Risk Of Developing Liver Cancer After HCV Treatment

Monday, October 11, 2010

Fatty Liver Disease, Genotype 3, Vitamin E and HCV

Fatty Liver Disease, Genotype 3, Vitamin E and HCV
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Fatty Liver disease in HCV has been proven to be caused directly from the virus. Genotype 3 patients are known to have a higher rate of fatty liver then other genotypes. Previously both genotype 2 and 3 were treated with the same treatment duration with the assumption both were the easier genotype to treat. Currently the data has shown that genotype 3 patients have a higher incidence of fatty liver and possibly the two genotypes may require different treatment protocols.
Treating with telaprevir alone (as shown below in this post) or monotherapy was not as potent against genotype 3 as it is in genotype 2. However, treating with Telaprevir showed the best results in combined therapy with interferon and ribavirin Only time will tell how genotype 3 will fair with the new drugs coming down the pipeline, and both boceprevir and telaprevir should soon be FDA approved.
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However until all the data is in there are other drugs making their way through clinical trials .
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RG7128 in phase one.
RG7128 in April of this year was presented at the "45th Annual Meeting of the European Association for the Study of the Liver (EASL)" in Vienna, Austria.
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The Link
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The Study
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LB10. Antiviral Activity Of The HCV Nucleoside Polymerase Inhibitor R7128 In HCV Genotype 2 And 3 Prior Non-Responders: Interim Results Of R7128 1500mg BID With PEG-IFN And Ribavirin For 28 Days.
E. J. Gane; M. Rodriguez-Torres; D. R. Nelson; I. M. Jacobson; J. G. McHutchison; L. Jeffers; A. Beard; S. Walker; N. Shulman; W. Symonds; E. Albanis; M. M. Berrey

Background:
Historically, HCV genotype (GT) 2 and 3 prior non-responders have demonstrated poor response rates to re-treatment with PEG-IFN/RBV (SOC).
No direct-acting antiviral agent in development has shown significant activity in individuals infected with HCV GT 2/3.
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R7128 is a potent nucleoside analog inhibitor of HCV polymerase, with activity against HCV GT 2/3 in vitro. When administered at doses of 1000-1500mg BID in combination with SOC for 28 days in treatment-naïve, HCV+ GT 1 patients, R7128 delivered an 85-88% rapid virologic response (RVR).
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This study was designed to evaluate R7128 with 180µg PEG-IFN and 1000-1200mg RBV for 28 days in patients with HCV GT 2 or 3.

