Deadly liver cancer on the rise, but half of cases preventable: Cancer Society

Video - Liver cancer risks
Liver cancer is one of the fastest rising cancers in Canada, but the need to educate about prevention isn't getting much attention. Kelly Crowe explains why.

TORONTO — Ground is being gained on many fronts in the war against cancer, but one of the deadliest — liver cancer — is still on the rise, the Canadian Cancer Society said Wednesday.

About half of liver cancer cases in Canada are probably preventable, the research and advocacy organization said as it released its annual estimates of the toll cancers will exact in Canada in 2013.

Overall, the society estimates 187,600 people will learn they have a new cancer this year (excluding non-melanoma skin cancers) and 75,500 Canadians will die from some form of the disease.

The big four remain breast cancer, prostate cancer, colorectal cancer and lung cancer, but rates of these diseases are either stable or declining, says Prithwish De, a cancer epidemiologist with the cancer society.

But the same is not true for liver cancer, which currently claims the lives of four out of five people diagnosed with it. Since 1970, the incidence of liver cancer has tripled in Canadian men and doubled in women.

Primary liver cancer — as opposed to cancer that spreads from another site to the liver — is still rare. The society estimates 2,000 people will be diagnosed with it in 2013 and 1,000 people will succumb to the disease. Worldwide, liver cancer is the third leading cause of cancer deaths, after lung and stomach cancer.

The cancer is so deadly because most cases are not found until the disease has progressed beyond the point of cure. When liver cancer is found early it generally responds well to treatment, says Dr. Sean Cleary, a liver surgical oncologist at Toronto’s University Health Network.

“One of the problems with this disease is that it does not develop symptoms or patients aren’t aware that they have the problem until the disease is very advanced, at a very large and untreatable stage,” he said.

Science has made little progress improving the survival chances of people with liver cancer. Over the past 20 years, the survival rate has risen by only between two and three per cent, De says.

But the toll the disease takes could be dramatically lowered if people at high risk of developing the liver cancer took some proactive steps, experts say.

Excess alcohol consumption, obesity and diabetes are known to be risk factors for developing liver cancer. Cutting back on alcohol and taking steps to maintain a healthy weight should lower one’s liver cancer risk, they suggest.

Another way to combat the disease is by addressing two related conditions that can be precursors to liver cancer — hepatitis B and C, which are viral infections of the liver. There is currently a vaccine against hepatitis B, but none for hepatitis C.

People who are at high risk of having one or the other infection should consider talking with their doctors about being tested for hepatitis. Treatment can often clear the infections, the experts say.

“Many individuals who are infected with either acute or chronic hepatitis infections may not be aware that they’re infected. And we’re trying to let Canadians know that there is a way to get tested and find out if you are infected by either hepatitis B or C,” says De.

Last year the U.S. Centers for Disease Control urged all baby boomers to have a one-time test for hepatitis C because of the liver cancer risk. The Canadian Liver Foundation later echoed that advice.

But the Public Health Agency of Canada is studying whether it makes sense to issue a similar recommendation in Canada, where the rate of hepatitis C is lower than in the U.S. While it deliberates, the cancer society is content to wait for evidence-based advice.

“Because we’re lacking that evidence in Canada it’s kind of premature to say whether (across-the-board) screening would be beneficial to that age group,” De says.

“And so, from the Canadian Cancer Society’s perspective, we’d like to wait until there’s a good solid base of evidence before we say anything about screening in specific age cohorts.”

Instead, they recommend a discussion about screening for people who had a blood transfusion before 1990, who use or used intravenous drugs or who moved to Canada from parts of the world where hepatitis B and C are common — Asia and sub-Saharan Africa for hepatitis B, Japan and southern Europe for hepatitis C, Cleary says.

Others at risk are people who’ve had high-risk sexual contacts and received tattoos in non-reputable tattoo parlours, he said.

