December 11, 2011

Hepatology. 2011 Dec 2. doi: 10.1002/hep.25508. [Epub ahead of print]

Petta S, Torres D, Fazio G, Cammà C, Cabibi D, Di Marco V, Licata A, Marchesini G, Mazzola A, Parrinello G, Novo S, Licata G, Craxì A.

Source

Sezione di Gastroenterologia, Di.Bi.M.I.S, Università di Palermo, Italia. petsa@inwind.it.

Abstract
BACKGROUND AND AIMS:

There are contrasting results in studies of cardiovascular risk in patients with genotype 1 chronic hepatitis C (G1 CHC). We evaluated the prevalence of carotid atherosclerosis compared with a control population in order to assess the potential association between atherosclerosis, host and viral factors, and liver histological features.

MATERIALS AND METHODS:

One hundred seventy-four consecutive biopsy-proven G1 CHC patients were evaluated by anthropometric and metabolic measurements. One hundred seventy-four patients attending an outpatient cardiology unit were used as controls. Intima-media thickness (IMT) and carotid plaques, defined as focal thickening of > 1.3 mm at the level of common carotid, were evaluated using ultrasonography. All G1 CHC biopsies were scored by one pathologist for staging and grading, and graded for steatosis.

RESULTS:

Carotid plaques were found in 73 (41.9%) G1 CHC patients compared with 40 (22.9%) control patients (p<0.001). Similarly, G1 CHC patients had a greater IMT compared with control patients (1.04±0.21 versus 0.90±0.16; p<0.001). Multivariate logistic regression analysis showed that older age (OR 1.047, 95%CI 1.014-1.082, p= 0.005), and severe hepatic fibrosis (OR 2.177, 95%CI 1.043-4.542, p=0.03), were independently linked to the presence of carotid plaques. In patients aged ≤55 years, 15/67 cases with F0-F2 fibrosis (22.3%) had carotid plaques, compared with 11/21 (52.3%) with F3-F4 fibrosis (p=0.008). By contrast, in patients >55 years the prevalence of carotid plaques was similar in those with or without severe fibrosis (25/43, 58.1% versus 22/43, 51.1%; p=0.51).

CONCLUSION:

Severe hepatic fibrosis is associated with a high risk of early carotid atherosclerosis in G1 CHC patients. (HEPATOLOGY 2011.).

Copyright © 2011 American Association for the Study of Liver Diseases

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Hepatology. 2011 Dec 2. doi: 10.1002/hep.25510. [Epub ahead of print]

McGarry LJ, Pawar VS, Parekh HH, Rubin JL, Davis GL, Younossi ZM, Capretta JC, O'Grady MJ, Weinstein MC.

OptumInsight, Medford, MA. lisa.mcgarry@optum.com

Abstract

Recent research has identified high hepatitis C virus (HCV) prevalence among older US residents who contracted HCV decades ago and may no longer be recognized as high-risk. We assessed the cost-effectiveness of screening 100% of US residents born 1946-1970 over 5 years (birth-cohort screening) compared with current risk-based screening, by projecting costs and outcomes of screening over the remaining lifetime of this birth cohort. A Markov model of the natural history of HCV was developed using data synthesized from surveillance data, published literature, expert opinion, and other secondary sources. We assumed eligible patients were treated with pegylated interferon plus ribavirin, with genotype 1 patients receiving a direct-acting antiviral in combination. The target population is US residents born 1946-1970 with no prior HCV diagnosis. Among the estimated 102 million (1.6 million chronically HCV-infected) eligible for screening, birth-cohort screening leads to 84,000 fewer cases of decompensated cirrhosis, 46,000 fewer cases of hepatocellular carcinoma, 10,000 fewer liver transplants and 78,000 fewer HCV-related deaths. Birth-cohort screening led to higher overall costs than risk-based screening ($80.4 billion vs. $53.7 billion), but yielded lower costs related to advanced liver disease ($31.2 billion vs. $39.8 billion); birth-cohort screening produced an incremental cost-effectiveness ratio (ICER) of $37,700 per quality-adjusted life-year gained versus risk-based screening. Sensitivity analyses showed that reducing the time horizon during which health and economic consequences are evaluated increases the ICER, whereas decreasing the treatment rates and efficacy increases the ICER. Model results were relatively insensitive to other inputs. CONCLUSION: Birth-cohort screening for HCV is likely to provide important health benefits by reducing lifetime cases of advanced liver disease and HCV-related deaths, and is cost-effective at conventional willingness-to-pay thresholds. (HEPATOLOGY 2011.).

