Worldwide 1 in 12 people have chronic hepatitis B or C = 500 million people

Latest Hepatitis News

Hepatitis C Project, vacancies x 3

 

The Hepatitis Foundation of New Zealand

Hepatitis C Programme

The Hepatitis Foundation of New Zealand is a national non-profit organisation whose mission is to promote positive health outcomes for the people of New Zealand. This is achieved through education and research into viral hepatitis; and early detection and long-term follow-up of chronic hepatitis B and C.

The Hepatitis Foundation (NZ) has been funded by the Ministry of Health to pilot and implement a national programme, to improve the health services for those living with hepatitis C.

We are looking to employ a team of self-motivated highly skilled professionals, based in our newly established office in Tauranga, to undertake this programme, commencing from early 2012.

This is an exciting opportunity to contribute to a new health initiative and make a significant difference to health outcomes of those with hepatitis C in New Zealand.

1.         Education and Training Development Officer

You will be a self motivated and innovative person with health or education experience who will be responsible within the team for developing educational resources, establishing and delivering educational and training programmes for key stakeholders involved in the pilot programme; as well as liaising with care providers; and developing a long term strategy for the training needs of the hepatitis nurses around the country.  Reference HepFNZ_HCV_2011/4

2.         Media Publications Officer / Communications Officer

This role includes overseeing the quarterly publication of a hardcopy and online magazine, and the setting up and management of an interactive website providing support and assistance for people with hepatitis C. It will also include working with the education officer to design and produce a wide range of educational materials. Reference HepFNZ_HCV _2011/5

3.         Senior Office Administrator/ Helpline Co-ordinator

This varied and interesting role combines office administration duties, secretarial support and a customer services (patient helpline) role. You will be responsible for the day to day management of the office and reception area, provide secretarial support to the team as required plus, with the support of the hepatitis nurse develop and manage a Hepatitis C information helpline.  Reference HepFNZ_HCV_2011/7

 

To request a Position Description please contact (or send your CV and cover letter to):

 

John Hornell

Chief Executive Officer

The Hepatitis Foundation of New Zealand

PO Box647

Whakatane

Email: john [at] hepfoundation [dot] org [dot] nz

DD: 07 3124563 ext 2

Mob: 021 739882

 

Closing date for applications:  16 December 2011

Liver cancer a deadly opponent

The death of legendary world heavyweight boxer Joe Frazier from liver cancer is a sad reminder of the seriousness of the disease.

Liver cancer often occurs after the cancer has originated somewhere else in the body, such as the large bowel or breast. This type of cancer is known as metastatic cancer.

However, it can also be a primary cancer. Although there are several organ structures in the liver, the most common type of cancer originating there is known as hepato cellular liver cancer (HCC), which originates from hepatocytes. This is what Frazier died of.

Liver cancer is very aggressive, with 98 per cent of those diagnosed with it dying within five years.

It is a common form of cancer, the third to fifth most common form of the disease in the world, depending on where you live.

In New Zealand, the average age of a liver cancer patient is between 60 and 80. In developing countries, where the risk factors for liver cancer (hepatitis B and C and excessive alcohol use) are more prevalent, people with the disease are in their 30s and 40s.

Men are three times more likely to develop liver cancer than women.

We began to offer hepatitis B vaccinations to children in New Zealand in the 1980s and hopefully this will result in a decrease in HCC during the next 10 to 20 years.

This is especially important in populations such as Maori, who have a higher prevalence of hepatitis B.

Hepatitis B can cause long-term inflammation in the liver if left untreated and can produce liver damage and cirrhosis, which may ultimately lead to HCC.

This is also true of hepatitis C, another virus.

Thankfully, there are medications which can eliminate these viruses and lower the risk of HCC developing.

It appears that chronic hepatitis B viremia can introduce genetic material into the liver cells. This material can upset the genetic makeup of the cells, thus causing them to become cancerous.

It is less clear how hepatitis C causes liver cancer, because its viral genetic material does not seem to make its way into the cells. It may well be that hepatitis C is an indirect cause.

Excessive alcohol use is the most common cause of liver cancer.

The symptoms of liver cancer, unfortunately, are ubiquitous. Unintentional weight loss, ascites (abdominal fluid and swelling) and becoming jaundiced may suggest the disease is present.

The key to prevention is to try to reduce the incidence of hepatitis B, in particular, as well as hepatitis C, and to make people aware of the dangers of alcohol.