“Individuals who have those risk factors are definitely candidates for speaking to their doctors about finding out whether testing for hepatitis B or C and whether any other types of counselling would be beneficial for them for reducing their risk of liver cancer,” De says.

http://www.thetelegram.com/News/Local/2013-05-29/article-3264208/Deadly-liver-cancer-on-the-rise,-but-half-of-cases-preventable%3A-Cancer-Society/1

UC Irvine study may point to new treatments for liver diseases

UC Irvine study may point to new treatments for liver diseases

May 22, 2013 – By discovering the new mechanism by which estrogen suppresses lipid synthesis in the liver, UC Irvine endocrinologists have revealed a potential new approach toward treating certain liver diseases.

With this finding, Dr. Ellis Levin and colleagues believe they are changing long-held views in the field. Study results appear in the May 21 issue of the journal Science Signaling.

“The dogma in the steroid receptor field for 50 years has been that only receptors located in the nucleus respond to steroid hormones by regulating genes that produce the developmental, functional and pathological effects of steroid hormones,” said Levin, professor of medicine, biological chemistry and pharmacology, and chief of endocrinology, diabetes and metabolism at UC Irvine and the VA Long Beach Healthcare System.

“In our study, we show that an estrogenic receptor compound acting at the cell membrane-based estrogen receptor alpha in the liver of transgenic and wild type mice suppresses all lipid synthesis. This includes cholesterol, triglycerides and fatty acids.”

Levin said this occurs through AMP kinase signaling, which inhibits the processing of the key transcription factor for many lipid-synthesis pathways genes. This causes the transcription factor to be retained in cytoplasm and prevents lipid synthesis gene expression.

“This action occurs without any participation of the nuclear receptor pool,” he added. “Thus, the membrane ER-alpha can regulate genes that produce a metabolic phenotype entirely unrelated to the nuclear receptor contributing.”

Estrogen plays a role in liver functions, and may be a deterrent to liver cancer, as men get this type of cancer at a rate of four-to-six times more than women and animals models of this cancer show clear suppression by estrogen. The hormone also helps suppress the development of fatty liver, which can lead to liver damage and failure, and inflammatory liver disease that result from chronic hepatitis.
Levin said that he and his colleagues are now testing compounds that target the membrane estrogen receptor in transgenic mice to see the impact for such diseases.

“We’re re-thinking the whole idea of hormone replacement of estrogen by exploring ways to boost estrogen receptor action selectively in a positive way,” he said. “This could include targeting one form of the receptor, or receptors at one location in cells but not all estrogen receptors.”

Last month, Levin was honored with the 2013 Solomon A. Berson Distinguished Researcher Award and Lectureship from the American Physiological Society, Endocrinology Division. The award is in recognition of Levin’s work on estrogen receptors outside the nucleus that mediates important functions of this steroid in breast cancer and the cardiovascular system, and is applicable to many other steroid receptors, including progesterone and androgen receptors in breast and prostate cancer, respectively.

Ali Pedram and Fiona O’Mahony with UC Irvine, Mahnaz Razandi with the VA Long Beach Healthcare System, and  Brian J. Harvey and Harry Harvey with the Royal College of Surgeons in Dublin, Ireland, contributed to the study, which was supported by grants from National Institutes of Health (CA-100366) and the Department of Veterans Affairs Merit Review Program (ERL). O’Mahony, who is also affiliated with the VA Long Beach Healthcare System was co-funded by Marie Curie Actions, the Irish Higher Education Authority Programme for Third Level Institutions Cycle 4, and the Italian National Research Council.

http://www.medicalnewstoday.com/releases/261002.php

Dietary Supplements for Hepatitis C? Not So Fast

Director's Page
Josephine P. Briggs, M.D.

Dietary Supplements for Hepatitis C? Not So Fast
May 16, 2013

An estimated 3.2 million Americans have chronic hepatitis C, a contagious liver disease caused by the hepatitis C virus. What is particularly worrisome about this disease is that most people do not have any symptoms until the virus has caused liver damage, which can take 10 years or more. Conventional medical therapies are available, but still, some people with hepatitis C try complementary health approaches, such as dietary supplements. In fact, we know from the HALT-C study, an NIH-sponsored clinical trial, that 23 percent of the study participants were using herbal products—the most common of which was silymarin (milk thistle).