Copyright © 2011 American Association for the Study of Liver Diseases.

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Boceprevir: Indication of added benefit for specific patients

December 9, 2011

The active ingredient boceprevir has been available since the middle of 2011 as a treatment for chronic hepatitis C of genotype 1. In an early benefit assessment pursuant to the "Act on the Reform of the Market for Medicinal Products" (AMNOG), the German Institute for Quality and Efficiency in Health Care (IQWiG) has now examined to establish whether boceprevir offers added benefit in comparison with the previous standard therapy.

According to this assessment, the dossier submitted by the pharmaceutical company provides indications of added benefit for patients who have not yet developed liver cirrhosis. However, the extent of this added benefit cannot be classified.

The pharmaceutical company provided no data - or inadequate data - for two other indications - patients with liver cirrhosis and patients for whom prior treatment was totally ineffective (zero response to prior interferon-based therapy) - and therefore added benefit for these patients is not proven.

An addition to previous standard drug therapy

Hepatitis C viruses attack the liver and can trigger inflammation there. If this becomes chronic, cirrhosis can develop and liver function progressively deteriorates. Moreover, the risk of liver cancer (hepatocellular carcinoma, HCC) increases. Boceprevir (trade name Victrelis®, manufacturer MSD Sharp & Dohme) inhibits the reproduction of hepatitis C viruses. Experts assume that if no viruses are detectable in the blood over a sustained period after treatment (sustained virological response, SVR), the risk of secondary disease is reduced.

Boceprevir is administered in addition to the active ingredients peginterferon alfa and ribavirin, which are already on the market. In accordance with the approval status, different patient groups are treated for different periods, as was allowed for in the assessment. The dual combination of peginterferon alfa and ribavirin has been the standard therapy and this was compared with boceprevir given in a triple combination with the former two drugs.

Reduction in secondary diseases: extent cannot be classified.

For the two indications of pretreated (treatment-experienced) and non-pretreated (treatment-naive) patients without cirrhosis, data from one approval study each (SPRINT-2 and RESPOND-2) were available. With the available studies, it is not possible to assess directly whether the new active ingredient influences secondary diseases, such as the development of liver cancer. This is partly because the studies have not lasted long enough for these patient-relevant outcomes to be recorded.

With respect to SVR, there was a clear advantage for boceprevir, both for pretreated patients and for non-pretreated patients without liver cirrhosis. However, SVR is not itself a patient-relevant outcome and cannot be equated with "cure", and there are no studies in which SVR is validated as a surrogate outcome in accordance with the usual criteria employed by IQWiG. Nevertheless, the Institute accepts SVR in the context of the assessment as a surrogate for the reduced incidence of liver cancer. This is because it is currently accepted that patients with no detectable hepatitis C virus in the blood are at lower risk of liver cancer. However, it is unclear how many cases of liver cancer can in fact be prevented by boceprevir.

For the outcome "secondary diseases", IQWiG recognizes an "indication" of a benefit for boceprevir. The requirements for a "proof" are not fulfilled, one reason being that the data are only derived from a single study each, with a comparatively small number of patients. Moreover, the scientific data do not permit a conclusive assessment of the number of patients in whom liver cancer is actually prevented. It is therefore unclear whether the added benefit is "minor", "considerable" or "major". For such a case, the corresponding legal ordinance specifies the assessment category of "unquantifiable".

Indication of greater harm for patients without prior treatment

The indication of greater benefit is in contrast to the indication of greater harm, but only in previously untreated patients. In these patients, boceprevir more often led to anaemia, although this was rarely serious. IQWiG classified the extent of this greater harm as "considerable". In contrast, in patients with prior treatment, anaemia was no more frequent than with standard treatment.