Gilead Announces Positive Five-Year Data Showing Effect of Viread(R) on Liver Fibrosis and Chirrhosis Caused by Chronic Hepattis B

SAN FRANCISCO, Nov 05, 2011

Gilead Sciences, Inc. (Nasdaq:GILD) today announced new five-year data from the open-label phase of two pivotal Phase 3 clinical trials (Studies 102 and 103) evaluating the efficacy of Viread(R) (tenofovir disoproxil fumarate) for the treatment of chronic hepatitis B virus (HBV) infection among primarily treatment-naïve patients. Results show that Viread maintains long-term viral suppression of HBV and is associated with a reduction in liver fibrosis and a reversal of cirrhosis. Among patients in both studies, the majority (88 percent) experienced an improvement in overall liver histology. Together, these two studies represent one of the largest datasets evaluating the impact of an oral antiviral therapy on histologic changes and showing a reduction in liver fibrosis. These findings are being presented Monday, November 7 at the 62nd annual meeting of the American Association for the Study of Liver Diseases (The Liver Meeting 2011) in San Francisco.

"We have long theorized that long-term antiviral therapy can not only help chronic hepatitis B patients achieve and maintain virologic suppression, but also help to improve clinical outcomes, including a reduction in the risk of fibrosis or cirrhosis," said Patrick Marcellin, MD, of Hôpital Beaujon in Clichy, France, INSERM CRB3 and University of Paris Denis Diderot, and the principal investigator of Study 102. "These results represent an important advance in HBV therapy because they elucidate Viread's potential to reduce or reverse signs of liver damage in patients with chronic hepatitis B."

Studies 102 and 103 were designed to compare Viread to Hepsera(R) (adefovir dipivoxil) in a blinded manner over 48 weeks, among both HBeAg-negative (Study 102) and HBeAg-positive (Study 103) patients with compensated liver disease. Patients originally randomized to Hepsera in both studies were switched to open-label Viread at 48 weeks and patients randomized to Viread continued on open-label Viread.

The data show that the majority of patients who received Viread continuously for 240 weeks experienced sustained suppression of HBV DNA (viral load) levels in the blood below 400 copies/mL (83 percent and 64 percent for Studies 102 and 103, respectively). Patients who were randomized to Hepsera and rolled over to Viread at week 48 and received Viread for a subsequent 192 weeks also maintained viral suppression (84 percent and 66 percent for Studies 102 and 103, respectively).

Notably, among the 331 patients who had paired biopsies at both baseline and week 240, 292 (88 percent) experienced an improvement in overall liver histology, as measured by an improvement of at least two points in Knodell necroinflammatory score without worsening in Knodell fibrosis score. Of the 94 patients who had cirrhosis (Ishak fibrosis score greater-than or equal to 5) at the start of therapy, 69 (73 percent) experienced regression of cirrhosis and 68 (72 percent) had at least a two-point reduction in Ishak fibrosis score.

Among HBeAg-positive patients receiving Viread through 240 weeks (Study 103), the cumulative probability (estimated by Two-State Markov model) of "s" antigen loss and seroconversion was 9 percent and 7 percent, respectively. Additionally, no resistance to Viread emerged over 240 weeks of treatment.

"Viral resistance is a significant challenge for physicians treating patients with chronic hepatitis B," said Jenny Heathcote, MD, of the University of Toronto, Canada, and the principal investigator for Study 103. "These five-year results are important in that they demonstrate Viread's high genetic barrier to resistance, which is essential for the long-term success of HBV therapy."

Viread for HBV was approved by the U.S. Food and Drug Administration (FDA) in 2008 and has since become the most-prescribed medicine for chronic HBV in the United States. These five-year data have been submitted to the FDA and to the European Medicines Agency for review and potential inclusion in the Viread label.

About Studies 102 and 103

Studies 102 and 103 were both multi-center, randomized, double-blind Phase 3 clinical trials comparing Viread to Hepseraamong HBeAg-negative (Study 102; n=375) and HBeAg-positive (Study 103; n=266) chronic hepatitis B patients with compensated liver disease. Patients had HBV DNA above 100,000 copies/mL and elevated levels of alanine aminotransferase (ALT, an enzyme that serves as a measure of liver inflammation) upon study initiation. The majority of patients were treatment-naïve.

Patients originally randomized to Hepsera in both studies rolled over to open-label Viread treatment (n=196) at week 48, while patients originally randomized to Viread continued open-label Viread (n=389). All patients were asked to undergo liver biopsy at 48 weeks of treatment and again at five years of treatment, and a total of 331 patients were evaluated in the histology analysis.

