High Referral of HCV Patients to Specialists But Low Treatment Initiation Rate - Barriers to Care & Treatment

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ID Week
October 2-6, 2013
San Francisco

IDWeek, October 2-6, 2013, San Francisco

from Jules: authors told me this study was conducted during the time period for pegylated interferon+ribavirin use. So for me a question is will these same barriers persist and to what degree if they do after new improved therapies about to be approved are available. In addition there are other barriers not addressed in this poster so how much will these barriers create difficulty in accessing care & treatment. Of course the barriers to initial diagnosis are the first concern, how will we diagnose the 75% we think are undiagnosed in the USA, estimated to be as many as 5 million undiagnosed. Second, how will we develop an adequate care infrastructure capable of accommodating so many patients, and will this care system be effective with adequately qualified care providers. I have doubts that primary care & untrained providers with no experience in hepatitis C can be trained to treat the disease. Third, how will we accommodate the hardest to treat patient populations: marginalized patient populations, IDUs, this will not be easy as this will take commitment to build a healthcare infrastructure with the ability to provide the specialized resource-intensive these patient populations will need. And within the IDU community there are gradations of difficult-to-treat patients, in particular there are patients that most providers do not want to treat, these are the most marginalized IV drug users who the healthcare system does not want to treat, they can be dirty, homeless, using IV drugs & alcohol, have psychiatric disorders, poor communication skills, unable to navigate healthcare system, mistrusting of the healthcare system, uneducated, but want to be cured, so we need to create a system that can & will treat these patients, it is doable. We can create a successful healthcare facilities system for them, we have to be creative.

Mark Mascolini

More than 90% of patients with HCV infection at an academic primary care practice got referred to a hepatitis specialist [1]. But for most patients more than a year passed between HCV diagnosis and referral, and only 18% of patients with a documented specialist visit started anti-HCV therapy.

Prompt diagnosis, referral, and possibly treatment of HCV infection are essential to preventing complications. Rapid referral and treatment might be considered even more urgent since licensing of direct-acting antiretrovirals that could induce sustained virologic response in more people. To assess HCV referral and treatment rates in their academic primary care practice, investigators at Baystate Medical Center/Tufts University in Massachusetts conducted this retrospective cross-sectional study. The researchers aimed both to describe referral and treatment patterns and to identify traits that favored or delayed referral and treatment.

The study focused on people making one or more office visits in the past 2 years who were diagnosed with HCV and not already in care with an infectious diseases or HCV specialist. Among 235 people eligible for the study, 215 (91.5%) got referred to a hepatitis specialist and 20 did not. But among those 215 referred patients, only 146 (68%) had a documented visit with an HCV specialist. Among the146 people with a documented specialist visit, 26 (17.8%) got treated for HCV infection and 120 did not. Among treated people, median time from referral to starting therapy was 226 days (interquartile range 157 to 376).

Among the 120 people not treated after a documented HCV specialist visit, reasons for lack of treatment included loss to follow-up, patient preference, psychiatric factors, substance abuse, and undetectable HCV load. Among the 20 patients with an HCV diagnosis not referred to an HCV specialist, (overlapping) reasons for lack of referral were active substance abuse (9 people), patient preference (7), psychiatric disorders (6), and other reasons (4).

Compared with the 146 referred people who had a documented HCV specialist visit, the 69 who did not were less likely to be married (5.8% versus 28.7%, P < 0.01) and marginally less likely to have any comorbidity (17.4% versus 29.7%, P = 0.07) or to be HIV-positive (4.4% versus 11.9%, P = 0.13). In this analysis, gender, race, age, injection drug use, psychiatric conditions, and severity of HCV infection did not distinguish between patients who did and did not have an HCV specialist visit.

Median time from HCV diagnosis to specialist referral was 411 days (interquartile range 33 to 1390). Time-to-event analysis identified three factors that favored a shorter median time to referral: being married (71 versus 184 days, P< 0.001), being HIV-positive (66 versus 156 days, P = 0.045), and having any comorbidity (83 versus 179 days, P = 0.009).

