.com.

For Enanta Investor Relations, please contact:
Paul Mellett
617-607-0761

For Enanta Public Relations, please contact MacDougall Biomedical Communications:
Kari Watson
781-235-3060 or kwatson@macbiocom.com

SOURCE Enanta Pharmaceuticals, Inc.

RELATED LINKS
http://www.enanta.com

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