Wednesday, December 30, 2015

Senator: Cut Medicaid for hepatitis C patients who drink alcohol, go off meds

Senator: Cut Medicaid for hepatitis C patients who drink alcohol, go off meds

TOPEKA – Medicaid recipients being treated for hepatitis C who drink alcohol or go off their medication would lose coverage under a recommendation passed by a legislative panel Tuesday.

Sen. Jim Denning, R-Overland Park, proposed that the state not cover high-cost medications for hepatitis C patients who don’t comply with treatment requirements. The proposal came toward the end of an all-day meeting of the KanCare Oversight Committee.

The seven-member committee passed the motion on a voice vote. The panel’s two Democrats, Rep. Jim Ward, D-Wichita, and Sen. Laura Kelly, D-Topeka, voted against it.

“Put me down as a ‘no’ for killing people,” Ward said after the vote.

Continue reading....

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Sunday, December 27, 2015

NPR- States Deny Pricey Hepatitis C Drugs To Most Medicaid Patients

States Deny Pricey Hepatitis C Drugs To Most Medicaid Patients

Medicaid in at least 34 states doesn't pay for treatment unless a patient already has liver damage, according to a report released in August. There are exceptions—for example, people who also have HIV or who have had liver transplants—but many living with chronic hepatitis C infection have to wait and worry. 
"It is just not feasible to provide it to everyone," says Matt Salo, director of the National Association of Medicaid Directors. "States have to make sure that we're going to prioritize and that those who need it the most get priority treatment, and that's what you're seeing."
Continue reading... 

Saturday, December 26, 2015

Hep C patient goes offshore for cure

Hep C patient goes offshore for cure
Home » News » Dunedin

By David Loughrey on Sun, 27 Dec 2015

A Dunedin woman who has imported new generation hepatitis C drugs she says will save her life wants to get her message out to others to source them from a ‘‘buyers' club'' in Australia.
Earlier this year, law student Hazel Heal was on the verge of needing a liver transplant, but this week the virus was all but undetectable in blood tests.
Ms Heal bought drugs in Australia for $3800, when in New Zealand they would have cost $84,000.
She found website www., which included information on a buyers' club, where people got together to buy drugs from overseas.
She then had a Skype appointment with Tasmanian GP Dr James Freeman.
That, she said, was ‘‘a good 40-minute appointment - he's very, very thorough'', which required blood results and other medical information.

Continue reading.... 

Wednesday, December 23, 2015

Australia bets $1B on pricey hep C drugs in broad effort to eradicate the disease

Australia bets $1B on pricey hep C drugs in broad effort to eradicate the disease
December 23, 2015 | 

Good news for Gilead Sciences ($GILD) and Bristol-Myers Squibb ($BMY): Australia's federal government wants to eliminate hepatitis C in the country. And it plans to shell out $1 billion on the drugmakers' meds to do that.

Australia is earmarking $1 billion to subsidize Gilead's Sovaldi and Harvoni, along with Bristol's Daklinza--as well as Pendopharm's ribavirin tablets, Ibavyr--for all hep C patients, regardless of their age or how they acquired the disease, Sky News reports. Authorities are hoping the investment can wipe the malady off the continental map within 20 years.

A different approach: High price of hepatitis C cure pushes health experts to promote prevention

A different approach: High price of hepatitis C cure pushes health experts to promote prevention

Nanci Hutson
The Daily Courier

Dr. Richard Pleva discusses the new medications that are leading to cures for people with this illness.

Hepatitis C is a "silent disease" as symptoms are often vague, fatigue-or flu-like, and can take decades to manifest themselves.

The repercussions of the illness, though, can be severe.

Left undiagnosed and untreated, hepatitis C can cause irrevocable liver disease or cancer such that liver transplant is the only patient option, according to local doctors and health professionals.

HCV Next: HCV and the Gastroenterologist, Exciting Real-World Data, New Regimens Emerge

The following articles appeared in the December print edition of HCV NEXT.

Table of Contents
A Conversation with Susanna Naggie, MD, MHS

The Liver Meeting 2015
HCV Next had the opportunity to sit down with leading experts in the field after they attended The Liver Meeting and they each provided insight into the data presented and how it will impact care of patients with HCV. These included Co-Chief Medical Editor, Ira M. Jacobson, MD, chair of the department of medicine at Mount Sinai Beth Israel Medical Center in New York City; and editorial board member, Catherine T. Frenette, MD, medical director of the department of Organ Transplantation at Scripps Green Hospital in San Diego.

Monroe County amid hepatitis C epidemic

State declares public health emergency for Monroe County amid hepatitis C epidemic



Watch Video

MONROE COUNTY, Ind. (December 22, 2015) – A public health emergency has been declared for Monroe County amid a hepatitis C epidemic. This allows the county health department to establish a syringe exchange program as part of a broader effort to reduce the spread of hepatitis C.

“Monroe County is experiencing an epidemic of hepatitis C tied to intravenous drug use,” said Dr. Adams. “The syringe exchange is part of a comprehensive approach that will connect residents with treatment, healthcare and other services critical to improving their health and halting the spread of disease.”

Senate Enrolled Act 461 made syringe exchange programs legal in Indiana for the first time. The law sets forth the procedural and substantive requirements that local communities must meet in order for an emergency declaration to be considered by the state health commissioner.

Steps in the process for local communities:

Local health officer must:
Declare that an epidemic of Hepatitis C or HIV exists
Determine that it is primarily transmitted through IV drug use
Deem that a syringe exchange program is medically appropriate as part of a comprehensive response

County commissioners must:
Hold a public hearing
Take official action adopting the declarations of the local health officer (above)
Describe other actions taken regarding the epidemic that have proven ineffective
Request a public health emergency declaration from the state

By declaring this public health emergency, the state health commissioner concurs with the declarations of the local health officer and county commissioners. By law, specific aspects of design and implementation of the program are left to local officials. No federal or state funding is appropriated for syringe exchange programs.

“What it means is that the local health officer has declared that there is an outbreak which means then access or more of reported cases than what it would be expected to see over the past five years,” said Pam Pontones, State Epidemiologist for the Indiana Department of Health.

The number of cases in Monroe County is up from just 93 cases in 2010. State officials say, intravenous drug use stemming from heroin abuse, is likely to blame.

“Reducing injection drug use is really a key way to eliminating the spread of Hepatitis C or HIV as well,” said Pontones.

After the state declared an emergency there, Monroe County health officials are able to implement a needle exchange program. Getting addicts to use clean needles is the state’s way to slow the surge.

It’s the same program that was implemented in Scott County, where nearly 200 new cases of HIV sprung up seemingly overnight this summer. It was the largest rural HIV outbreak in the country’s history.

“I think this really illustrates that there’s more rural communities vulnerable to having dramatic increases in HIV whenever you have injection drug use,” said Dr. William Yarber, a public health professor at Indiana University, and the Director of the Rural Center for STD and AIDS prevention.

Rural areas Yarber says are more likely to see outbreaks and less likely to see fast and easy solutions. Many of the state’s resources Yarber says are concentrated in urban areas like Indianapolis and the Chicago suburbs.

“This is going to have a lasting impact. Over $80 million in lifetime healthcare in Scott County, I mean that’s one part of it of course economics, but how about the human suffering?” he said.

The public health emergency will last through December 20, 2016. Monroe County is now the fourth county in the state to utilize a needle exchange program because of a disease outbreak.

For questions regarding the syringe exchange program, contact Kathy Hewett at the Monroe County Health Department at (812) 349-2722.

Visit the Indiana State Department of Health at for important health and safety information, or follow us on Twitter at @StateHealthIN and on Facebook at

Hoosiers who do not have health care coverage or access to a doctor are encouraged to check availability for the new Healthy Indiana Plan—HIP 2.0—by visiting or calling 1-877-GET-HIP-9.

Friday, December 11, 2015

Abbott and UC San Francisco Discover New Virus is Linked to Hepatitis C

Abbott and UC San Francisco Discover New Virus is Linked to Hepatitis C


ABBOTT PARK, Ill., Dec. 11, 2015 /PRNewswire/ -- Abbott and University of California San Francisco (UCSF) published research identifying a newly discovered human virus, known as human pegivirus 2 (HPgV-2), and proving it is found among some patients with hepatitis C (HCV). This research, published today in PLOS Pathogens, identified eight complete strains of HPgV-2, which makes it the first study to reveal the entire genetic makeup of this new virus. Although infection with this bloodborne virus was found to be tightly associated with HCV, it is not yet known whether this new virus can cause disease.