The researchers suggested the high referral rate reflects a practice setup in which primary care and specialty services share electronic medical records and ancillary staff. The correlation between being married and prompter referral may mean marital status is a proxy for social support that could enhance adherence. The link between HIV coinfection or comorbid conditions and faster referral may reflect more frequent clinic visits by these patients and thus increased provider awareness.

The investigators called for prospective studies to confirm their findings. They suggested that new, simpler, less toxic HCV regimens may prompt faster patient referral and treatment initiation.

Reference

1. Ooi WB, Madero-Gorostieta F, Dahiya S, et al. Referral and treatment patterns in chronic hepatitis C. IDWeek 2013. October 2-6, 2013. San Francisco. Abstract 465.

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Reported by Jules Levin

Referral and Treatment Patterns of Chronic Hepatitis C
Wei B. Ooi MD, Fernando Madero-Gorostieta MD, Saurabh Dahiya MD, Michael Rosenblum MD, Alexander Knee, Armando Paez MD, Daniel Skiest MD Baystate MedicalCenter/Tufts University School of Medicine

Program Abstract

Background: Hepatitis C virus (HCV) infection is a common blood-borne disease in the United States; approximately 3.2 million people are infected chronically. Prompt evaluation for possible treatment is important to avoid complications of HCV infection.

Methods: This was a retrospective cross-sectional study at an academic primary care practice. The objectives were to describe referral and treatment patterns of HCV infection and identify patient characteristics associated with delay in HCV care. HCV-infected patients were identified based on ICD-9 billing codes.

Exclusion criteria included missing electronic medical records and patients followed by a HCV specialist prior to their initial presentation to our practice. Patient characteristics associated with delay in HCV care were determined using time-to-event methods. Differences were evaluated using Kaplan-Meier plots and log-rank tests.

Results: Two hundred and thirty five patients were included, of which 215 were referred to a HCV specialist. Mean age was 50 years. Sixty four percent were male and fifty six percent were white. Median duration from HCV diagnosis to referral to HCV specialist was 411 days. Median duration from referral to HCV specialist visit was 71 days. Thirty two percent of 215 patients who were referred did not have a documented specialist visit. Only twenty six patients (11%) were started on HCV treatment and the median duration from referral to initiation of treatment was 226 days. Primary care providers or HCV specialists' reasons for no referral and no HCV treatment, respectively, included patient preference, substance abuse, psychiatric disorders, lost to follow-up and others. Patient characteristics associated with an earlier assessment of Hepatitis C included marital status, HIV co-infection and history of any medical co-morbidity.

Conclusion: Most HCV- infected patients were referred to a HCV specialist. However, HCV treatment was infrequent with a prolonged duration from time of diagnosis to treatment. Patient, physician and system factors need to be addressed to improve care.

Continue here to view posters …..

Dr. Graham Foster to Present a Poster on Spring Bank Pharmaceuticals' HCV Drug SB 9200 at the AASLD

MILFORD, Mass., Oct. 7, 2013 /PRNewswire/ -- Dr. Graham R. Foster and his team from Queen Mary, University of London, London, United Kingdom, will be presenting a poster titled "Pangenotypic anti-HCV activity of SB 9200 assessed in the 'Capture-fusion' replication assay" (Abstract No. 473) at the 64^th Annual Meeting of The American Association for the Study of Liver Diseases (AASLD), November 1-5, 2013, Washington, DC.  Details can now be viewed at the AASLD website at www.aasld.org.

The Poster is scheduled for presentation on Saturday, November 2, 2013, 2:00 pm –7:30 pm EDT.