Effect on mortality unclear

IQWiG established that the approval studies contained inadequate data on quality of life for patients with or without prior treatment. There were no statistically significant differences in mortality between the treatment groups. It thus remains unclear if and how boceprevir influences mortality.

Provided by Institute for Quality and Efficiency in Health Care

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Taxes Could Fill AIDS Funding Crunch: U.N.

By Aaron Maasho

ADDIS ABABA (Reuters) Dec 07 - The fight against AIDS risks being set back years by a global financial crisis, the head of the United Nations campaign against the disease warned Wednesday.

Incidence rates of HIV infection have been falling and access to treatment is expanding. However, a decline in donor contributions has caused a funding crisis for the Global Fund to Fight AIDS, Tuberculosis and Malaria, the largest body for HIV funding, and is dampening optimism about an eventual end to the disease, UNAIDS director Michel Sidibe told Reuters in an interview.

"It is not the time to stop, to reverse all this achievement. The financial crisis is there ... but when we have a financial crisis we need to be innovative," Sidibe said.

Annual funding for HIV/AIDS programs fell to $15 billion in 2010 from $15.9 billion in 2009, well below the $22-24 billion the U.N. agency says is needed annually by 2015 to pay for a comprehensive, effective global response.

Speaking on the sidelines of an international AIDS conference in the Ethiopian capital, Addis Ababa, Sidibe said donors could raise funds through taxes.

"If we have a global financial transaction tax, say of 0.5%, we will have $226 billion. Ten percent of that resource is enough for financing the fight against HIV/AIDS, stopping the epidemic, because we can reduce by 96% the number of new infections by putting people early on treatment," Sidibe said.

"We can have taxation on cigarettes and alcohol. We can find different ways to mobilize new resources."

With many large international donor countries struggling with looming recession and debt crises, public health experts say it is crucial for countries affected by HIV/AIDS to increase their own funding, especially developing countries.

"Sustainability and particularly reducing dependency, making sure that African leaders are taking responsibility to initiate a new discussion around treatment and (the) AIDS financing crisis in Africa, those for me will be the most important messages to come out from Addis Ababa," Sidibe said.

The Global Fund is already cutting new grants for countries battling HIV. The public-private fund contributes about 70% of the money spent on life-saving antiretroviral drugs in developing nations.

Former President George W. Bush, whose President's Emergency Plan for AIDS Relief (PEPFAR) program committed $15 billion dollars for a five-year period in 2003, urged Americans to contribute despite their own economic woes.

"It's essential our country not retreat from the world, it's essential that we continue to show our compassion by funding programs that work," Bush told reporters ahead of the meeting, which opened Sunday.

The U.S. government provided the Global Fund with its founding contribution and has been its largest single donor since its inception in 2001.

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GEN News Highlights: Nov 28, 2011

Blocking activity of the 5-HT2B serotonin receptor on fibrogenic hepatic stellate cells (HSCs) in the liver may provide a new approach to boosting liver regeneration in injury and disease, scientists suggest. They report on research demonstrating that scar-causing hepatic stellate cells (HSCs) in the liver are negative regulators of hepatocyte regeneration, and that this negative regulatory activity requires stimulation of the 5-hydroxytryptamine 2B receptor (5-HT2B) on HSCs by serotonin.

The studies, which were led by the Newcastle University’s Institute of Cellular Medicine, showed that selective antagonism of 5-HT2B on HSCs enhanced hepatocyte growth in rodent models of acute and chronic liver injury. Similar effects were also seen in mice lacking 5-HT2B. The findings are reported in Nature Medicine in a paper titled “Stimulating healthy tissue regeneration by targeting the 5-HT2B receptor in chronic liver disease.”

Liver disease is characterized by reduced hepatocyte regeneration, which is accompanied by fibrogenesis and the development of liver cirrhosis and cancer, the authors explain. Unfortunately, the complexity of pathways that regulate hepatocyte proliferation, including the contribution of fibrogenic HSCs, is not well understood.

What has been shown, however, is that in the diseased liver HSCs transdifferentiate into activated myofibroblasts that drive fibrogenesis and secrete soluble factors such as hepatocyte growth factor, TGF-β1, and interleukin-6 (IL-6), which might impact on hepatocyte proliferation.