"Based on our findings, our team used the genetic makeup of the virus to develop both a molecular test for detecting it in the bloodstream and an antibody test for determining an immune response to the virus. Our next step is to explore whether this new virus can cause disease, and if so, work with blood banks to continue to help safeguard the world's blood supply against these types of new viruses," said John Hackett Jr., Ph.D., divisional vice president of applied research and technology at Abbott. "Research such as this is ultimately focused on unlocking new technologies that hold the potential for significant improvements to the practice of healthcare."

This study was conducted by the UCSF-Abbott Viral Diagnostics and Discovery Center (VDDC), which was established through a multi-year collaboration between Abbott and UCSF. To identify the new virus, researchers used techniques for sequencing fragments of the genetic makeup of it, including deep sequencing and ultra-rapid pathogen identification technologies. The patient blood sample from which the virus was first discovered was provided by the Center for Liver Diseases at University of Chicago Medical Center.

"By characterizing eight complete genomes and four partial genomes of human pegivirus 2, this study provides new insights into the evolution and diversity of this virus in infected individuals," said Dr. Charles Chiu, M.D., Ph.D., an associate professor of laboratory medicine at UCSF and director of the UCSF-Abbott VDDC. "Discoveries like these are one of the reasons our partnership with Abbott is so important, as they provide us with information that push the boundaries of scientific knowledge and may have significant downstream implications with respect to human health."

About Abbott:

At Abbott (NYSE: ABT), we're committed to helping you live your best possible life through the power of health. For more than 125 years, we've brought new products and technologies to the world -- in nutrition, diagnostics, medical devices and branded generic pharmaceuticals -- that create more possibilities for more people at all stages of life. Today, 73,000 of us are working to help people live not just longer, but better, in the more than 150 countries we serve.

Connect with us at, on Facebook at and on Twitter @AbbottNews and @AbbottGlobal.

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Scientists discover a potential treatment for cirrhosis

Scientists discover a potential treatment for cirrhosis

A study by IRB Barcelona and IDIBAPS reveals a therapeutic target to prevent the development of the many abnormal blood vessels that cause gastrointestinal bleeding—the main complication in cirrhosis.

Cirrhosis is the main risk factor for liver cancer. The same target may be the key to preventing and treating this condition.

Cirrhosis figures among the top twenty causes of death from disease worldwide.

Scientists headed by Raúl Méndez, ICREA research professor at the Institute for Research in Biomedicine (IRB Barcelona), and Mercedes Fernández, at IDIBAPS reveal that the inhibition of CPEB4 protein may prevent the development of the abnormal blood vessels associated with cirrhosis. Pathological angiogenesis is one of the most serious complications in patients with cirrhosis and a key factor in the development and worsening of the disease. Consequently, many research efforts focus on identifying treatments for this condition. The results of the study have been published in the most recent issue of Gastroenterology

In Western countries, cirrhosis is among the 10 leading causes of death among adults. It is a very common disease in Spain and the leading cause of liver transplantation in this country. It is responsible for a high rate of hospital admissions and use of health resources due to complications that occur in advanced stages of the disease.

Perverse repairing effect

Tissue sample of human cirrhotic liver, in which changes in the structure and elevated CPEB4 protein expression can be appreciated in the regeneration nodules. Credit: IRBBarcelona/IDIBAPS

Cirrhosis is a chronic lesion characterised by the accumulation of scar tissue (fibrous nodules), which alters the normal structure and function of the organ. Chronic hepatic lesions are caused mainly by alcoholism, hepatitis C, and increasingly by obesity.

The accumulation of scar tissue impedes blood circulation in the liver, thus leading to portal hypertension (the portal vein). To relieve the pressure in the vein, collateral blood vessels develop outside the liver. The problem is then two-fold, first because the liver receives even less blood, thereby causing greater damage to the organ, and second because the blood vessels are of poor quality (pathological angiogenesis).

"Hepatic cells try to repair liver lesions, but the way by which they do this turns out to be fatal for the organ. This is a loop that gets bigger and finally threatens the patient's life. Also, the collateral blood vessels form varicose veins in the oesophagus and stomach of patients with cirrhosis; these veins are fragile and have a high tendency to burst, causing heavy bleeding that is difficult to stop," explains Mercedes Fernández, from IDIBAPS and co-leader of the study. "This is why a treatment that regresses and/or prevents pathological veins—which is not currently available—would be efficient," she adds.

A target named CPEB4

VEGF (vascular endothelial growth factor) is the main effector protein in the development of blood vessels. "All current drugs that aim to prevent neovascularisation are based on inhibiting VEGF or VEGF receptors, but the problem is that indiscriminate attack of this protein impairs the normal development of blood vessels, thus causing unbearable adverse effects," explains Méndez, from IRB Barcelona. 

Pathological blood vessels (white circles), with abundant CPEB4 expression in cirrhotic tissue. Credit: IRBBarcelona/IDIBAPS

In a previous study published in Nature Medicine, Méndez, together with researchers at the Hospital del Mar in Barcelona, had already discovered that CPEB proteins are involved in blood vessel development in pancreatic and brain cancer. Given the urgent need to identify new targets for pathological angiogenesis, Méndez and Fernández started collaborating to examine the role of CPEB4 in this process in the context of cirrhosis, a disease characterised by profound neovascularisation.

"The best about the study is that we demonstrate that the development of pathological blood vessels can be stopped by interfering with CPEB4 proteins while positive vascularisation remains intact," says Méndez. The experiments in cells in vitro, in animal models, and in samples taken from patients with cirrhosis have revealed the molecular mechanisms through which the increase in CPEB4 favours the overexpression of VEGF in cirrhosis.

From cirrhosis to liver cancer

The researchers uphold that the repair cycle that the liver enters worsens the situation to the extent that the regeneration nodules, which show high levels of CPEB4, form liver carcinomas. In this context, the Spanish Association against Cancer (Asociación Española Contra el Cáncer (AECC)) has awarded more than one million euros to the Méndez-Fernández tandem, who, together with Jordi Bruix (IDIBAPS-Hospital Clínic), will work in a coordinated manner to unravel the role of this molecule and to propose a treatment for liver carcinomas, the main liver cancer and third cause of death by cancer worldwide, with a 5-year survival rate of less than 10%.

In parallel, Méndez's lab at IRB Barcelona is working on a research project on CPEB4 inhibitors. Last year they resolved the structures of these proteins at the atomic level—the previous step to the computational design of inhibitors, which is being undertaken in collaboration with Modesto Orozco, at the same centre. Furthermore, and with the support of the Botín Foundation, Méndez has fine-tuned an assay to test CPEB4 inhibitors, with the aim to speed up the detection of molecules with the greatest therapeutic potential.

Reference article:
Sequential Functions of CPEB1 and CPEB4 Regulate Pathologic Expression of VEGF and Angiogenesis in Chronic Liver Disease.

Calderone V, Gallego J, Fernandez-Miranda G, Garcia-Pras E, Maillo C, Berzigotti A, Mejias M, Bava FA, Angulo-Urarte A, Graupera M, Navarro P, Bosch J, Fernandez M*, Mendez R*.

Gastroenterology (2015). doi: 10.1053/j.gastro.2015.11.038

Fighting liver fibrosis, the wound that never heals

From left: Nasun Hah, Ruth Yu, Mara Sherman, Ron Evans, Michael Downes, Chris Liddle and Ann Atkins

Image: Courtesy of the Salk Institute for Biological Studies

Fighting liver fibrosis, the wound that never heals

LA JOLLA—Chronic damage to the liver eventually creates a wound that never heals. This condition, called fibrosis, gradually replaces normal liver cells--which detoxify the food and liquid we consume--with more and more scar tissue until the organ no longer works.

Scientists at the Salk Institute have identified a drug that halts this unchecked accumulation of scar tissue in the liver. The small molecule, called JQ1, prevented as well as reversed fibrosis in animals and could help the millions of people worldwide affected by liver fibrosis and cirrhosis, caused by alcoholism and diseases like hepatitis. These results were published in PNAS the week of December 7, 2015.

Liver cells in a dish (left) become scar tissue when exposed to carcinogens (center). The Salk team found that the molecule JQ1 blocks scarring in animals by preventing normal liver cells from changing into scar-producing cells (right).

Credit: Salk Institute for Biological Studies

"After too much damage in the liver, the scar tissue itself causes more scar tissue," says Ronald Evans, professor and director of Salk's Gene Expression Laboratory and a Howard Hughes Medical Institute investigator. "We can actually reverse liver fibrosis in animals and are now exploring potential therapeutic applications for humans."

When the liver is damaged, small collections of hepatic stellate cells that specialize in storing vitamin A are called upon to tend to the wound. These activated stellate cells shed their vitamin A, travel to the site of injury and create thick, fibrous scar tissue to wall off and repair the damage. However, with prolonged organ stress, healthy liver cells become replaced by scar tissue, eventually leading to organ failure.