About Spring Bank Pharmaceuticals   
Spring Bank Pharmaceuticals is engaged in the discovery and development of an entirely new class of pharmaceuticals based on the Company's proprietary SMNH, "Small Molecule Nucleic Hybrid" technology program. The company's lead compound, SB 9200, a potential breakthrough drug for the treatment of HCV and HBV, is currently in Ph. 1 clinical studies for HCV. In addition, the Company has preclinical programs for Respiratory Syncytial Virus (RSV) infections, a Broad-Spectrum Antiviral agent, and COPD. For more information, please visit our website: www.springbankpharm.com

Contact: Douglas Jensen (508) 473-5993 Ext.105

SOURCE Spring Bank Pharmaceuticals, Inc.

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Scientist tackle HIV from unusual angles to find cure

October 7, 2013 8:15 am by Allday, Erin |  MedCity News

In the race for a cure for HIV, the wins are stacking up.

We have the Berlin Patient and the Mississippi Baby. There's the Visconti Cohort -- 14 patients in France -- and most recently, two men in Boston who were declared to be HIV-free just this summer.

Through a variety of mechanisms and treatments, all of these people were able to shake the virus and stop taking the drugs that HIV-infected patients ordinarily need to survive. They represent possibility -- that modern science is capable of curing a deadly infection.

But possibility and reality aren't in the same place just yet. And the hunt has taken off to find a cure that won't just halt the disease one patient at a time, but put up a global blockade to HIV. Scientists are searching for a cure that's affordable and safe, and will shut down the epidemic entirely.

In the Bay Area, the Gladstone Institutes this summer has collected more than $12 million in funding from the National Institutes of Health for research aimed largely at exploring untapped avenues toward finding a cure.

UCSF is one of three institutions nationally to start research programs -- again, with NIH funding -- specifically focused on developing cures. Conversations about curing HIV have dominated locally and globally, from last year's International AIDS Conference in Washington, D.C., to a town hall meeting in San Francisco on Tuesday night.

"There have been anecdotal cases of individuals who have been for all intents and purposes cured, or whose disease has been put in remission," said Dr. Mike McCune, chief of the UCSF division of experimental medicine. "Now you have a groundswell for an effort to come up with interventions. It's a high-risk venture, but a lot of us are taking it up now because we think it's doable."

HIV under control

HIV has for more than a decade been a treatable disease. With daily antiretroviral drugs, patients can keep their infection under control, and stave off death from AIDS, for decades. But the drugs aren't a cure, and the virus lingers in a latent state, from which it can reawaken and wreak havoc if patients don't keep on medication.

Plus, the latent virus, even when kept under control by drugs, appears to cause subtle but constant damage that leads to premature aging and early death from heart disease and other age-related illnesses.

So while antiretroviral drugs have been a boon to the millions suffering from HIV and made a huge dent in the global epidemic, they aren't a permanent solution -- they aren't a cure.

The word "cure" itself is tricky when applied to HIV infection. Scientists for the most part don't expect to find an absolute cure any time soon -- a cure in which the virus is wiped out entirely. Instead, they are looking for a "functional" cure, which would mean patients could live, and stay healthy, with a small amount of virus that's kept under control either by the body's own immune system or with the help of cheap, easy-to-access drugs.

The first cure, functional or otherwise, came in 2008 with the Berlin Patient -- a man since identified as Timothy Brown who was treated in Germany and now lives in San Francisco. Brown was given a bone marrow transplant to treat cancer, but the therapy also killed off his HIV infection. Since then, a similar bone marrow treatment appears to have cured two HIV patients in Boston.

Meanwhile, scientists have 15 documented cases -- a baby in Mississippi and the 14 patients in France -- of people being cured of HIV by taking high-dose antiretroviral drugs immediately after becoming infected. All of those patients have, so far, been able to avoid the drugs long term and stay healthy.

These cases are thrilling and all cause for celebration, doctors and scientists say. But the treatments behind them aren't practical for stopping the HIV epidemic. In the case of bone marrow transplants, the therapy is too expensive and risky, and it would require finding donors for every HIV patient -- impossible on a global level.

Early antiretroviral therapy may be a reasonable treatment for many cases, but it would require a huge effort to get people tested and treated almost immediately after infection, and it isn't an option for the millions already sick.