Methods:
25 patients (20 active/5 placebo) with genotype 2 (n=10) or genotype 3 (n=15) who had not previously achieved a sustained virologic response (SVR) with interferon-based therapy were enrolled.
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Patients received R7128 1500mg BID or placebo along with PEG-IFN/RBV for 28 days, followed by PEG-IFN/RBV alone for a minimum of 20 weeks. All patients were non-cirrhotic and all had been previously treated with at least 12 weeks of interferon-based therapy.
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Results:
Antiviral Activity
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· 90% RVR was demonstrated in this cohort of treatment failure HCV GT 2 or 3 patients with R7128 + SOC .
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· Prior treatment response had no impact upon R7128 + SOC response, RVR was 60% in SOC prior relaspers
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· The antiviral activity observed with R7128 + SOC was maintained across genotype 2 and 3; and consistent with in vitro data
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· Compared to prior therapy, the addition of R7128 resulted in a more rapid decline in plasma HCV RNA, based upon those subjects with available prior treatment histories
· HCV RNA values in the SOC alone group declined with a -3.7 log 10 change from baseline compared to -5.0 in the R7128 cohort
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Summary
· A mean 5.0 log 10 decline in plasma HCV RNA was demonstrated following 28 days of combination therapy with R7128 + SOC in HCV genotype 2 or 3 infected subjects
· Compared to prior treatment responses, R7128 provided additional antiviral activity in these subjects
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· R7128 was generally well-tolerated and demonstrated no evidence of acute target organ toxicity
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· Serum ALT levels normalized during R7128 therapy in 54% of subjects with elevated ALT at baseline
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· Pharmacokinetic data demonstrate that the ‘new’ formulation results in slightly higher plasma exposures compared to the previous formulation.
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Conclusions
· R7128 has provided positive proof-of-concept that a direct acting antiviral can deliver additional antiviral potency in an HCV genotype 2 or 3 treatment failure population with an RVR of 90%. Longer term data is needed to determine adequate length of treatment in this population.
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· As predicted by in vitro data, R7128 demonstrated similar potency against HCV genotype 2 or 3 compared to a previous study of R7128 again genotype 1 HCV
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· The absence of virologic breakthrough reinforces the implications from monotherapy studies that nucleo0side polymerase inhibitors have a high genetic barrier to resistance
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· The safety and efficacy of this combination study support further development of R7128 in combination with the standard of care (pegylated interferon and ribavirin) in this difficult to rreat, HCV genotype 2/3 non-responder population and provides appropriate potency and safety to progress to Phase 2b studies to explore optimal treatment duration in HCV genotype 2 or 3 treatment-naive patients.
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Clinical Phase Phase I RG7128
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lDrug Name RG7128 (Polymerase Inhibitor)
Drug Category RG7227 (ITMN-191) (Danoprevir) Protease Inhibitor
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Comments: AASLD 2009:
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Comments: AASLD 2009: Results from 13 days of treatment with RG7128 & RG7227: 63% (5 out of 8) genotype 1 treatment-naive patients were HCV RNA negative (less then 15 IU/mL) and 25% (2 out of 8) of null responders were HCV RNA negative (less then 15 IU/mL). The drugs were well-tolerated; no treatment discontinuations due to side effects.
Special Presentation
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On November 17 2009, InterMune announced that an independent data monitoring committee recommended the company stop testing the therapy in the RG7227 900 milligram dosage given once every 12 hours after three patients had elevated levels of ALT, a liver enzyme.
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EASL 2010: A small study using ritonavir (100 mg) to boost danoprevir (200 mg) both given twice a day achieved 100% undetectable HCV RNA after 15 days and was generally well-tolerated. Based on these findings an additional two study arms of prior complete non-responders will be retreated with danoprevir, ritronavir, PEG/RBV for 12 weeks. A larger study titled INFORM-3 is being planned that will include ritonavir.
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Since then Roche has bought full rights to the drug and other drugs from Intermune.
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Roche buys full rights to danoprevir from InterMune
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Agreement reinforces Roche’s leadership in the fight against hepatitis C
"The latest news is that Danoprevir is a second generation protease inhibitor for hepatitis C that has shown promising efficacy in pre-clinical and early clinical development. Following co-development between Roche and InterMune since 2006, Roche now assumes sole ownership of danoprevir. This results in increased flexibility to develop and market its portfolio of drugs against hepatitis C, which also includes Pegasys (40 kDa pegylated interferon alfa 2a, the current standard of care) and RG7128, a nucleosidic polymerase inhibitor which has shown a promising resistance profile."
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Information/links related to geno 3 treatment and fatty liver disease.
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Also the study on Vitamin E and fatty liver disease.
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Steatosis is a condition characterised by the build up of fat within the liver, sometimes triggering inflammation of the liver. It is also known as fatty liver. It is only recently that the significance and relationship of steatosis to HCV has begun to be understood.
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There are two different forms of steatosis (Fatty Liver) that may be found in people with HCV: Metabolic steatosis and HCV-induced steatosis
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Metabolic steatosis can result from obesity, raised blood fat levels (hyperlipidemia), insulin resistance and type II diabetes and is similar to the type of fatty infiltration caused by excessive alcohol consumption and that is also found in Non-Alcoholic Fatty Liver (NASH).
Metabolic steatosis is not triggered by the hepatitis C virus; however the combination of this form of steatosis and the presence of HCV can lead to a more rapid progression of scarring or fibrosis.
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HCV-induced steatosis is fatty infiltration that is directly caused by the presence of the virus. It is possible for people with HCV to have both forms of steatosis simultaneously.
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Genotypes and Fatty Liver Disease:
Although it seems that all genotypes can trigger steatosis, the risk of developing steatosis is significantly higher for people with genotype 3. There is a complex reaction between the genotype 3 virus and liver cells that is not seen in other genotypes that makes this group at much higher risk of developing the condition. Around 40% of people with hepatitis C have steatosis, compared to about 14% to 31% of the general population. However, 60% - 80% of people with genotype 3 have moderate or severe steatosis.