"Traditional therapies targeting inflammation don't work because these cells have multiple ways to bypass the drug," says Michael Downes, a Salk senior scientist and author of the paper. "In contrast, our strategy was to stop the fibrotic response at the genome level where these pathways converge."

The search for the critical genome pathway struck gold, uncovering a regulatory protein, called BRD4, that is a master regulator of liver fibrosis.

With this new knowledge in hand, the Salk team found JQ1 successfully inhibited BRD4 and halted the transformation of hepatic stellate cells into fiber-producing cells. This is good news, as JQ1 is a prototype of a new class of drugs currently being tested in human clinical trials for various cancers.

"JQ1 doesn't just protect against the wound response, but also reverses the fibrotic response in mice," says Ruth Yu, a Salk staff researcher and one of the authors of the paper.

"Our results indicate that BRD4 is a driver of chronic fibrosis and a promising therapeutic target for treating liver disease," says Evans, who also holds the March of Dimes Chair in Molecular and Developmental Biology. "We think this discovery may also treat fibrosis in other organs, like the lung, pancreas and kidney."

Other authors include Ning Ding, Nasun Hah, Mara Sherman, Chris Benner, Mathias Leblanc and Mingxiao He of the Salk Institute, and Christopher Liddle of the University of Sydney.

The work was funded by the NIH, the National Health and Medical Research Council of Australia Project Grants, the Leona M. and Harry B. Helmsley Charitable Trust, the Samuel Waxman Cancer Research Foundation and Ipsen/Biomeasure.

BRD4 is a novel therapeutic target for liver fibrosis

Ning Ding, Nasun Hah, Ruth T. Yu, Mara H. Sherman, Chris Benner, Mathias Leblanc, Mingxiao He, Christopher Liddle, Michael Downes, and Ronald M. Evans

Thursday, December 10, 2015

Activists dressed as Gilead butchers greeted participants at the European Conference on HIV and Hepatitis Coinfection


On the morning of Thursday 10th December 2015, a public action targeted specifically at big pharma profiteering from the lives of people with hepatitis C happened in central London. Activists dressed as Gilead butchers greeted participants as they arrived at the European Conference on HIV and Hepatitis Coinfection

The ACT UP LONDON (2) activists were demanding Gilead and other drug companies drop the prices of the new medicines which can cure hepatitis C. The companies are charging extortionate prices – tens of thousands of pounds for pills that cost just a few hundred pounds to make (3).

Gilead were revealed last week by US congress to have sent internal emails saying “let’s hold our price higher regardless of the uproar.” Kevin Young, Gilead’s executive vice president for commercial operations, wrote to colleagues in November 2013 …”Two sincere requests…Let’s not fold to advocacy pressure in 2014. Let’s hold our position whatever competitors do or whatever the headlines” (4).

Read more here....

December Updates
Reducing the cost of new hepatitis C drugs
An index of articles pointing the reader to the current controversy over the high price of Sovaldi, Harvoni (ledipasvir/sofosbuvir) and AbbVie Viekira Pak.

Also See
Sovaldi Investigation Finds Revenue-Driven Pricing Strategy Behind $84,000 Hepatitis Drug
Dec 1 2015
A report released Tuesday by US Senators Ron Wyden and Charles Grassley claims that Gilead Sciences priced the hepatitis C treatments Sovaldi (sofosbuvir) and Harvoni (ledipasvir/sofosbuvir) with the sole goal of maximising revenue. The report was based on an investigation of 20 000 pages of internal company documents, dozens of interviews with health care experts and data from Medicaid programmes in all 50 states and the District of Columbia.
“Gilead pursued a calculated scheme for pricing and marketing its Hepatitis C drug based on one primary goal, maximizing revenue, regardless of the human consequences. There was no concrete evidence in emails, meeting minutes or presentations that basic financial matters such as R&D costs or the multi-billion dollar acquisition of Pharmasset, the drug’s first developer, factored into how Gilead set the price....

Wednesday, December 9, 2015

Sudden drop-off in VA hepatitis C treatments alarms veterans community

Sudden drop-off in VA hepatitis C treatments alarms veterans community
By Diane Zumatto

Despite the fact that Congress appropriates VA’s medical services account a full year in advance precisely to avoid a slowdown in VA services and treatment should there be any fiscal uncertainty with the rest of the government at the start of a new fiscal year, VA’s treatment of veterans with HCV dropped astoundingly to less than 400 for the first week of October, and has remained alarmingly low since then.

Continue reading....

Senate Hearings To Investigate Rising Price Of Medications

Tuesday, December 8, 2015

European Physicians Report Strong but Variable Uptake of All-Oral Interferon-Free Hepatitis C Virus Regimens Across EU5 Countries

European Physicians Report Strong but Variable Uptake of All-Oral Interferon-Free Hepatitis C Virus Regimens Across EU5 Countries

BURLINGTON, Mass.Dec. 8, 2015 /PRNewswire/ -- Decision Resources Group finds that surveyed EU5 physicians report that more than half of their hepatitis C virus (HCV) patients were being treated with interferon (IFN)-free regimens. Factors such as regulatory approval date and pricing and reimbursement negotiations contributed to wide variation in the uptake dynamics of novel HCV therapies. Differences between EU5 markets were most apparent in the treatment of non-cirrhotic patients with lower liver fibrosis scores, who are typically deprioritized for access to IFN-free therapies. This effect is exemplified in the United Kingdom, where 45 percent of non-cirrhotic treatment-naive genotype-1 patients were being treated with IFN dual therapy or first generation protease inhibitor triple therapy, according to survey results, though this will change rapidly with the recent approval of new direct acting antivirals in the UK in late 2015.
Other key findings from the special report entitled "TreatmentTrends: Hepatitis C Virus 2015 (EU)":
  • Surveyed EU5 physicians report that nearly two-thirds of their genotype-1 and -2/3 HCV patients are non-cirrhotic and thus are not prioritized for treatment. However, only one-quarter of treatment-naive non-cirrhotic HCV patients in the EU5 are being actively warehoused, down from 30 percent a year ago, suggesting EU5 countries are increasingly treating HCV-infected patients regardless of liver disease stage.
  • Across EU5 countries, Gilead's Harvoni and a combination of Gilead's Sovaldi and Bristol-Myers Squibb's Daklinza are the leading regimens for treatment-experienced cirrhotic patients with genotype-1 and -2/3 infection, respectively. Uptake of these agents in the EU5 was primarily driven by France and Germany. Surveyed EU5 physicians rate both regimens highly on overall safety, efficacy in both compensated and decompensated cirrhotic patients, as well as efficacy in HCV genotype-1 and -3 infections.
  • Surveyed EU5 physicians indicate the need for novel therapies with pan-genotypic activity, regimens with treatment duration under 12 weeks and for increased patient access to efficacious but costly therapies. In addition, physicians expect Merck & Co.'s grazoprevir/elbasvir to bring the most immediate benefit to their patients, likely due to improved treatment efficacy in difficult-to-treat populations, such as patients with renal impairment.
Comments from Decision Resources Business Insights Analyst James T. Heeres, Ph.D.:
  • "Although EU5 physicians rate Gilead's Harvoni and Bristol-Myers Squibb's Daklinza highly on efficacy, they are clearly critical of the cost of these therapies. However, according to our research, cost issues may recede in the near future as some EU5 countries work to lift access barriers. This still leaves the door open for emerging therapies to compete on efficacy in niche populations and, to some degree, on cost."
  • "As our primary research had predicted, drug treatment rates and patient shares for Harvoni, Abbvie's Viekirax, and Daklinza have grown in the EU5, largely in response to lowering of market access barriers. However, the potential approval of several pan-genotypic regimens (e.g. Gilead's Sovaldi + velpatasvir) and regimens targeting niche populations (e.g. Merck & Co.'s grazoprevir/elbasvir) will likely kick-start another round of pricing negotiations. Alternatively, currently approved regimens may retain market share if physician preference and cost present substantial market access barriers for emerging therapies."
For more information on purchasing this report, please email
About Decision Resources GroupDecision Resources Group offers best-in-class, high-value data, analytics and insights products and services to the healthcare industry, delivered by more than 900 employees across 14 global locations. DRG provides the pharmaceutical, biotech, medical device, financial services and payer industries with the tools, insights and advice they need to compete and thrive in an increasingly complex and value-based marketplace.
Media contact:
SHIFT CommunicationsTheresa Masnik
SOURCE Decision Resources Group

NEW DELHI - Hetero gets DCGI approval to market Gilead's Harvoni Hepatitis C drug

Hetero gets DCGI approval to market Hepatitis C drug  

NEW DELHI: Drug maker Hetero has received approval from DCGI to market generic version of Gilead's Harvoni, a drug used in the treatment of Hepatitis C, in the country.