To investigate the role of HSCs in hepatocyte regeneration the team first evaluated the effects of triggering selective apoptosis-mediated depletion of HSCs on hepatocyte proliferation in bile duct-ligated (BDL) mice, a well-established rodent model of extrahepatic cholestasis. To effect selective apoptosis, HSCs were targeted using a single-chain antibody, C1-3, conjugated to gliotoxin. This mycotoxin is specific to synaptophysin, an antigen expressed on myofibroblasts positive for α-smooth muscle actin (α-SMA+ myofibroblasts), which are specifically derived from the transdifferentation of HSCs.

Treatment of BDL mice using C1–3 gliotoxin resulted in marked but not complete, deletion of hepatic α-SMA+ cells in mice ( α-SMA+ myofibroblasts derived from other cell types weren’t affected) and the stimulation of hepatocyte proliferation. Importantly, there was no accompanying change in the expression of the hedgehog target gene Gli2, which indicated that stimulation of hepatocyte growth after HSC depletion wasn’t due to activation of the hedgehog pathway, the authors note.

The team’s previous work had identified functional 5-HT2B serotonin receptors on activated HSCs in liver disease. Hence, they next looked at whether paracrine signaling between HSCs and hepatocytes might explain the antiregenerative properties of HSCs. To investigate the influence of 5-HT2B on hepatocyte regeneration during liver injury the researchers used a drug called SB-204741, which is a highly specific 5-HT2B antagonist but has negligible effects on the 5-HT2A and 5-HT2C receptor subtypes.

Studies in the experimental mice showed that administration of SB-204741 stimulated hepatocyte proliferation in progressive BDL-induced liver injury and in liver damage induced by acute carbon tetrachloride (CCl4) administration. These results indicated a specific antiregenerative role for 5-HT2B signal, a notion supported by studies in 5-HT2B knockout mice (Htr2b-/-).

Partial hepatectomy (PHX) in these knockout animals led to elevated hepatocyte proliferation. Levels of IL-6 and TNF-α, which are primers of hepatocyte regeneration and expressed transiently shortly after surgery, were modestly increased in 5-HT2B knockout mice at four hours of PHX. Crucially, though, the production of TGF-β1, which is induced in the end stage of liver regeneration and acts to repress hepatocyte proliferation, was evident in the livers of wild-type mice at 36 hours after PHX but not in the livers of 5-HT2B knockout animals.

Interestingly, the investigators report, the liver-to-bodyweight ratios of wild-type mice treated using SB-204741 increased after PHX, indicating that selective antagonism of 5-HT2B results in sustained stimulation of liver regeneration.

5-HT2B is expressed on HSCs in diseased liver but at lower levels on cholangiocytes and Kupffer cells, the researchers continue. Studies indicated that 5-HT2B was induced in HSCs after PHX, but its expression was reduced in hepatocytes. Treatment with C1-3-gliotoxin increased hepatocyte proliferation after PHX, and this was associated with reduced hepatic expression of TGF-β1.

Thus far, it appeared that HSC depletion and 5-HT2B antagonism had similar effects on hepatocyte proliferation in models of liver damage, but what wasn’t known was whether they acted through independent mechanisms. If so, then additive effects should be observed when combining HSC depletion with 5-HT2B antagonism. However, while the combination of HSC depletion and SB-204741 treatment in CCl4-injured mice enhanced hepatocyte proliferation and inhibited TGF-β1 expression, there were no additive effects.

The investigators next designed chromatin immunoprecipitation studies to identify the intracellular signaling pathways through which serotonin and 5-HT2B exert their antiregenerative effects. They found that either antagonism of 5-HT2B or treatment using the ERK inhibitor PD98059 suppressed serotonin-induced recruitment of JunD, which is one half of the heterodimer making up the AP-1 transcription factor that controls transcription of TGFβ1. Likewise serotonin-induced phosphorylation of JunD was also suppressed on administration of PD98059 or SB-204741.

“On the basis of these data, we propose that phosphorylation and activation of JunD by ERK mediates the stimulation of TGF-β1 transcription by serotonin and 5-HT2B in HSCs,” the authors conclude. “If this pathway operates in the context of the injured liver, then JunD would be predicted to function as a transcriptional repressor of hepatocyte proliferation.”