Seventy-two percent of patients in Study 102 and 50 percent of patients in Study 103 achieved normalized ALT at week 240. Viread was well-tolerated in both studies. The most commonly observed adverse events were abdominal pain, nasopharyngitis, headache, influenza, back pain and hypertension. Across both studies, 2.1 percent of patients who received Viread for five years discontinued treatment due to an adverse event and 0.9 percent of patients experienced a confirmed increase in serum creatinine of at least 0.5 mg/dL or calculated creatinine clearance less than 50 mL/min.

Important Information About Viread for Chronic Hepatitis B

Viread (tenofovir disoproxil fumarate) is indicated for the treatment of chronic hepatitis B in adults. The following points should be considered when initiating therapy with Viread for the treatment of HBV infection: This indication is based primarily on data from the treatment of nucleoside-treatment-naïve patients, and a smaller number of patients who had previously received lamivudine or adefovir. Patients were adults with HBeAg-positive and HBeAg-negative chronic hepatitis B with compensated liver disease. Viread was evaluated in a limited number of subjects with chronic hepatitis B and decompensated liver disease. The number of patients in clinical trials who had lamivudine- or adefovir-associated substitutions at baseline was too small to reach conclusions of efficacy.

Lactic acidosis and severe hepatomegaly with steatosis, including fatal cases, have been reported with the use of nucleos(t)ide analogs, including Viread, in combination with other antiretrovirals.

Severe acute exacerbations of hepatitis have been reported in HBV-infected patients who have discontinued anti-hepatitis B therapy, including Viread. Hepatic function should be monitored closely with both clinical and laboratory follow-up for at least several months in patients who discontinue anti-hepatitis B therapy, including Viread. If appropriate, resumption of anti-hepatitis B therapy may be warranted.

New onset or worsening of renal impairment including cases of acute renal failure and Fanconi syndrome has been reported with the use of Viread. It is recommended to assess creatinine clearance (CrCl) before initiating treatment with Viread and monitor CrCl and serum phosphorus in patients at risk, including those who have previously experienced renal events while receiving Hepsera. Administering Viread with concurrent or recent use of nephrotoxic drugs should be avoided.

Viread should not be used with other tenofovir-containing products (e.g., Atripla(R), Complera(R), Truvada(R)). Viread should not be administered in combination with Hepsera.

Due to the risk of development of HIV-1 resistance, Viread should only be used as part of an appropriate antiretroviral combination regimen in HIV-infected patients with or without HBV coinfection. HIV antibody testing should be offered to all HBV-infected patients before initiating therapy with Viread.

Decreases in bone mineral density (BMD) have been observed in HIV-infected patients. It is recommended that BMD monitoring be considered for patients with a history of pathologic fracture or who are at risk for osteopenia. The bone effects of Viread have not been studied in patients with chronic HBV infection. Cases of osteomalacia (associated with proximal renal tubulopathy and which may contribute to fractures) have been reported in association with the use of Viread.

In controlled clinical trials in patients with chronic hepatitis B with compensated liver disease, the most common adverse reaction (all grades) was nausea, observed in 9 percent of patients taking Viread at week 48. Other adverse reactions observed at week 48 in greater than 5 percent of patients treated with Viread include abdominal pain, diarrhea, headache, dizziness, fatigue, nasopharyngitis, back pain and skin rash.

In HBV-infected patients with decompensated liver disease, the most common adverse reactions (all grades) reported in greater-than or equal to 10 percent of patients treated with Viread were abdominal pain (22 percent), nausea (20 percent), insomnia (18 percent), pruritus (16 percent), vomiting (13 percent), dizziness (13 percent), and pyrexia (11 percent).

Coadministration of Viread with didanosine increases didanosine concentrations. Use with caution and monitor for evidence of didanosine toxicity (eg, pancreatitis, neuropathy). Didanosine should be discontinued in patients who develop didanosine-associated adverse reactions. In adults weighing >60 kg, the didanosine dose should be reduced to 250 mg when it is coadministered with Viread. Data are not available to recommend a dose adjustment of didanosine for patients weighing <60 kg. Coadministration of Viread with atazanavir decreases atazanavir concentrations and increases tenofovir concentrations. Use atazanavir with Viread only with additional ritonavir; monitor for evidence of tenofovir toxicity. Coadministration of Viread with lopinavir/ritonavir increases tenofovir concentrations. Monitor for evidence of tenofovir toxicity.

The recommended dose for the treatment of chronic hepatitis B is 300 mg once daily taken orally without regard to food. The dosing interval of Viread should be adjusted and renal function closely monitored in patients with moderate and severe renal impairment.