Hetero is the first company in India to receive the approval for the fixed-dose combination Ledipasvir-Sofosbuvir (90mg/400mg) from Drug Controller General of India (DCGI), the company said in a statement.

Read more at:

Monday, December 7, 2015

HCV genotype 3: a wolf in sheep’s clothing

Journal: Expert Review of Anti-infective Therapy

HCV genotype 3: a wolf in sheep’s clothing

José-R. Blancoa* & Antonio Rivero-Juarez
1a Infectious Diseases Area. Hospital San Pedro - Center for Biomedical Research of La Rioja (CIBIR) . Piqueras 98, 26006 Logroño , La Rioja ( Spain ).
2b Infectious Diseases Unit. Instituto Maimonides de Investigación Biomédica de Córdoba (IMIBIC) . Hospital Universitario Reina Sofía de Córdoba. Universidad de Córdoba . Avda. Menendez Pidal s/n, 14004 Córdoba , Córdoba ( Spain ).

Publishing models and article dates explained

Received: 16 Sep 2015
Accepted: 30 Nov 2015
Accepted author version posted online: 03 Dec 2015

Keywords: Hepatitis C, Genotype 3, Metabolic syndrome, Hepatocellular carcinoma

Download as PDF or Interactive PDF

HCV genotype 3: a wolf in sheep’s clothing

"All truths are easy to understand once they are discovered; the point is to discover them". Galileo Galilei"

At present, the hepatitis C virus (HCV) is a major cause of morbidity and mortality affecting over 185 million people worldwide,[1] equivalent to a global prevalence of about 2.5% in 2015. Genotype 3 (HCV G3) is one of the seven recognized genotypes.[2] HCV G3 is the second most common genotype overall and is estimated to account for 54.3 million cases throughout the world (30.1%).[1] Although three-quarters of them occur in South Asia where it is endemic, the 3a subtype is an “epidemic subtype“ widely distributed geographically, probably associated with injecting drug use.[3]

 In the last two years, the history of HCV infection has changed radically with the appearance of the new direct-acting antiviral agents (DAAs).[4] Although HCV G3 was one of those genotypes who achieved a better sustained viral response (SVR) using pegylated interferon and ribavirin (PEG-IFN/Rbv) therapy,[5] the current effectiveness of the new DAAs against HCV G3 leaves a lot to be desired compared with the results obtained with other genotypes.[6] This is a major problem since, compared to other genotypes, HCV G3 is associated with faster progression of fibrosis,[7,8] a greater risk for hepatocellular carcinoma (HCC),[8-10] and a higher mortality.[11] Why is it so pathogenic and resistant to treatment? The reasons for this “aggressiveness” are without doubt multiple, complex and not well known.

First, it is important to remember that the host immune response plays an important role in HCV G3 infection because of its potential to contribute to viral clearance. So, acutely HCV-infected patients are much more likely to spontaneously clear HCV if they are infected with HCV G3 than HCV G1.[12] Indeed, chronically infected HCV G3 patients had higher SVR rates after shorter treatment with PEG-IFN/Rbv therapy when compared to those with chronic HCV G1 infection.[13] One of the possible reasons could be that in monocytic cell and plasmacytoid dendritic cell lines and in macrophages differentiated from monocytes with macrophage colony-stimulating factor, HCV G3 induces greater interferon transcription than either genotype 1a or 1b.[14] However, this apparent benefit may backfire because of the increased rate of fibrosis progression of HCV G3, probably due to the higher non-parenchymal cell transcription of IFN genes following intracellular HCV G3 sensing.[14]

It has been reported previously that HCV G3 is associated with a significantly increased risk of developing cirrhosis and HCC compared to HCV G1, and association that is independent of the patients’ age, diabetes, body mass index, or antiviral treatment.[8] The high viremia observed in HCV G3-infected patients may be a marker of rapid disease damage, reflecting either the inability of the immune system to control the infection or the existence of some escape mechanisms in HCV G3 which prevents the immune system response from being effective.[15]

Secondly, another problem that is not well understood is the interaction between HCV and lipid metabolism.[16] So, HCV G3 selectively interferes with the late cholesterol synthesis pathway,[17] although this interference is resolved after the SVR. Other mechanisms that alter lipid metabolism are increased the novo lipogenesis and the inhibition of mitochondrial fatty acid degradation.[18] At what level of lipid metabolism does HCV G3 work? Is the damage the consequence of the virus or of its proteins in infected hepatocytes? Given that, in previous studies, the variables independently associated with SVR were high LDL levels,[19,20] low HDL levels [19] and statin use,[19] one might think that statins would be a useful option for such patients. Nonetheless, this is not actually the case with HCV G3. In one analysis of patients with HCV 1-3 genotypes who received combination therapy with PEG-IFN/Rbv, the significant impact of statin use was only observed among the HCV G1 patients.[20] Similar findings were reported by Selic Kurincic et al.[21]

Steatosis is a common histologic finding in patients infected by HCV G3, independently of the presence of fibrosis, diabetes, hepatic inflammation, ongoing alcohol abuse, higher body mass index, and older age.[22] Indeed, steatosis in HCV G3 infected patients is not the result of overexpression of genes involved in lipogenesis.[23] The higher rates of hepatic steatosis in HCV G3 patients, even in absence of other metabolic complications, suggest that some specific viral sequences may be involved in the etiology of steatosis.[18] In fact, after reaching SVR, hepatic steatosis in these patients had disappeared.[24,25] Another possible explanation for the high presence of steatosis could be that HCV G3 steatosis induces the liberation of proinflammatory chemokines that increase the recruitment of inflammatory cells to the liver.[14] In support of this idea, the depletion of liver Kupffer cells prevents the development of diet-induced hepatic steatosis and insulin resistance.[26]

It is important to bear in mind that there is a significant correlation between the steatosis score and the titer of intrahepatic HCV RNA in patients with HCV G3, providing virological and some clinical evidence that steatosis is the morphological expression of a viral cytopathic effect in patients infected with this genotype.[27] This finding has important implications, such as lower SVR rates or higher relapse rates after HCV treatment.[28,29] Is steatosis a marker of rapid progression or bad prognosis in HCV G3 infected patients?

Non-alcoholic fatty liver disease (steatosis/steatohepatitis) is similarly recognized as the hepatic manifestation of metabolic syndrome (MS). HCV virus genotype 3 infection increases the risk of insulin resistance and diabetes, probably due to the direct effect of the virus on intracellular insulin signaling.[30] This situation not only increases the cardiovascular risk but also reduces the likelihood of achieving a SVR.[31] Another common manifestation of MS is obesity, a problem that also increases the expression of some inflammatory cytokines and activates several signaling pathways involved in the pathogenesis of insulin resistance.[32] The inflammation may also contribute to the pathogenesis of liver damage.[33] Obesity has also been correlated with a lower SVR rate.[34] Once again, this opens up an interesting way to research the mechanisms involving MS and SVR in these patients. Are insulin resistance and/or obesity indicators of the the existence of an established liver damage, even though we are unable to diagnose it? Is there some symbiotic relationship between the adipocytes and HCV G3 that reduces the efficacy of the DAAs? In view of the higher rates of SVR using the new DAAs, is the presence of MS still important in chronic HCV infection?.[35] Probably not, but there is as yet no concrete answer for this question and so the controversy about steatosis and HCV remains. Valenti et al also reported that the rs738409 genotype, a polymorphism that influences liver fat without affecting insulin resistance and body composition, was associated with severe hepatic steatosis in patients infected with a non-3 HCV genotype, and also with fibrosis stage and cirrhosis (OR = 1.47; P = 0.002).[36] Similarly, Cai et al [37] reported that rs738409 was associated with an increased risk of steatosis in patients infected with a non-3 HCV genotype. These results suggest distinct pathogenic mechanisms in the 3 and non-3 genotypes.

Moving on to the third point, and so concluding this topic, it is necessary to understand the clinical implications of the different HCV G3 subtypes (in other words, immunity, inflammation, prognosis, response to DAAs). This is something we already known for HCV G1a and 1b.[38] At least 10 HCV G3 subtypes have been described so far.[39] Are some of these HCV G3 subtypes able to evade the immune response? Can we expect the same SVR for different subtypes? The correct identification of HCV G3 subtypes would probably be necessary because they are crucial in clinical trials evaluating the new DAAs. No data have so far stratified the response of HCV G3 to the new DAAs, which could be an essential issue that requires further investigation.