Unusual angles

That's why scientists are tackling HIV from some unusual angles these days in their hunt for a cure. At Gladstone, for example, the recent NIH funding has gone toward three projects: looking at genetically engineered mice, hijacked viruses and suicidal cells.

"These proposals, some of them are really a shot in the dark," said Leor Weinberger, a Gladstone scientist who on Monday won an NIH grant for his work in hijacking viruses. "But you have to diversify your portfolio, you have to have some high-risk products you're invested in, if you're going to find solutions."

Weinberger's research is in harnessing bits of HIV and using them to attack the virus itself. The therapy would involve replacing some of the genetic material in the virus and disrupting its ability to replicate.

If it works, it might require a one-time injection, and while it wouldn't kill off all the virus in the body, it would render it essentially harmless, said Weinberger.

'Cellular suicide'

Dr. Warner Greene, director of the virology and immunology division at the Gladstone Institutes in San Francisco, has uncovered a surprising explanation for the deaths of certain immune cells that are associated with HIV infection. He's found that "bystander" cells -- those that haven't been infected by the virus -- appear to self-immolate when they're exposed to HIV but not yet taken over by it.

The cellular suicide is probably a protective gesture meant to prevent spread of the virus, but in fact it sets off a chain of events that leads to widespread destruction of the immune system, Greene said.

He's exploring whether anti-inflammatory drugs could halt that self-destructive process and even destroy some or all of the HIV reservoirs. Patients might still have to take regular medication, but perhaps not antiretroviral drugs, which can have tough side effects, and they might avoid the long-term damage done by latent HIV infection.

"We're looking at cell death by an intensely inflammatory response," Greene said. "It turns out the dying cells, because of inflammation, attract new cells to come to their aid, and they fall prey too. It starts a vicious cycle. Now the question is, what can we do about that? How can we interrupt this cycle?"

A popular thread of cure research is in the viral reservoirs, which are still largely undefined -- in fact, scientists aren't entirely sure where those reservoirs are located in the body.

But if doctors can find those reservoirs, or prevent them from forming, that might mean the end to HIV. The focus of UCSF's cure team is on finding the reservoirs and understanding how they're created.

Turning to mice

At the same time, Gladstone scientist Shomyseh Sanjabi, who also won NIH funding this week, is developing a strain of mice whose immune systems have been removed and replaced with human systems. These mice will be engineered to reflect both humans with normal immune systems and humans who are knowns as "elite controllers" -- able to stave off HIV infection without any treatment.

Elite controllers are rare, but scientists have recognized them as priceless for research into how the body can naturally fight HIV. Sanjabi hopes her mice will help other scientists finally unravel some of the mysteries behind HIV.

She has her own theories on HIV latency and the reservoirs, she said, but "we're just really excited by the idea that no matter what we find, whether our hypothesis is right or not, we're going to get a lot of information out of our work."

"We have to first know the beast that we're trying to kill," she said.

Erin Allday is a San Francisco Chronicle staff writer. E-mail: eallday@sfchronicle.com ___

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Visit the San Francisco Chronicle at www.sfgate.com

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Crucial Hep C vaccine stalled due to lack of funding

Lucie van den Berg medical reporter

From: Herald Sun

October 08, 2013 12:01AM

Money is needed to fund a crucial Hep C vaccine that could save lives. Source: ThinkStock

A GAME-CHANGING vaccine that could help eradicate a debilitating virus plaguing almost 150 million people worldwide has stalled over a funding shortfall.

Melbourne scientists have successfully tested the hepatitis C vaccine in animal models, but it cannot progress to human trials until it secures funding.

Hep C is the leading cause of liver disease and puts an incredible strain on the health system.

But the Burnet Institute vaccine, which could prevent the virus, is stuck in the medical research "valley of death".

Associate Professor Heidi Drummer said it had developed a preventive vaccine that - together with new direct acting antiviral agents - could eradicate the virus.