The parent compound of Viread was discovered through a collaborative research effort between Dr. Antonin Holy, Institute for Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic (IOCB) in Prague and Dr. Erik DeClercq, Rega Institute for Medical Research, Katholic University in Leuven, Belgium.

Please see full Prescribing Information for Viread, Complera, Truvada and Hepsera (including BOXED WARNINGS).

About Gilead Sciences

Gilead Sciences is a biopharmaceutical company that discovers, develops and commercializes innovative therapeutics in areas of unmet medical need. The company's mission is to advance the care of patients suffering from life-threatening diseases worldwide. Headquartered in Foster City, California, Gilead has operations in North America, Europe and Asia Pacific.

Forward-Looking Statement

This press release includes forward-looking statements, within the meaning of the Private Securities Litigation Reform Act of 1995, that are subject to risks, uncertainties and other factors, including the risks that the FDA and the European Medicines Agency may not agree to the inclusion of the five-year data in the Viread label. In addition, the data may not impact physicians' decisions to prescribe Viread over other existing or future HBV medications. In addition, as Viread is used over longer periods of time by many patients with underlying health problems, taking numerous other medicines, safety, resistance, drug interaction or other issues may arise, which could reduce the market acceptance of Viread. These risks, uncertainties and other factors could cause actual results to differ materially from those referred to in the forward-looking statements. The reader is cautioned not to rely on these forward-looking statements. These and other risks are described in detail in Gilead's Quarterly report on Form 10-Q for the quarter ended June 30, 2011, as filed with the U.S. Securities and Exchange Commission. All forward-looking statements are based on information currently available to Gilead, and Gilead assumes no obligation to update any such forward-looking statements.

U.S. full prescribing information for Viread is available at www.Viread.com.

U.S. full prescribing information for Hepsera is available at www.Hepsera.com.

Complera, Hepsera, Truvada and Viread are registered trademarks of Gilead Sciences, Inc. or its related companies.

Atripla is a registered trademark of Bristol-Myers Squibb & Gilead Sciences, LLC.

For more information on Gilead Sciences, please visit the company's website at www.gilead.com or call Gilead Public Affairs at 1-800-GILEAD-5 or 1-650-574-3000.

SOURCE: Gilead Sciences, Inc.

Gilead Sciences, Inc.
Susan Hubbard, 650-522-5715 (Investors)
Soleil Harrison, 650-522-5283 (Media)

Hepatitis C now a bigger killer than HIV

SAN FRANCISCO -- Mortality associated with hepatitis C has surpassed that of HIV, a researcher said here.

The declining death rate from HIV crossed the rising rate associated with hepatitis C infection in about 2006, according to Scott Holmberg, MD, of the CDC.

On the other hand, the rate of deaths associated with hepatitis B has been relatively flat, Holmberg reported at the annual meeting of the American Association for the Study of Liver Diseases.

The finding, from an analysis of death statistics from 1999 through 2007, comes as another study presented here suggested that as many as 800,000 new cases of hepatitis C could be diagnosed under a proposed new screening approach.

Indeed, Holmberg told an oral session here that the figures he and colleagues turned up are probably underestimates of the mortality burden of viral hepatitis in the U.S., partly because many people with viral hepatitis have yet to be diagnosed.

The issue also arises with HIV, he noted, but current estimates are that about 20% of those with HIV in the U.S. are not yet diagnosed. For hepatitis C, he said, the rate of diagnosis is probably less than half of those who actually have the virus.

The researchers looked at 21.8 million death certificates from the National Center for Health Statistics. Deaths were defined as being related to one of the three viruses if they were listed as either underlying or contributing causes of death.

Those data were used to construct the temporal trends, Holmberg said. The researchers also analyzed data for 2007 to get a picture of cause and variables associated with the incidence and prevalence of the diseases.

Holmberg reported that the rate of deaths related to hepatitis B was almost constant over the study period, at less than one per 100,000 people. In 2007, for instance, there were 1,815 such deaths.

On the other hand, he said, deaths associated with hepatitis C increased significantly, with a yearly age-adjusted mortality rate change of plus 0.18 deaths per 100,000 people. The toll reached 15,106 deaths in 2007.

In contrast, HIV deaths fell to 12,734 in 2007, the researchers found.

The highest toll of hepatitis deaths was among the middle-aged – those 45 through 64.

Holmberg reported that 59% of deaths related to hepatitis B occurred in that age group, as did 73% of the deaths linked to hepatitis C. In both cases, the rate was significantly higher than in the reference group – those 44 and younger.