In summary, given the aggressiveness of HCV G3, it is increasingly necessary to initiate antiviral treatment as soon as possible in all patients, including those with steatosis and/or MS. In these patients, even those with SVR, continued surveillance is necessary, paying careful attention to patients with cirrhosis. There is no doubt that better knowledge of HCV G3 should be a priority for us all.

Financial & competing interests disclosure
JR Blanco has carried out consulting work for Abbvie, Bristol-Myers Squibb, Gilead Sciences, Janssen, Merck, and ViiV Healthcare; has received compensation for lectures from Abbvie, Bristol-Myers Squibb, Gilead Sciences, Janssen, Merck, and ViiV Healthcare, as well as grants and payments for the development of educational presentations for Gilead Sciences and BristolMyers Squibb. A Rivero-Juarez is the recipient of a Postdoctoral Perfection Grant from Fundación Progreso y Salud, Consejería de Salud y Políticas Sociales, Junta de Andalucia (0024-RH-2013). He has received compensation for lectures from Bristol-Myers Squibb, Janssen, Merck, and ViiV Healthcare.The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. 

1. Mohd Hanafiah K, Groeger J, Flaxman AD, Wiersma ST. Global epidemiology of hepatitis C virus infection: new estimates of age-specific antibody to HCV seroprevalence. Hepatology. 2013;57(4):1333-1342.
2. Smith DB, Bukh J, Kuiken C, Muerhoff AS, Rice CM, Stapleton JT, et al. Expanded classification of hepatitis C virus into 7 genotypes and 67 subtypes: updated criteria and genotype assignment web resource. Hepatology. 2014;59(1):318-327.
3. Pybus OG, Cochrane A, Holmes EC, Simmonds P. The hepatitis C virus epidemic among injecting drug users. Infect. Genet. Evol. 2005;5(2):131- 139.
4. Gentile I, Buonomo AR, Zappulo E, Borgia G. Interferon-free therapies for chronic hepatitis C: toward a hepatitis C virus-free world? Expert. Rev. Anti. Infect. Ther. 2014;12(7):763-773.
5. Hoofnagle JH, Seeff LB. Peginterferon and ribavirin for chronic hepatitis C. N. Engl. J. Med. 2006;355(23):2444-2451.
6. AASLD/IDSA HCV Guidance Panel Hepatitis C guidance: AASLD-IDSA recommendations for testing, managing, and treating adults infected with hepatitis C virus. Hepatology. 2015;62(3):932-54.
7. Probst A, Dang T, Bochud M, Egger M, Negro F, Bochud PY. Role of hepatitis C virus genotype 3 in liver fibrosis progression--a systematic review and meta-analysis. J. Viral Hepat. 2011;18(11):745-759.
8. Kanwal F, Kramer JR, Ilyas J, Duan Z, El-Serag HB. HCV genotype 3 is associated with an increased risk of cirrhosis and hepatocellular cancer in a national sample of U.S. Veterans with HCV. Hepatology. 2014;60(1):98- 105.
9. Nkontchou G, Ziol M, Aout M, Lhabadie M, Baazia Y, Mahmoudi A, et al. HCV genotype 3 is associated with a higher hepatocellular carcinoma incidence in patients with ongoing viral C cirrhosis. J. Viral Hepat. 2011;18(10):e516-522.
10. McCombs J, Matsuda T, Tonnu-Mihara I, Saab S, Hines P, L'italien G, et al. The risk of long-term morbidity and mortality in patients with chronic hepatitis C: results from an analysis of data from a Department of Veterans Affairs Clinical Registry. JAMA Intern. Med. 2014;174(2):204-212.
11. van der Meer AJ, Veldt BJ, Feld JJ, Wedemeyer H, Dufour JF, Lammert F, et al. Association between sustained virological response and all-cause mortality among patients with chronic hepatitis C and advanced hepatic fibrosis. JAMA. 2012;308(24):2584-2593.
12. Lehmann M, Meyer MF, Monazahian M, Tillmann HL, Manns MP, Wedemeyer H. High rate of spontaneous clearance of acute hepatitis C virus genotype 3 infection. J. Med. Virol. 2004;73(3):387-391.
13. Hadziyannis SJ, Sette H Jr, Morgan TR, Balan V, Diago M, Marcellin P, et al. Peginterferon-alpha2a and ribavirin combination therapy in chronic hepatitis C: a randomized study of treatment duration and ribavirin dose. Ann. Intern. Med. 2004;140(5):346-355.
14. Mitchell AM, Stone AE, Cheng L, Ballinger K, Edwards MG, Stoddard M, et al. Transmitted/founder hepatitis C viruses induce cell-type- and genotypespecific differences in innate signaling within the liver. MBio. 2015;6(2):e02510.
15. Buti M, Esteban R. Hepatitis C virus genotype 3: a genotype that is not 'easy-to-treat'. Expert Rev. Gastroenterol. Hepatol. 2015;9(3):375-385.
16. Clement S, Peyrou M, Sanchez-Pareja A, Bourgoin L, Ramadori P, Suter D, et al. Down-regulation of phosphatase and tensin homolog by hepatitis C virus core 3a in hepatocytes triggers the formation of large lipid droplets. Hepatology. 2011;54(1):38-49.
17. Clark PJ, Thompson AJ, Vock DM, Kratz LE, Tolun AA, Muir AJ, et al. Hepatitis C virus selectively perturbs the distal cholesterol synthesis pathway in a genotype-specific manner. Hepatology 2012;56(1):49-56.
18. Negro F. Hepatitis C virus-induced steatosis: an overview. Dig Dis. 2010;28(1):294-299.
19. Harrison SA, Rossaro L, Hu KQ, Patel K, Tillmann H, Dhaliwal S, et al. Serum cholesterol and statin use predict virological response to peginterferon and ribavirin therapy. Hepatology 2010;52(3):864-874.
20. Pandya P, Rzouq F, Oni O. Sustained virologic response and other potential genotype-specific roles of statins among patients with hepatitis Crelated chronic liver diseases. Clin. Res. Hepatol. Gastroenterol. 2015;39(5):555-565.
21. Selic Kurincic T, Lesnicar G, Poljak M, Meglic Volkar J, Rajter M, Prah J, et al. Impact of added fluvastatin to standard-of-care treatment on sustained virological response in naive chronic hepatitis C patients infected with genotypes 1 and 3. Intervirology. 2014;57(1):23-30.
22. Leandro G, Mangia A, Hui J, Fabris P, Rubbia-Brandt L, Colloredo G, et al. Relationship between steatosis, inflammation, and fibrosis in chronic hepatitis C: a meta-analysis of individual patient data. Gastroenterology, 2006;130(6):1636-1642. Downloaded by [] at 12:46 07 December 2015
23. Ryan MC, Desmond PV, Slavin JL, Congiu M. Expression of genes involved in lipogenesis is not increased in patients with HCV genotype 3 in human liver. J. Viral Hepat. 2011;18(1):53-60.
24. Poynard T, Ratziu V, McHutchison J, Manns M, Goodman Z, Zeuzem S, et al. Effect of treatment with peginterferon or interferon alfa-2b and ribavirin on steatosis in patients infected with hepatitis C. Hepatology. 2003;38(1):75-85.
25. Kumar D, Farrell GC, Fung C, George J. Hepatitis C virus genotype 3 is cytopathic to hepatocytes: Reversal of hepatic steatosis after sustained therapeutic response. Hepatology 2002;36(5):1266-1272.
26. Huang W, Metlakunta A, Dedousis N, Zhang P, Sipula I, Dube JJ, et al. Depletion of liver Kupffer cells prevents the development of diet-induced hepatic steatosis and insulin resistance. Diabetes 2010;59(2):347-357.
27. Rubbia-Brandt L, Quadri R, Abid K, Giostra E, Malé PJ, Mentha G, et al. Hepatocyte steatosis is a cytopathic effect of hepatitis C virus genotype 3. J. Hepatol. 2000;33(1):106-115.
28. Aziz H, Gill U, Raza A, Gill ML. Metabolic syndrome is associated with poor treatment response to antiviral therapy in chronic hepatitis C genotype 3 patients. Eur. J. Gastroenterol. Hepatol. 2014;26(5):538-543.
29. Restivo L, Zampino R, Guerrera B, Ruggiero L, Adinolfi LE. Steatosis is the predictor of relapse in HCV genotype 3- but not 2-infected patients treated with 12 weeks of pegylated interferon-alpha-2a plus ribavirin and RVR. J. Viral Hepat. 2012;19(5):346-352.
30. Kawaguchi T, Yoshida T, Harada M, Hisamoto T, Nagao Y, Ide T, et al. Hepatitis C virus down-regulates insulin receptor substrates 1 and 2 through up-regulation of suppressor of cytokine signaling 31. Am. J. Pathol. 2004;165(5):1499-1508. 31. Poustchi H, Negro F, Hui J, Cua IH, Brandt LR, Kench JG, et al. Insulin resistance and response to therapy in patients infected with chronic hepatitis C virus genotypes 2 and 3. J. Hepatol. 2008;48(1):28-34.
32. Chen L, Chen R, Wang H, Liang F. Mechanisms linking inflammation to insulin resistance. Int. J. Endocrinol. 2015;2015:508409.
33. Szabo G, Petrasek J. Inflammasome activation and function in liver disease. Nat. Rev. Gastroenterol. Hepatol. 2015;12(7):387-400.