Hep C has been a difficult virus to tackle with a single vaccine because of its clever ability to change its structure and evade our immune response.

"Hep C is classed into 7 different genotypes and 100 different sub types, which means it has been a really big challenge to try and make a vaccine that will protect against all circulating strains," Prof Drummer said.

Her team at the Viral Fusion Laboratory discovered that even though the virus protein, which the antibodies have to stop infiltrating the cells, was highly variable, it still had consistent characteristics across the strains.

They designed a vaccine containing a protein with only those consistent components.

In mice and guinea pigs injected with the vaccine, they found the body produced antibodies that were able to tackle the consistent components across all virus strains, stopping the infection.

She said it was a real step forward, but the crucial test was replicating the result in humans.

The Burnet Institute has been unable to secure funding to carry out phase 1 clinical trials.

Commercial development and industry engagement manager Serina Cucuzza said it was difficult to attract funding for the crucial proof of concept stage, known as the valley of death.

"We have passed the initial valley of death by highlighting that we have a vaccine that is a potential game-changer," she said.

"It's now in the second valley of death where we need to trial it in humans, which is an expensive exercise."

She said vaccines were traditionally the best low cost, high value intervention, but they were struggling to attract Government or investor funding to progress the project.

The majority of Australia's 11,000 new hep C cases each year are caused by injecting drugs, but in the developing world infections are mostly due to unsterilised medical equipment.

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Simeprevir data from COSMOS study in Hepatitis C patients will be presented as late-breaking presentation at AASLD

Stockholm, Sweden — Medivir AB (OMX: MVIR) announced that data from the phase IIa COSMOS study (Combination Of SiMeprevir and sOfosbuvir in HCV genotype 1 infected patientS) of the investigational protease inhibitor simeprevir (TMC435) administered once daily with Gilead’s investigational nucleotide inhibitor sofosbuvir (GS-7977), with and without ribavirin, in genotype 1 chronic hepatitis C adult patients with compensated liver disease has been accepted as a late-breaking oral presentation at the upcoming Annual Meeting of the American Association for the Study of Liver Diseases (AASLD). AASLD will take place November 1 to 5 in Washington, D.C.

The COSMOS data will be presented during the late-breaking oral session on Monday, November 4, 2:45-4:30 p.m. (EST) in Hall E:
SVR results of a once-daily regimen of simeprevir (TMC435) plus sofosbuvir (GS-7977) with or without ribavirin in cirrhotic and non-cirrhotic HCV genotype 1 treatment-naïve and prior null responder patients: The COSMOS study.

• Lead Author: Ira M. Jacobson, Weill Cornell Medical College, New York, USA

Full session details and data presentation listings for the 2013 AASLD Annual Meeting can be found at http://www.aasld.org/livermeeting.

For more information please contact:
Rein Piir, EVP Corporate Affairs & IR
Mobile: +46 708 537 292.

About Simeprevir
Simeprevir is an investigational NS3/4A protease inhibitor jointly developed by Janssen R&D Ireland and Medivir AB, for the treatment of genotype 1 and genotype 4 chronic hepatitis C in adult patients with compensated liver disease, including all stages of liver fibrosis. Simeprevir works by blocking the protease enzyme that enables the hepatitis C virus to replicate in host cells.

Janssen is responsible for the global clinical development of simeprevir and has acquired exclusive, worldwide marketing rights, except for in the Nordic countries. Medivir will retain marketing rights for simeprevir in these countries.

Simeprevir was approved in Japan in September 2013 for the treatment of genotype 1 hepatitis C. In the U.S., the New Drug Application (NDA) filed by Janssen for simeprevir administered once daily in combination with pegylated interferon and ribavirin for the treatment of genotype 1 chronic hepatitis C in adult patients was granted Priority Review designation by the Food and Drug Administration (FDA) in May. A Marketing Authorisation Application was submitted to the European Medicines Agency (EMA) in April seeking approval of simeprevir for the treatment of genotype 1 or genotype 4 chronic hepatitis C.