What we know from current research is that no dietary supplement has been shown to be effective for hepatitis C or its complications. NCCAM’s Web site has information on what the science says about dietary supplements, such as milk thistle, probiotics, zinc, and other supplements, for hepatitis C.

If you or a loved one has hepatitis C, I encourage you to take a look at this information. Get the facts on the research so you can be an informed consumer. And be sure to talk with your health care provider before using any dietary supplement to make certain that it is safe for you and compatible with any medical treatment you are receiving.

Take care, and as always, be well!

5 Things You Should Know About Dietary Supplements for Hepatitis C

Hepatitis C is a liver disease caused by a virus. It is usually chronic (long-lasting), but most people do not have any symptoms until the virus causes liver damage, which can take 10 or more years to happen.  Without medical treatment, chronic hepatitis C can eventually cause liver cancer or liver failure. Conventional medical treatments are available for chronic hepatitis C. Some people with hepatitis C also try complementary health approaches, especially dietary supplements.

If you are considering any dietary supplement for hepatitis C, here are some things you should know.
 

1.  No dietary supplement has been shown to be effective for hepatitis C or its complications.
     
2.  The results of research supported by the National Institutes of Health have shown that silymarin, the active extract of milk thistle and the most popular complementary health product taken by people with liver disease, was no more effective than placebo in people with hepatitis C.
     
3.  Research on other dietary supplements for hepatitis C, such as zinc, licorice root (or its extract glycyrrhizin), SAMe, and lactoferrin, is in its early stages, and no firm conclusions can be reached about the potential effectiveness of these supplements.
     
4.  Colloidal silver is sometimes promoted for treating hepatitis C, but is not safe. Colloidal silver can cause irreversible side effects, including a permanent bluish discoloration of the skin.
     
5.  Check with your health care provider before using any dietary supplement to make sure that it is safe for you and compatible with any medical treatment that you are receiving for hepatitis C or any other health problem.

  http://nccam.nih.gov/about/offices/od/hepatitisC?nav=rss

Consumption of Coffee Associated With Reduced Risk of Liver Cancer - A Meta-Analysis

Consumption of Coffee Associated With Reduced Risk of Liver Cancer
  

What does the latest scientific evidence say about the connection between coffee consumption and liver cancer? Does it offer protective benefits?

 

May 23, 2013  

 

BMC Gastroenterology


Consumption of Coffee Associated With Reduced Risk of Liver Cancer - A Meta-Analysis

Li-Xuan Sang, Bing Chang, Xiao-Hang Li, Min Jiang

BMC Gastroenterol. 2013;13(34)

Abstract

Background

Methods

Results

Discussion

Conclusion

Discussion Only
Coffee consumption has been suggested as a protective factor in the development of liver cancer, but evidence from observational studies is inconsistent.^[11–25] The results of the current meta-analysis of seven prospective and nine case–control studies suggest that there is an inverse association between coffee consumption and liver cancer among different groups according to consumption level. There were significant reductions of 50% in the risk of liver cancer with the highest consumption of coffee compared with non/almost never consumption. The meta-analyses of Bravi et al.^[30] found significant reductions of 55% in the risk of liver cancer with the high drinkers compared with non-drinkers, and Larsson & wolk^[31] found a risk reduction of 43% per 2 cups of coffee per day increment. Our results are consistent with these two previous articles, partly because all of the studies in these two articles are included in the our meta-analysis.

Some results in this meta-analysis were heterogeneous, because the included studies had differences in study design, study region, study sex distribution, and control for confounding factors. In separate analyses by study design, we found an inverse association between coffee consumption and liver cancer among hospital- based case–control studies and among cohort studies.

There was also an inverse association between coffee consumption and liver cancer among European and Asian populations, and the significant risk reduction was stronger among Asian than European populations. The different results may be explained by racial differences. Differences in coffee drinking habits may be a partial explanation for the discrepancy.