All truths are easy to understand once they are discovered
; the point is to
discover them
Galileo Galilei

St. Louis VA says it’s not turning away any patients with Hepatitis C seeking expensive prescriptions

St. Louis VA Supplying an Expensive Cure to Hep C

December 7, 2015 8:16 AM
The new drug, Sofosbuvir, can cost the VA $42,000 for each patient’s 12-week treatment.
Complaints are reported elsewhere about VA patients being put on a waiting list, but in St. Louis Dr. Leela Nyak, a liver specialist at the John Cochran Medical Center says the cost isn’t forcing them to turn people away.
Read more... 

The Impact Of New Hepatitis C Drugs On National Health Spending

The Impact Of New Hepatitis C Drugs On National Health Spending
Charles Roehrig

Those who follow Altarum Institute’s monthly health sector briefs and trend reports are well aware that the five-year run of record low growth rates in national health spending (from 2009 through 2013) has come to an end, or at least been interrupted. According to data just released by the Centers for Medicare & Medicaid Services (CMS), health spending grew by 5.3 percent in 2014, compared to 2.9 percent in 2013 and roughly 4 percent from 2009 through 2012. Our estimates for the first eight months of 2015 show growth of 6.2 percent, though on a downward path, indicating that the year could finish at around 6 percent growth.

Many analysts had predicted well in advance an increased health spending growth rate for 2014 due to the implementation of the Patient Protection and Affordable Care Act (ACA). The expanded coverage provisions of the ACA were expected to increase the number of persons with health insurance and hence health spending (Note 1).

However, the huge jump in prescription drug spending that occurred in 2014 was unforeseen. In 2013, spending on prescription drugs grew by only 2.4 percent, but in 2014, it skyrocketed to 12.2 percent. Some of this increase in spending on prescription drugs is due to expanded coverage, and some is due to the acceleration in prescription drug prices.

A major source of this growth was the introduction of Sovaldi in December 2013, and Harvoni in October 2014. Both are very expensive breakthrough drugs for the treatment of hepatitis C (a disease of the liver, affecting approximately 3 million Americans). The new hepatitis C drugs have had a significant impact on growth rates in spending on prescription drugs and on national health spending.
Company Sales Of New Hepatitis C Drugs

I use company reports to track quarterly U.S. sales of the four bestselling new prescription drugs for the treatment of hepatitis C: Harvoni and Sovaldi (Gilead Sciences, Inc.), Viekira Pak (AbbVie), and Olysio (Janssen Pharmaceutical Companies of Johnson & Johnson). While these sales figures are not identical to the final sales captured in health spending, they provide a basic sense of the impact of hepatitis C drugs on overall health spending growth rates (Note 2).

The quarterly sales are shown in Figure 1. Combined sales were $100 million in Q4 2013, jumping to $2.4 billion and $3.8 billion in Q1 and Q2 2014. In Q3, sales of the existing drugs fell to $2.9 billion, presumably due to the expected release of a more appealing drug, Harvoni, in October. Starting in Q4 2014, sales moved back to $3.5 billion and have stayed in that range during the first three quarters of 2015.

Source: Altarum Center for Sustainable Health Spending, computed from Gilead, AbbVie, and Johnson & Johnson Company reports.

Impact On 2014 Growth In Health Spending

National health spending in 2013 was about $2.9 trillion. In 2014, company sales of the new hepatitis C drugs were $12.3 billion higher than in 2013. This represents 0.4 percent of total health expenditures in 2013, and suggests that the new hepatitis C drugs added 0.4 percentage points to the 2014 health spending growth rate. In the absence of these new drugs, national health spending would have grown by about 4.9 percent rather than 5.3 percent.

Prescription drug spending in 2013 was $265 billion. Similar math suggests that the new hepatitis C drugs added about 4.6 percentage points to the growth in prescription drug spending in 2014. The total growth rate in prescription drug spending in 2014 was 12.2 percent, so we estimate that it would have been 7.6 percent in the absence of the new hepatitis C drugs. That latter would still have been a large increase relative to the 2.6 percent growth seen in 2013 for prescription drugs and is likely due to a combination of expanded coverage and accelerated price growth.
Likely Impact On 2015 Growth In Health Spending

While spending on hepatitis C drugs in 2015 remains very high ($14.4 billion is a reasonable estimate, assuming $3.5 billion in Q4), it represents a much smaller increase ($1.9 billion) than experienced in 2014 ($12.3 billion). This means that in 2015, hepatitis C drugs will have added less than 0.1 percentage points to the growth rate in national health expenditures and 0.6 percentage points to the growth rate in prescription drug spending.

To put it another way, the relatively small increase in hepatitis C spending in 2015 should reduce the overall rate of growth in national health expenditures by more than 0.3 percentage points compared to the growth rate in 2014. For prescription drugs, it should bring the growth rate down by about 4 percentage points (Note 3).

Our November health sector spending brief shows that the growth rate in spending on prescription drugs has indeed been falling in 2015 and, as of September, was at 8.4 percent, year over year. This is 3.8 percentage points below the growth rate in 2014, and we attribute much of the decline to the leveling off in spending on hepatitis C (Note 4).

The decline in the prescription drug spending growth rate in 2015 has been more than offset by a higher rate of growth in spending on health care services so that, in September, the health spending growth rate of 5.5 percent was actually higher than the rate for 2014. In the absence of the prescription drug spending slowdown, the September growth rate would have been about 5.9 percent.
Implications For 2016 And Beyond

I conclude with speculation about the future using rough estimates that I believe nonetheless provide some useful information. U.S. sales of hepatitis C drugs seem to have stabilized at about $14 billion per year, which equates to about 150,000 persons treated per year (at a rate of $90,000 per person treated).

The number of new cases per year is about 30,000 so our current rate of spending should be sufficient to reduce prevalence by about 120,000 per year. There are about 3 million people with hepatitis C in the U.S., so our current rate of spending could continue for many years before we run out of cases to treat. (Because hepatitis C is spread by those already infected, the number of new cases should dwindle toward zero as the overall prevalence falls toward zero.)

Of course, the amount we actually spend per year over the next few years could be higher or lower than what we spent in 2015. Recent recommendations argue for treatment of nearly all diagnosed cases, yet many states and other payers continue to prioritize candidates for treatment based on severity of illness and other factors. This means that the near-term rate of spending is quite unpredictable and depends upon how much effort is put toward identifying and treating existing cases, how much resistance there is to approving treatment, and what competition might do to reduce drug prices. In the longer term, the curative powers of these drugs should drive hepatitis C prevalence, and therefore spending, to very low levels.
Note 1

Estimates from the American Community Survey show that the percentage of the population with health insurance grew by 2.8 percentage points between 2013 and 2014.
Note 2

One difference is the lag between when the sale (to an intermediary) is recorded by the company and when the final sale is made to the consumer. Another is that retail markups are included in health spending but not in company sales. Finally, prescription drug sales in the national health accounts refer only to retail sales, while company sales include sales to hospitals and physicians for drugs administered during the health encounter and whose costs are embedded in the hospital or physician bill.The vast majority of hepatitis C drugs are sold at retail.
Note 3

For further analysis of prescription drug spending, see: R. Kamal and G. Claxton, October 30, 2015, “Recent trends in prescription drug spending and what to look out for in coming years,” Peterson-Kaiser Health System Tracker.
Note 4

The leveling off we observe in company sales in 2015 runs counter to a recent report stating that Medicare spending on these drugs grew by $4.5 billion in 2015. Some of this may be due to lags between company sales to intermediaries and the subsequent sales to Medicare patients. We have not built lags into our analysis, and this could mean we have somewhat overstated the 2014 impact and understated the 2015 impact.
tags: harvoni, hepatitis c, prescription drugs, sovaldi, spending growth


Saturday, December 5, 2015

December Hepatitis Newsletters: Highlights From AASLD 2015 - Treating Genotype 3, Cirrhosis and Liver Cancer

December Hepatitis Newsletters: Spotlight On Daryl Luster, With Highlights From AASLD 2015

Greetings everyone, welcome to this months index of Newsletters filled with highlights from the 66th American Association for the Study of Liver Diseases Annual Meeting. 