In confirmation of this, the team found that compared with wild-type mice, JunD-knockout mice recovering from CCl4 injury demonstrated higher numbers of mitotic hepatocytes, which was associated with reduced TGF-β1 expression.

The researchers finally moved on to evaluate whether 5-HT2B antagonism would have an antifibrogenic effect in mouse models of progressive liver disease in which both fibrogenesis and regeneration result in remodeling of the hepatic architecture. Experimental animals were given CCl4 injections over three weeks to establish fibrotic disease, and then CCl4 treatment was continued either with or without treatment with SB-204741.

“Treatment with SB-204741 significantly reduced the number of hepatic α-SMA+ fibrogenic cells, fibrotic matrix, hepatic expression of TGF-β1, and expression of the fibrogenic genes encoding TIMP-1 and pro-collagen I, confirming an antifibrogenic effect at the molecular level,” they write.

Moreover, SB-20741 administration was linked with a higher rate of cellular apoptosis in the fibrotic matrix. Administration of SB-20471 in the model of progressive BDL-induced liver disease also resulted in a protective antifibrotic effect as well as improvements in liver function.

The overall results demonstrate that the negative regulation of hepatocyte regeneration by HSCs in the liver requires stimulation of the 5-HT2B receptor on HSCs by serotonin, which activates expression of TGF-β1 through signaling by ERK1 and the transcription factor JunD, the authors conclude.

“5-HT2B is selectively expressed by activated human HSCs and the signaling pathway we describe here is conserved in human HSCs. Potent and selective antagonists of 5-HT2B are already available and have been reported as being safe for clinical use in humans. This class of drug may therefore have therapeutic potential in liver disease, both as stimulants of hepatocyte regeneration and as anti-fibrotic agents.”

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From Morbidity & Mortality Weekly Report

Massachusetts, 2010

Daniel Church, MPH; Kerri Barton, MPH; Franny Elson, MS; Alfred DeMaria, MD; Kevin Cranston, MDiv; Norma Harris, PhD; Stephen Liu, MPH; Dale Hu, MD; Deborah Holtzman, PhD; Scott Holmberg,

Posted: 12/08/2011; Morbidity & Mortality Weekly Report. 2011;60(42):1457-1458. © 2011 Centers for Disease Control and Prevention (CDC)MD; Rania A. Tohme, MD

Abstract and Introduction

Introduction

During 2002–2009, rates of newly diagnosed hepatitis C virus (HCV) infection increased from 65 to 113 cases per 100,000 population among persons aged 15–24 years in Massachusetts.[1] Accordingly, the Massachusetts Department of Public Health (MDPH) and CDC interviewed persons aged 18–24 years with HCV infection reported to MDPH during July 1–December 31, 2010, to elicit detailed information regarding demographic, clinical, and risk characteristics.

Of the 394 patients indentified, 193 (49%) had a valid telephone number; of those 193 patients, 101 (52%) did not answer after three call attempts, 19 (10%) were either in a drug treatment facility or incarcerated, 19 (10%) refused to participate, 31 (16%) agreed to participate but did not come on the scheduled interview day, and 23 (12%) completed the interview. An additional five persons aged 18–24 years with diagnosed HCV infection during July 1– December 31, 2010, but not reported to MDPH, were interviewed in a correctional facility, where they were incarcerated.

Mean age of the 28 respondents was 21.9 years (range: 19–24 years); 15 (54%) patients were female, 23 (82%) were white, nine (32%) did not finish high school, nine (32%) were unemployed, and 25 (89%) had health insurance. Twenty-six (93%) had used drugs; of these, 100% reported marijuana use, with a median age of initiation of 13 years (range: 9–17 years); 92% reported opioid analgesic abuse (oxycodone and/or Oxycontin), with a median age of initiation of 17 years (range: 12–23 years); and 89% reported heroin use, with a median age of initiation of 18 years (range: 14–21 years). Nearly all respondents (95%) used opioid analgesics before switching to heroin. During the preceding 6 months, the most frequently injected drugs among respondents were heroin (50%) and opioid analgesics (30%).