We also found an inverse association between coffee consumption and liver cancer among male and female populations, but this result was derived from only four studies with a small number of cases, so we could not draw a firm conclusion. A history of liver disease may be a risk factor for liver cancer, and after adjustment for this, a significant inverse association remained between coffee consumption and liver cancer among two subgroups.

There are several potential mechanisms through which high consumption of coffee may reduce the risk of liver cancer. Coffee contains a variety of chemicals including caffeine, cafestol, kahweol, and chlorogenic acids. It remains uncertain which ingredient of coffee is protective against liver cancer. Some studies have indicated that caffeine can prevent oxidative DNA damage, modify the apoptotic response and reverse cell cycle checkpoint function.^[32–34] Caffeine has strong antioxidant properties.^[35] In an animal experiment, caffeine significantly reduced the incidence of chemically-induced hepatocellular carcinoma in rats.^[36] Furthermore, cafestol and kahweol have been shown to be anti-carcinogenic.^[37,38] Cafestol and kahweol have demonstrated a protective effect against aflatoxin B1-induced genotoxicity.^[39] In addition, a study by Feng et al. showed that chlorogenic acids can scavenge reactive oxygen species and have an anti-tumor effect.^[40] These studies suggest that ingredients in coffee may play an important role in protecting against the occurrence and development of liver cancer.

Our meta-analysis had some merits.

First, the total number of cases included in this meta-analysis was substantial (n = 3622 liver cancer cases). The summary ORs of the highest compared with the lowest coffee consumption categories for risk of liver cancer were consistent with those in a previously published meta-analyses (n = 2260 liver cancer cases).^[30,31]

Second, we found little evidence of publication bias in our meta-analysis. Third, we performed a comprehensive search of the literature on the association between coffee consumption and liver cancer risk up to May 2012.

Our meta-analysis had several limitations. First, we used the highest and lowest coffee consumption levels as measures of exposure, but we were not able to determine whether different amounts of coffee consumption could decrease liver cancer risk. Second, misclassification bias should be considered. Each study presented coffee consumption in different units (cups/week, cups/day, days/week, drinks/day, times/week). Therefore, differential misclassification could bias the results.

Third, because liver cancer is a multifactorial disease, it is uncertain whether other factors may have influenced the results. Fourth, the study areas covered in our meta-analysis only included Asia (Japan, China, Hong Kong) and Europe (Finland, Greece, Italy). Therefore, the value of our results is limited for other areas (Africa, America and Australia). Fifth, potential publication bias might have influenced the results, despite no bias indicated from either the funnel plot or Egger's test.

View Full Text Available @ Medscape

Links Of Interest
Is It Time To Write A Prescription for Coffee? Coffee and Liver Disease -  Commentary

Sofosbuvir Works for Patients Who Cannot Take Peginterferon

 
Sofosbuvir Works for Patients Who Cannot Take Peginterferon

Two phase III studies confirm the efficacy of a sofosbuvir and ribavirin therapy in patients with HCV genotype 2 or 3 infection for whom peginterferon is not an option.

In patients infected with hepatitis C virus (HCV) genotype 2 or 3, treatment with peginterferon plus ribavirin has a sustained virologic response (SVR) of 70% to 85%. However, adverse effects of peginterferon are a barrier to treatment for many patients. Now, two industry-funded, phase III trials have evaluated the efficacy of sofosbuvir (400 mg daily) plus ribavirin (1000 mg–1200 mg daily) in these patients.

In a blinded, placebo-controlled trial, investigators randomized 280 patients for whom peginterferon therapy was not an option (e.g., adverse effects, contraindications for interferons, and patient refusal) to receive sofosbuvir/ribavirin or matching placebo for 12 weeks. In a blinded, active-control trial, researchers randomized 202 patients with prior nonresponse to peginterferon therapy to receive 12 or 16 weeks of sofosbuvir/ribavirin. The primary endpoint in both studies was SVR at 12 weeks after therapy ended.