Your favorite bloggers have written some wonderful articles as well, plus a new interview with Daryl Luster, our very own advocate, author and President of the Board of Directors at Pacific Hepatitis C Network

Daryl was featured in an interview recently on; The American Journal Of Medicine Hepatitis C Resource Center Blog, which tackled some of the following powerful topics; HCV treatment restrictions, stigma, discrimination, drug cost, harm reduction and access to care, to name a few.

It begins, here...

Daryl’s Articles
Read all of Daryl’s articles on
On a personal level connect with Daryl on Facebook, and follow him on Twitter.

AASLD 2015 - Review
In case you missed it, review key data presented at the meeting over at ViralEd and CCO. 

If that seems too clinical, scroll through this months newsletters for additional AASLD highlights, written by devoted HCV advocates, with you, the patient in mind. 

December Newsletters

HCV Advocate
The HCV Advocate newsletter is a valuable resource designed to provide the hepatitis C community with monthly updates on events, clinical research, and education.

Read The HCV Advocate Daily
Current edition


This month’s HCV Advocate newsletter is all about The Liver Meeting held in San Francisco, CA. There was much information about hepatitis C (HCV) presented, and there were demonstrations held—what more could anyone want? In Part 1 of our Liver Conference coverage Lucinda and I report on the following: 

Snapshots – I cover some of the most exciting late-breaking posters about HCV treatment including treating genotype 3, cirrhosis and post-transplant HCV and those pesky RAVs with multiple drug combinations in clinical development. 
HealthWise – Lucinda covers advocacy issues including the protests at AASLD and she discusses her favorite posters and presentations.

What’s New!
We have overhauled our medical glossary and herbal glossary to make it easier to navigate. Check them out!

We have begun a new feature highlighting some of the best websites for our readers. In this edition we are recommending that has tons of information, brochures and informational videos that you can download free of charge.

Lastly, we would like to take this time to ask you to think about donating to our organization—the Hepatitis C Support Project, a Project of the Tides Center. Any contribution you can afford will help us to provide the much-needed education and support that we provide to the hepatitis C community. Click here to learn more. 

In Case You Missed It

November Mid-Month Newsletter
Feds to Medicaid: Stop HCV Treatment Restrictions
by Alan Franciscus
This is good news for patients who have been denied HCV treatment by Medicaid. It will also mean that the government will investigate HCV pricing policies and insurance denial practices.

by Alan Franciscus
The combination of sofosbuvir plus velapasvir (with and without ribavirin) to treat genotypes 1 through 6 has completed Phase 3 clinical studies, and Gilead has submitted the data to the Food and Drug Administration for marketing approval. Read about the results.

Social Security and Medicare Changes for 2016
by Jacques Chambers
It is that time of year that some people need to start making changes to their Social Security or Medicare. Read this informative article by Jacques to find out the latest information and changes to these two important programs.

HCV Drugs
by Alan Franciscus
There was a lot of news in the world of HCV drugs — such as a teaser to a study that will be released at AASLD — curing people with 3 weeks of treatment, a safety warning about Viekira Pak and Technivie, and going bananas to treat HIV, HCV and the flu.

HCV SnapShots
by Alan Franciscus
This month’s column features two abstracts including HCV and the risk of preterm birth, and how statins reduce the progression to cirrhosis.

The Five: Pan-Genotypic Drugs
by Alan Franciscus
This month’s The Five discusses the various aspects of pan-genotypic drugs and why they are the future of HCV treatment.

View past newsletters here....

Connect With HCV Advocate


Hepatitis B and C Public Policy Association 
The Hepatitis Public Policy Association aims to urge and facilitate the formulation of public policies at national and international level for the communication, prevention and management of the spread of viral Hepatitis B and C. The Association’s unique approach in furtherance of this aim is to gather together, and work in partnership with, the major stakeholders in the field of these diseases including regulators, patients, clinicians, public health and civil society communities and the private sector.

December 2015 – Newsletter
Editor-in-Chief, Prof Massimo Colombo MD

In This Issue

What’s new at AASLD 2015
Several novelties concerning the advances in the field of hepatitis C were reported at the AASLD 2015 meeting. I will focus my report on the real-world data on treatment with direct acting antivirals (DAA), those obtained in some selected populations (genotype 3, acute hepatitis C, persons who inject drugs [PWID], decompensated cirrhosis), the problem of NS5A-associated resistance associated variants (RAVs), and some of the results of soon-to-be-approved medications.

A report from The 2015 Liver Meeting: The AASLD Global Forum
The 2015 Liver Meeting in San Francisco offered an occasion for experts from around the world to meet and discuss the latest findings in hepatology. The Global Forum was an event dedicated to the advances in treatment of chronic hepatitis C and the challenges that remain to fight the battle against HCV worldwide.

Next-generation sequencing as an emerging weapon of molecular epidemiology to track patients at risk of hepatocellular carcinoma
Q. Professor Zucman-Rossi, is our understanding of the risk factors of hepatocellular carcinoma exhaustive?
The vast majority of hepatocellular carcinomas (HCC) occur on a cirrhotic background developed after a chronic liver disease usually related to infections by hepatitis B or C viruses, high alcohol consumption, metabolic genetic diseases or obesity. Apart from these major risk factors, the contribution of others such as tobacco remains to be ascertained. Whereas HCC risk increases with the severity and duration of cirrhosis development, an increased number of HCC are discovered in non-cirrhotic patients. Particularly in these cases, we can hypothesize that exposure to additional risk factors and/or genetic predisposition could contribute significantly to the development of HCC.

Metabolic steatohepatitis and liver cancer
Q. Professor Dufour, when was the link between liver cancer and metabolic syndrome established?
In the last decades, research in the field of hepatocellular carcinoma has been focused on the link with hepatitis B virus and hepatitis C virus and, on the therapeutic front, on the development of systemic target therapy which lead to the approval of sorafenib in 2007. The landscape is changing with the realization that effective treatment of chronic viral hepatitis will reduce the number of patients at risk of developing hepatocellular carcinoma.

An update on treatment for hepatocellular cancer (HCC)
Q. Professor Galle, is liver cancer a hard to treat disease?
Hepatocellular cancer (HCC) is a disease with dismal prognosis and worldwide the third leading cause of cancer-related mortality, behind lung and stomach cancers. In the majority of patients, HCC is a deadly complication of liver cirrhosis resulting from underlying liver disease such as viral hepatitis. The remaining hepatic reserve of the cirrhotic patient contributes significantly to the availability of therapeutic options and often dictates outcome.

Extra-hepatic manifestations of hepatitis C
Q. What organs besides the liver are affected by HCV
A higher prevalence of immune-related disorders has been found in patients with HCV infection compared to uninfected controls, one above all mixed cryoglobulinemia and its sequelae, ranging from cutaneous and visceral vasculitis to glomerulonephritis and B cell non-Hodgkin’s lymphoma. The ability of HCV to target lymphocytes-the most important step in the pathogenesis of virus-related immunological disorders- can explain also the important role of HCV in the genesis of systemic autoimmune diseases like Sjögren syndrome, rheumatoid arthritis, hemolytic anemia and severe thrombocytopenia. The virus has been implicated also in organ-specific autoimmune diseases like thyroid disorders and autoimmune hepatitis.

Emerging and re-emerging infections in the era of globalization
Q & A session on emerging and re-emerging infections in the era of globalization with Prof Alessandro Zanetti, Department of Public Health-Microbiology-Virology, Faculty of Medicine, University of Milan, Italy.

NYC Hep C Task Force
The New York City Hepatitis C Task Force is a city-wide network of service providers and advocates concerned with hepatitis C and related issues. The groups come together to learn, share information and resources, network, and identify hepatitis C related needs in the community. Committees form to work on projects in order to meet needs identified by the community

December 2015 Hep Free NYC Newsletter

In This Newsletter
Upcoming Events
New Tools
Training & Technical Assistance
Journal Articles & Reports
Job Board
Funding Board
Join our network!

Upcoming Activist Webinars
The Cost of Production for HCV Treatment
Treatment Action Group. Dec 8 (10 AM)

DAAs Drastically Simplify Hep C Diagnosis and Monitoring.
Treatment Action Group. Dec 10 (9 AM).

Meeting Highlights
The Brooklyn Hep C Task Force meeting included informative and exciting presentations on various hepatitis topics. Check out our meeting notes to view these presentations! 
11-4-2015 Brooklyn Hep C Task Force Meeting Notes

View our past meeting reports here

View all newsletters, here.

Subscribe to this Newsletter

Join Us



HepCBC Hepatitis C Education and Prevention Society

The hepc.bull, has been “Canada’s hepatitis C journal” since the late 1990′s and has been published nonstop since 2001. The monthly newsletter contains the latest research results, government policy changes, activities and campaigns you can get involved in, articles by patients and caregivers, and a list of support groups plus other useful links.