Medical record reviews showed that five respondents had visited emergency departments on multiple occasions complaining of pain and were prescribed opioid analgesics. Most respondents (70%) reported sharing syringes and drug paraphernalia within networks of injection drug users that included persons with known HCV infection (43%). One in four respondents reported never being informed of their HCV infection by their health-care provider, and 11 (39%) were tested for HCV in a drug treatment program or during incarceration.

The findings in this report are subject to at least three limitations. First, only a small number of persons agreed to be interviewed, which limits the ability to generalize these findings. The low response rate might be attributed, in part, to the characteristics of the targeted population (young injection drug users) coupled with lack of provision of incentives. Second, comparison of the demographic and clinical characteristics of persons who were interviewed with those who could not be interviewed was not possible because information was lacking for nearly 60% of the 394 hepatitis C cases reported during July 1–December 31, 2010. However, of those cases with available information, 229 (58%) occurred among females and approximately 80% occurred among whites, which is consistent with the demographic characteristics of interviewed respondents. Finally, persons with HCV infection who were in drug rehabilitation centers could not be interviewed because of federal confidentiality regulations specific to these centers.

Consistent with other studies, most respondents reported opioid analgesics abuse before switching to heroin (which is less expensive).[2,3] Health-care providers should routinely ask about prescription and illicit drug use and screen all persons with risk factors for HCV infection, regardless of age.[4] They also need to be aware of warning signs of prescription opioid and drug abuse, such as frequent complaints of pain and request for opioids. Drug treatment programs and prisons are potential venues for education regarding the risk for hepatitis C from sharing needles and other injection paraphernalia and for providing vaccination against hepatitis A and B. School and community-based education programs also are needed to prevent initiation of illicit and prescription drug use.[5] Several harm reduction interventions have been conducted to assess the effectiveness of reducing incidence of both human immunodeficiency virus and HCV infection. Overall results from a recent meta-analysis did not indicate a statistically significant decrease in incident HCV infection from a single programmatic strategy; however, the results did indicate that combined interventions were effective.[6] Thus, combining current interventions and identifying new evidence-based approaches to preventing drug use and unsafe injection practices in young adults are needed to control and prevent HCV infections.

References

  1. CDC. Hepatitis C virus infection among adolescents and young adults—Massachusetts, 2002—2009. MMWR 2011;60:537–41.
  2. Lankenau SE, Teti M, Silva K, Bloom JJ, Harocopos A, Treese M. Initiation into prescription opioid misuse amongst young injection drug users. Int J Drug Policy 2011; June 19 [Epub ahead of print].
  3. Grau LE, Dasgupta N, Harvey AP, et al. Illicit use of opioids: is OxyContin a "gateway drug"? Am J Addict 2007;16:166–73
  4. CDC. Recommendations for prevention and control of hepatitis C virus (HCV) infection and HCV-related chronic disease. MMWR 1998;47(No. RR-19).
  5. National Institute on Drug Abuse. Preventing drug use among children and adolescents: a research-based guide for parents, educators, and community leaders. Bethesda, MD: US Department of Health and Human Services, National Institutes of Health; 2003. Available at http://www.drugabuse.gov/prevention/index.html. Accessed October 25, 2011.
  6. Hagan H, Pouget ER, Des Jarlais DC. A systematic review and meta-analysis of interventions to prevent hepatitis C virus infection in people who inject drugs. J Infect Dis 2011;204:74–83.

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Friday, December 09, 2011 by Angela Kean

Resonance Health (ASX: RHT) is moving to protect the intellectual property associated with its diagnostic test for the assessment of fatty liver, HepaFat Scan, through the lodgement of a Provisional Patent Application.

The company has also registered the HepaFat Scan trademark and, importantly, begun discussions with interested parties on its potential use and licence.

Results of a clinical study conducted earlier in the year demonstrate that the MRI-based diagnostic product can accurately assess the severity of fatty liver disease, replacing the need for an invasive liver biopsy.

According to Resonance, nearly one in three Americans have fatty liver, and non-alcoholic fatty liver disease is the most common liver disease in the U.S. and Europe.

An accurate diagnosis of early stage fatty liver disease provides a better outcome for patients, to address the condition before the onset of liver damage.