For instance, just 8% of hepatitis C deaths occurred in the reference group, compared with 39% among those ages 45 through 54 and 34% among those 55 through 64.

As expected, coinfection with HIV significantly increased the risk of death from the hepatitis viruses, with adjusted odds ratios of 1.8 and 4.0 for hepatitis B and C, respectively.

But those risks paled compared with some other comorbidities. Specifically:

  • Having chronic liver disease led to an adjusted odds ratio for death of 32.1 for hepatitis B and 34.4 for hepatitis C, with the respective 95% confidence intervals from 31.0 to 38.1 and from 31.0 to 33.3.
  • Being coinfected with the other virus led to an adjusted odds ratio of between 29.9 and 31.5, depending on which virus was considered the primary cause of death.

Holmberg cautioned that death certificate data have some inherent limitations, including incomplete ascertainment of causes, misclassification, and missing data.

A key finding of the analysis is that most of the hepatitis deaths are occurring in people 45 through 64, according to AASLD president Jake Liang, MD, of the National Institute of Diabetes and Digestive and Kidney Diseases in Bethesda, Md.

The causes remain unclear, he told reporters, although one possibility is the "youthful indiscretions" of the Baby Boomers.

From a public health standpoint, he added, "this is a population we really need to be concerned with ... We really need to be more aggressive in identifying them and trying to treat them."

Some People with Hepatitis B May Need Liver Cancer Screening sooner and More Often
Written by Liz Highleyman

Asian immigrants in the U.S. who have chronic hepatitis B virus (HBV) infection may develop hepatocellular carcinoma (HCC) at younger-than-expected ages, suggesting that people with risk factors such as smoking and family history should start liver cancer screening sooner and receive it more frequently, according to a report in the September 13, 2011, advance edition of the American Journal of Gastroenterology.

Over years or decades, chronic hepatitis B (and C) can lead to serious liver damage including cirrhosis and HCC. In the U.S., hepatitis B is much more prevalent among people from Asia, where HBV is endemic and many people became perinatally infected before the advent of widespread vaccination.

HCC is more easily treated if caught early. Routine liver cancer screening is recommended for chronic hepatitis B patients with cirrhosis and certain for high-risk populations -- including Asian men age 40 and older and Asian women age 50 and older -- even if cirrhosis is not present. However, many younger hepatitis B patients develop HCC before they are advised to start screening.

David Wan from New York University and colleagues aimed to determine risk factors for the development of early-onset HCC -- that is, occurring in men under age 40 or women under 50 -- among U.S. Asian immigrants with chronic hepatitis B.

The investigators retrospectively collected clinical, demographic, and laboratory data for all Asian immigrants with hepatitis B at Bellevue Hospital Center in New York between 2003 and 2009. A total of 168 patients with HCC were identified and compared with age-matched control subjects with hepatitis B but not HCC.

Results

  • 74% of all identified HCC cases (124 out of 168) were late-onset, while 26% (44 out of 168) were early-onset.
  • In a comparison of the 124 late-onset HCC patients with 199 age-matched control subjects without HCC, the following factors were found to be significantly (P < 0.05) associated with liver cancer development:

o      Male sex: odds ratio (OR) 4.4, or more than a 4-fold risk;

o      Liver cirrhosis: OR 9.6;

o      Surrogate marker lab tests (i.e., platelets, international normalized ratio, total bilirubin, albumin).

  • Comparing the 44 early-onset HCC patients with 432 age-matched control subjects with hepatitis B, the following were independent (P < 0.05) predictors of liver cancer:

o      Male sex: PR 2.7, or nearly a 3-fold risk;

o      Family history of HCC: OR 2.7;

o      History of smoking: OR 3.4.

o      Liver cirrhosis: OR 19.5;

o      Surrogate marker lab tests.

  • Overall, 54.8% of people with late-onset HCC had cirrhosis, compared with 29.5% of early-onset HCC cases.

"HCC occurs in Asian immigrant HBV patients younger than currently recommended screening guidelines," the study authors concluded. "A large majority of these early-onset patients did not have cirrhosis at the time of their HCC diagnosis; therefore, factors other than cirrhosis need to be considered when evaluating HCC risk in young patients."

"Factors associated with HCC development across all ages include cirrhosis and male gender, while family history and smoking history may identify younger Asian immigrant HBV patients at risk for HCC," they continued. "[O]ur results suggest that younger Asian HBV patients, especially those with a smoking history or family history of HCC, appear to have an increased risk for HCC and should be considered for enrollment in early screening programs regardless of their age."