December Newsletter
hepc.bull -- 12 2015


Generic Drug Company
Before my visit to Lupin Limited in Pune, India, on November 20, 2015: OK, this is to prepare you for what I learned about generic drugs on November 20th. Close your eyes. What do you envision when I say: “Generic Drug Company in India”? If you’re like me, you probably have viewed these companies as inferior to companies which research and develop new drugs, rightfully hold the patents, and make the big bucks. After all, generic companies simply copy what someone else has spent years—in many cases, decades—working on, discovering the uses and analyzing the structure of unique new Active Pharmaceutical Ingredient (API) molecules. They perfect the dosage and discover side-effects through clinical trials, while at the same time they’ve had to explore many research ‘dead ends’ which result in zero ‘payback’ before finally hitting on the ‘pay dirt’ of a commercially viable product.

SVR-HCC risk
Hepatocellular carcinoma (HCC) is the most common liver cancer suffered by those with hepatitis C; it is often found in those who have not been treated whose disease has progressed. The new treatments, direct-acting antivirals (DAAs) are curing almost everyone, but researchers in Houston, TX wanted to know if the risk of HCC goes away.

Other viruses that affect the Liver
Those of us who have or have had hepatitis C must take extra care so as to not get other infections, since many if not most of us still have scarring, even if the virus is gone. This means taking care, as before, not to expose our bodies to toxins or anything that can cause liver inflammation (such as tobacco, alcohol and fast foods).

Treatment Map
The Canadian Treatment Action Council (CTAC) in Toronto has developed a great new free online tool for getting the most current HCV treatment news in Canada

Holiday Letter from HepCBC
Gilead GT 4-6
Would YOU?/
Honour Roll

Begin here...

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GI & Hepatology News
GI & Hepatology News is the official newspaper of the AGA Institute and provides the gastroenterologist with timely and relevant news and commentary about clinical developments and about the impact of health-care policy. The newspaper is led by an internationally renowned board of editors.

GI & Hepatology Newsletter

December 2015 PDF ( 13.7MB) | December 2015 Interactive Version

FDA warns of serious liver injury from HCV drugs
Sofosbuvir/velpatasvir works in HCV
IDWeek: Despite better drugs, HCV deaths keep rising
GI and liver diseases remain public health burden

Read breaking news stories now: visit the GI & Hepatology News website.

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HCV Action brings together hepatitis C health professionals from across the patient pathway with the pharmaceutical industry and patient representatives to share expertise and good practice.

In November, HCV Action published three new case studies, each highlighting hepatitis C services or projects that are both innovative and highly successful in terms of improving outcomes for patients.

NICE publishes final guidance for three new hepatitis C treatmentsThe National Institute for Health and Care Excellence (NICE) have this month published final guidance recommending the use of Harvoni, Daklinza and Viekirax (with or without Exviera) for the treatment of people with hepatitis C. The guidance will result in significantly wider access to the new, non-interferon, direct acting anti-viral treatments, which have shorter treatment durations and much less severe side-effects for patients when compared to interferon-based

A new report on sustainable healthcare
3 Dec 15

Call in Parliament for a national hepatitis C improvement framework
1 Dec 15

NICE releases final guidance for access to Harvoni, Viekirax and Daklinza hepatitis C treatments
25 Nov 15

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Blogs Around The Web

AJM Hepatitis C Resource Center - Hepatitis C Blog 
The AJM Hepatitis C Resource Center provides both primary care providers and specialists with continually updated treatment guidelines, and an up-to-date repository of informative, freely-available, full-text articles to encourage effective HCV screening and diagnosis, and to highlight the promise of novel treatment regimens.

Exclusive Hepatitis C Interview: Daryl Luster
In your experience as a patient and also as someone who now works in this area, what are the biggest challenges associated with the hepatitis C epidemic in the U.S.?

DARYL LUSTER: In the U.S. and the world, the issue is access to screening, quality care, and treatment. I mean, really, that’s a major issue. It’s quite complicated in the U.S. because of the fact that there is no real universal health care in America. In fact, some people have no insurance, no coverage whatsoever.

In Case You Missed It - Exclusive HCV Interview: Lucinda K Porter, RN

The Hepatitis B Foundation is a national nonprofit organization dedicated to finding a cure for hepatitis B and helping to improve the lives of those affected worldwide through research, education and patient advocacy. Visit

Top Stories

India Launches Drive to Eradicate Hepatitis B Virus
Nov 30 – The health ministry in collaboration with UNICEF launched a media campaign, including megastar Amitabh Bachchan, with the resolve to make India Hepatitis B Virus-free by the next decade.
Read more.

Functional Liver Cells Grown in the Lab
Nov 30 – Researchers have developed a new technique for growing human liver cells in the laboratory, described as the “holy grail of liver research”, and would allow for a more efficient, lower cost means of studying viral hepatitis, liver cancer, fatty liver, and drug toxicity.
Read more.

Coffee Linked to Reduced Liver Fibrosis in People with HBV, HCV, and NAFLD
Nov 30 – Drinking coffee was associated with lower liver stiffness, a non-invasive measure used to estimate liver fibrosis, in people with hepatitis B, hepatitis C, and non-alcoholic fatty liver disease (NAFLD). 

Tuesday, December 1, 2015
World AIDS Day - Coinfection with HIV and Viral Hepatitis
An estimated 1.2 million persons are living with HIV in the United States. Of people living with HIV in the United States, about 25 percent are coinfected with hepatitis C virus (HCV), and about 10 percent are coinfected with hepatitis B virus (HBV). People living with HIV infection are disproportionately affected by viral hepatitis, and those who are coinfected are at increased risk for serious, life-threatening complications. HIV coinfection more than triples the risk for liver disease, liver failure, and liver-related death from HCV. Because viral hepatitis infection is often serious in people living with HIV and may lead to liver damage more quickly, CDC recommends all persons at risk for HIV be vaccinated against hepatitis B and be tested for HBV and HCV infection. December 1st has been designated World AIDS Day, creating an opportunity not only for raising awareness about HIV infection, but educating health professionals and the general public worldwide about the overwhelming burden of HIV and viral hepatitis coinfection, and the importance of testing, care, and treatment.

View more @ HBV Advocate Blog

Creating a World Free of Hepatitis C
Welcome to my website and blog. My name is Lucinda Porter and I am a nurse committed to raising awareness about hepatitis C. I believe that we can create a world free of hepatitis C. We do this together, one step at a time.

Gilead’s Pricing of Hepatitis C Drugs Investigated by Senate
on DECEMBER 3, 2015

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Blogs At
Hep is an award-winning print and online brand for people living with and affected by viral hepatitis. Offering unparalleled editorial excellence since 2010, Hep and are the go-to source for educational and social support for people living with hepatitis.

Kim Bossley
Hepatitis C Advocate and Co-Founder, The Bonnie Morgan Foundation
Getting your TEAM formed - part 1 
The important part is that your get your life on track and have someone there to help you hold yourself accountable. Everyone deserves to be cured....regardless.
Click here

HIV/Hep C Co-infection activist; on treatment
1 December 2015: World AIDS Day
On World AIDS Day I am grateful for all the activists who fought hard for access to the life saving medication which keeps me, and many hundreds of thousands of others, alive today. I also remember the thousands of men and woman who didn't live long enough to benefit from the medication.

Greg Jefferys
My Hep C Travel Diary, Hepatitis C Advocate
Dare we Dream of a Hep C-free Australia? 
The Liver Clinic at St Vincent's Hospital in Sydney will now monitor patients who are having their Hepatitis C treated with Indian generics.
Click here

Grace Campbell
A nom de guerre for a person living with hepatitis C on Viekira Pak + Ribavirin
Last Entry: Hepatitis C: It's 4 in the morning ...
It's 4am, I'm wide awake and for the first time in many years I am not frightened about the future.
Click here

Connie M. Welch
Passionate Encourager for Christ, Writer, Speaker, and Hep C Warrior
Overcoming Obstacles with Hep C
Hep C has many stages. Overcoming obstacles with Hep C is possible. No matter where you're at in fighting Hep C
click here 

Matt Starr
Hepatitis, Liver Disease Support Coach
The Grouse and Waiting with Hep C
I have hepatitis C. I waited a long time for changes in my health, as a decade of battles with ongoing disease that changed my life. Ups and downs occurred, with lowlights that included a liver transplant, different treatments with low chances of success, and complications that continued beyond my sister's loving gift of her live liver donation. I won't go into details here, as it would end up reading like the long story that it is.
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Enjoy the weekend, be safe.