Meanwhile, Resonance has also recorded substantial growth in the sales volumes of its non-invasive, MRI-based service for the measurement of liver iron overload, FerriScan, in the 2012 financial year.

From July to November 2011 there has been a 30% month-on-month increase in the numbers of FerriScans sold, compared to the same period in 2010.

Resonance announced earlier this week it has expanded the distribution of FerriScan into the Middle East with the appointment of Gulf Drug Establishment as a distributor.

Gulf Drug Establishment will distribute the FerriScan service in the United Arab Emirates, Saudi Arabia and Egypt where there is a high number of patients with iron overload caused by regular blood transfusions to treat an underlying condition.

FerriScan is currently available through over 120 centres in more than 20 countries. Resonance witnessed strong growth in new FerriScan users in Brazil, Japan, Italy and China in 2010-11.

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AHF Targets Merck Over AIDS Drug Pricing

Dec. 8, 2011, 3:10 p.m. EST

AIDS group launches advocacy campaign pressuring the drug giant to heed President Obama's call for drug companies to "do their part" to help Americans get access to life-saving AIDS treatments

LOS ANGELES, Dec 08, 2011 (BUSINESS WIRE) -- As part of its ongoing campaign to lower AIDS drug prices and increase access, AIDS Healthcare Foundation (AHF) today announced that it is launching a new advocacy campaign calling for the drug company Merck to lower its prices for cash-strapped AIDS Drug Assistance Programs (ADAPs). ADAPs, a network of federal and state funded programs that provide life-saving HIV treatments to low income, uninsured, and underinsured individuals living with HIV/AIDS nationwide, are facing a severe financial crisis that has left as many as 10,000 people with AIDS without access to treatment.

The campaign comes days after Gilead Sciences, Inc., the largest manufacturer of AIDS drugs in the U.S., announced it has agreed to provide additional discounts to the programs. Gilead is the second company, following Boehringer Ingelheim, to agree to additional discounts for ADAPs.

On December 1st -- World AIDS Day -- President Obama proclaimed the need for all stakeholders to do more to help the struggling ADAP programs, saying: "The federal government can't do this alone, so I'm also calling on state governments, and pharmaceutical companies, and private foundations to do their part to help Americans get access to all the life-saving treatments."

"We want to state loud and clear that Merck's refusal to lower its prices for ADAPs is a death sentence for people with AIDS," said Michael Weinstein, AIDS Healthcare Foundation President. "Our campaign will feature a series of actions near Merck headquarters in New Jersey, including print and television advertisements, protests at Merck's main campus, direct mail, and contact with Merck investors," said Weinstein. Weinstein added: "At a cost to ADAPs of roughly $8,000-$9,000 per person per year, Merck's Isentress is one the highest priced AIDS drugs in the US today. Merck employees and the public should know about the company's shameful pricing and policies on AIDS."

"Gilead and other companies have agreed to provide additional discounts to ADAPs, and the President has asked the companies to do more to help these programs. There's no reason for Merck to refuse other than greed," said Tom Myers, Chief of Public Affairs for AIDS Healthcare Foundation.

The first ad in AHF's campaign will be a "Merck: Breaking the Bank" direct mail postcard sent to the communities surrounding Merck's headquarters in Whitehouse Station, NJ. The postcard highlights that Merck has made billions of dollars on AIDS drugs, lending to a nearly $100 billion market capitalization for the company, yet it refuses to lower prices for the publicly funded ADAPs.

As part of its strategy to raise the pricing issues with Merck investors, in October AHF testified before the board of CalPERS (California Public Employees Retirement System) about the pricing policies of Merck and other drug companies. At that meeting the CalPERS board agreed to contact Merck and others about their pricing policies in light of the financial difficulties experienced by ADAPs. The CalPERS action followed the move by California State Treasurer Bill Lockyer, and state Treasurer John Chiang, to write to Merck and other companies and urge them to provide additional discounts to ADAPs.

AIDS Healthcare Foundation (AHF), the largest global AIDS organization, currently provides medical care and services to more than 124,000 individuals in 23 countries worldwide in the US, Africa, Latin America/Caribbean the Asia/Pacific region and Eastern Europe. www.aidshealth.org

SOURCE: AIDS Healthcare Foundation

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