In patients for whom peginterferon therapy was not an option, SVR was 78% for treatment with sofosbuvir/ribavirin compared with 0% for placebo (P<0.001). In previously treated patients, SVR was 50% for 12 weeks of therapy versus 73% for 16 weeks (P<0.001). SVR rates were lower for patients with genotype 3 versus genotype 2 in both treatment-naive patients (61% vs. 93%) and treatment-experienced patients who received therapy for 12 weeks (30% vs. 86%) or 16 weeks (62% vs. 94%).

SVR rates were lower in patients with cirrhosis than without, both in treatment-naive patients (overall, 61% vs. 81%; genotype 3 vs. 2, 21% vs. 94%) and treatment-experienced patients (overall, 66% vs. 76%; genotype 3 vs. 2 in 16-week group, 61% vs. 78%). In both studies, investigators found no evidence of resistance development, and discontinuation rates were low (1%–2%).

Comment: Oral sofosbuvir plus ribavirin is effective in patients with HCV genotypes 2 or 3 for whom peginterferon-based therapy is not an option or was previously ineffective. Of note, these sustained virologic response rates for sofosbuvir plus ribavirin are comparable to or higher than those previously reported for therapy with peginterferon plus ribavirin in this population.

— Atif Zaman, MD, MPH

Published in Journal Watch Gastroenterology May 24, 2013

 CITATION(S):
Jacobson IM et al. Sofosbuvir for hepatitis C genotype 2 or 3 in patients without treatment options. N Engl J Med 2013 May 16; 368:1867. (http://dx.doi.org/10.1056/NEJMoa1214854)

Medline abstract (Free)

Hepatitis C: Am I At Risk For Liver Cancer?

Hepatitis C: Am I At Risk For Liver Cancer?

Offered on the blog today are a few studies that look at the risk for developing liver cancer in people who are - or who have been - infected with chronic hepatitis C.   The CDC reported hepatitis C is the leading cause of liver cancer which is the fastest rising cause of cancer-related death in the U.S. Without a doubt this disease can lead to serious health problems including liver damage, cirrhosis, liver cancer and liver failure.

In the United States the CDC has implemented screening strategies to identify people at high risk for hepatitis C. Included in the risk group are people born between 1945 and 1965 - age 47 to 67, who currently account for about 75% of the estimated 2.7 and 3.9 million people infected with the virus.

*Learn more about who is at risk and why here.

I often ask myself why people forgo HCV testing if they fall into this high risk population. Most people would agree, preventive strategies for cancer or liver damage are worth the time it takes for a routine blood test.

Additionally a large portion of people are unaware they are infected. These people are in need of clinical evaluation and counseling including prevention strategies; using alcohol, supplements, over-the-counter medications or prescription drugs can cause additional liver damage.

Alcohol And HCV

Older studies have confirmed in patients with hepatitis C heavy alcohol intake contributes to HCV-associated liver disease and can cause significantly more liver scarring or cirrhosis, a more recent study has shown even moderate alcohol increases the risk for liver-related mortality. Last month in the medical journal Alimentary Pharmacology & Therapeutics, researchers concluded; Although chronic hepatitis C is associated with increased risks for overall and liver-related mortality, these risks are even higher for patients consuming moderate and excessive amounts of alcohol. Here is a comment from the study's lead author Zobair Younossi; For instance, the risk of liver-related death among people with hepatitis C who averaged two or fewer drinks a day was 74 times that of similar people without hepatitis C. Check out the interview here.

Disease Progression

Medscape reported: Out of 100 people that contract the infection, 75–85 people will develop chronic infection, 60–70 people will develop chronic liver disease, five to 20 people will develop cirrhosis over the course of their chronic infection and one to five people will die of complications including hepatocellular carcinoma (HCC). The good news is that the overall percentage of people with HCV who develop cirrhosis or liver cancer is low, unless that person is you, then its at 100%.

Liver Cancer Without Cirrhosis?

In the June 2013 issue of American Journal of Roentgenology researchers investigated liver cancer in patients with chronic HCV - without advanced fibrosis or cirrhosis.