To date, more than 3,700 patients have been treated with simeprevir in clinical trials. Simeprevir is also being studied in several interferon-free regimens using selected combinations of direct-acting antiviral agents with different mechanisms of action.

For additional information about simeprevir clinical trials, please visit www.clinicaltrials.gov.

About Sofosbuvir
Sofosbuvir (formerly referred to as GS-7977) is a once-daily nucleotide analog polymerase inhibitor for the treatment of HCV infection being developed by Gilead Sciences, Inc. Sofosbuvir is being evaluated as part of multiple therapeutic regimens, including programs with RBV alone and in combination with peg-IFN and RBV.

About Medivir
Medivir is an emerging research-based pharmaceutical company focused on infectious diseases.
Medivir has world class expertise in polymerase and protease drug targets and drug development which has resulted in a strong infectious disease R&D portfolio. The Company’s key pipeline asset is simeprevir, a novel protease inhibitor for the treatment of hepatitis C that is being developed in collaboration with Janssen R&D Ireland. Medivir has also a broad product portfolio with prescription pharmaceuticals in the Nordics.

For more information about Medivir AB, please visit the Company’s website: www.medivir.com

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Oversight Reduces HIV Prescription Errors

Laird Harrison

Oct 05, 2013

SAN FRANCISCO — Better record keeping, education, and vigilance by infectious disease clinicians and pharmacists can reduce the rate of prescription errors for HIV-infected patients hospitalized for other reasons, new research shows.

Such reforms significantly reduced the rate of prescribing errors from 50% to 34% at the Cleveland Clinic(P = .008), said Elizabeth Neuner, PharmD, an infectious diseases clinical pharmacist. "They allow more effective prescribing."

Dr. Neuner presented the research to reporters attending a news conference here at IDWeek 2013.

Antiretroviral drug regimens for HIV are typically complicated and can be difficult for patients to follow, she noted.

When HIV-infected patients are hospitalized for non-HIV conditions, hospital providers who are unfamiliar with the complexities of HIV therapy can make errors. The consequences include adverse effects, a loss of viral protection, and drug interactions, she told Medscape Medical News.

"We wanted to take a more focused look at those patients because they are at such high risk for medication errors," she said.

To reduce these errors, the Cleveland Clinic implemented a program that involved education, modification of the electronic drug file to help guide the accurate prescribing of medications, a daily medication profile review by a pharmacist specializing in HIV, and the involvement of an infectious disease physician.

In their study, Dr. Neuner and her team evaluated 162 HIV-infected patients hospitalized for another reason before the program was implemented and 110 patients hospitalized after it started.

Table. Prescribing Errors Before and After Program Implementation

Outcome	Preprogram	Postprogram	P Value
Errors resolved	36%	74%	.001
Time to resolve errors	180 hours	23 hours	.002
Cases with errors	50%	34%	.008

The researchers found that infectious disease specialists provided valuable input. Errors were corrected more often when patients were evaluated by a specialist than when they were not (68% vs 32%; P = .002).

For example, the specialists corrected inaccurate antiretroviral medications and dosages, adjusted regimens in which a new medication, such as for heart problems or diabetes, was interacting with an antiretroviral medication, and revised therapy to address a new problem, such as kidney injury.

In some cases, physicians opted not to correct the error because the patient was doing well on the therapy and the benefits outweighed the risks.

Michael Horberg, MD, national director for HIV/AIDS at Kaiser Permanente Medical Group in Rockville, Maryland, pointed out that Kaiser hospitals are using a similar system to prevent errors.

"When these patients come in, they sometimes remember to bring their medications, and they sometimes don't," he told Medscape Medical News. "If we can't get hold of their primary care physician, we're at a loss. In such cases, the roles of the infectious disease clinician and pharmacist are increasingly critical to quality of care and quality outcomes."

Dr. Horberg and Dr. Neuner have disclosed no relevant financial relationships.

IDWeek 2013. Abstract 176. Presented October 3, 2013.

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