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Hepatitis C virus genotypes 2 and 3 are both responsive to antiviral treatment, they have been regarded as similar. However, recent evidence has shown there may be differences between these two genotypes with regard to their clinical features and possibly responses to combined interferon and ribavirin therapy.
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As demonstrated in recent studies considering rapid virologic response (RVR) as a criterion for shortening treatment from the standard 24 weeks to 12 or 16 weeks in patients with genotype 2 or 3, the reason for lower response in genotype 3 versus genotype 2 patients may be a lower response rate in patients without an RVR. As a consequence, treatment longer than the currently recommended 24 weeks may be required for patients with genotype 3 but not for those with genotype 2 in the absence of an RVR. Whether this lower sensitivity to treatment in a subgroup of patients with genotype 3 may be attributed to viral heterogeneity or other associated cofactors is not yet known
Genotype 3 patients, SVR rates were lower overall :
G3 telaprevir alone: SVR 50%;
G3 telaprevir/pegylated interferon/ribavirin: SVR 67%;
G3 pegylated interferon/ribavirin: SVR 44%.
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Therapy response to interferon-based regimen in patients with HCV genotype 3 infection is negatively affected by increasing age, suggesting that elderly patients (> 50 years old) with genotype 3 infection may need longer duration of therapy."
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Steatosis and HCV treatment
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There is increasing evidence that steatosis can reduce the effects of treatment.
Some retrospective studies have shown that people with steatosis were less likely to achieve a sustained virologic response (SVR) even when taking into account other factors that might induce steatosis.
One study found that sustained virologic response rates were 18-32% lower in people with steatosis compared to people without steatosis after adjusting for other co-factors that affect treatment such as genotype, fibrosis score, and viral load level. /
Diet and Excercise: A recent study found that HCV patients who participated in a diet and exercise program for three months lowered their grade of steatosis and, remarkably, their fibrosis score.
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The Study
In this study we show that, besides alcohol consumption, an unbalanced diet is an important factor of hepatitis C evolution and nonresponse to antiviral treatment. Specific nutritional education and severe alcohol restrictions might, synergistically, improve the response to antiviral therapy
Symptoms
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Many people with steatosis experience no symptoms.
Symptoms that people do experience are non-specific and liver enzymes levels are not necessarily raised. As with fibrosis, the definitive way to diagnose steatosis is a liver biopsy.
Vitamin E appears to be more effective in treating obesity-associated chronic liver disease than a prescription drug, U.S. researchers found.......
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Vitamin E, diabetes drug may reverse fatty liver disease
In a notable research, scientists claim to have found that vitamin E pills may help treat chronic liver disease.
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Vitamin E, diabetes drug may reverse fatty liver disease
In a notable research, scientists claim to have found that vitamin E pills may help treat chronic liver disease.'
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The research conducted by Virginia Commonwealth University (VCU), U.S., and funded by National Institutes of Health and Takeda Pharmaceutical revealed that vitamin E tablets could reverse nonalcoholic fatty liver disease --steatohepatitis.
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Project scientist, Patricia Robuck, National Institute of Diabetes and Digestive and Kidney Diseases was quoted by Los Angeles Times as saying, “This is an important landmark in the search for effective treatmentsfor (the disease).”
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How Many People In The Study
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247
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How Long Was The Study ?
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A 96-week study including 247 adults in their mid-40s, suffering from steatohepatitis (Fatty Liver)
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None of them were diabetics or excessive drinkers, but all were obese.
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Assigned To Three Groups For Two Years
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For the study, the subjects were randomly assigned three varied treatments for two years wherein they were given certain amount of medication on a daily basis.
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The First Group
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The first group was given 800 International Units (IU) of vitamin E
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The Second Group
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The second group was given 30 milligrams of the diabetes drug pioglitazone(an insulin-sensitizer)'
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Third Group
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The third group was administered a *placebo treatment instead of medication. (*Placebo dummy medication
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All Had A Liver Biopsy After Treatment
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All the subjects underwent a liver biopsy at the commencement and finishing of the trial such that the researchers could arrive at comparative results. .
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The Big Reveal
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First Group; Results of liver tissue characteristics during liver biopsies revealed that 43 percent of the vitamin E group had improved significantly.
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Second Group; 34 percent of the group given the diabetes drug pioglitazone showed improvements
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Third Group; 19 percent improvement was shown of those given placebo treatment.'
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Furthermore, the biopsy data revealed that vitamin E considerably reduced liver inflammation, fat accumulation and presence of dying ‘ballooning cells’ that appear in fatty liver tissue.
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The Second Group (diabetes drug pioglitazone) was found to improve insulin signaling, which helps diabetics metabolize sugar. However, it could also diminish the amount of fat in the liver, the researchers added.
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“This confirms a long-term benefit for pioglitazone and gives an alternative option in the form of vitamin E,” Kenneth Cusi, endocrinologist, University of Texas Health Science Center was quoted in ScienceNews as saying.
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Robuck cautioned that vitamin E should only be taken under a doctor’s supervision. He was cited in Business Week as saying, “The trial included only a relatively healthy population with no diabetes and no cardiovascular disease.
For those people, it can be an important treatment.”Arun Sanyal, MD, VCU stressed on further research and told ScienceNews, “It’s too early to recommend (vitamin E) as a panacea for fatty liver disease.”

The study appears in New England Journal of Medicine.

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