AJR Am J Roentgenol. 2013 Jun;200(6):W610-W616.

Hepatocellular Carcinoma in Chronic Hepatitis C in the Absence of Advanced Fibrosis or Cirrhosis.

Lewis S, Roayaie S, Ward SC, Shyknevsky I, Jibara G, Taouli B.

Source
1 Department of Radiology/Body MRI and Translational and Molecular Imaging Institute, Ichan School of Medicine at Mount Sinai, One Gustave Levy Pl, Box 1234, New York, NY 10029.

Abstract

OBJECTIVE. The objective of our study was to describe the cross-sectional imaging appearance of hepatocellular carcinoma (HCC) in patients with chronic hepatitis C virus (HCV) infection in the absence of advanced fibrosis and cirrhosis.

MATERIALS AND METHODS. This study is a retrospective review of our surgical database to identify patients with chronic HCV infection and HCC who underwent hepatectomy and who had undergone preoperative CT or MRI. Only patients with a Metavir fibrosis score of F0, F1, or F2 on pathology were included. Patients with hepatitis B virus coin-fection or other causes of chronic liver disease and patients with histopathologic evidence of advanced fibrosis or cirrhosis (Metavir scores F3 and F4) were excluded. Contrast-enhanced CT or MRI examinations performed within 2 months before surgery were reviewed for the number, size, and location of tumors; tumor enhancement characteristics; and presence of macrovascular invasion.

RESULTS. Two hundred forty-five resections of HCC in patients with HCV were performed in our institution from 1987 to 2012. Of this group, 26 patients (10.6%) had a Metavir fibrosis score of F0, F1, or F2; of those patients, 19 (18 men and one woman; 18 non-Asian patients and one Asian patient; mean age, 64 years) had imaging studies available for review. Twenty-one HCCs (mean size, 4.5 cm; range, 0.9-14.8 cm) were evaluated at imaging. Typical wash-in and washout characteristics were seen in 16 of 19 viable lesions (84.2%). The remaining two HCCs were completely necrotic after transarterial chemoembolization. Eighteen patients had a solitary tumor. Most tumors (15/21, 71.4%) developed in the right hepatic lobe.

CONCLUSION. HCC can develop in patients with chronic HCV without advanced fibrosis or cirrhosis, most frequently in older non-Asian men, and usually appears as a large solitary tumor with a typical wash-in-washout enhancement pattern.

Liver Cancer With Cirrhosis After Successful HCV Therapy

Last month in Clinical Infectious Diseases, researchers concluded: The risk for HCC, liver decompensation, and death in patients with liver cirrhosis related to HCV was markedly reduced after SVR, but a long-term risk of developing HCC remains for up to 8 years.

This month the in-depth clinical information website, Healio.com featured the study:

HCC risk persists 8 years after HCV eradication

May 9, 2013

The long-term risk for hepatocellular carcinoma among patients with hepatitis C remains up to 8 years after sustained virological response to antiviral therapy, researchers reported in Clinical Infectious Diseases.

The number of patients with cancer was too low to draw any firm conclusion, but it was nevertheless somewhat surprising that the risk remained for such a prolonged time period,” Soo Aleman, MD, PhD, of the departments of gastroenterology and hepatology and infectious diseases at Karolinska Institutet in Stockholm, told Infectious Disease News.

“We need to know how long this risk persists and which subgroups of patients are at the highest risk after achieving sustained virological response (SVR). Future studies are needed to answer these questions.”

Aleman and colleagues conducted a prospective study that included patients who had HCV-related cirrhosis.

Among the 351 patients, 110 reached SVR, 193 did not and 48 were untreated. The study was initiated in 2001 and the patients were followed for a mean of 5.3 years.

Six patients who achieved SVR developed hepatocellular carcinoma (HCC), for an incidence of 1 per 100 person-years. Two patients were diagnosed within a year after achieving SVR at 0.5 and 7.7 months, and the remaining four were diagnosed at 2.4, 7.4, 7.4 and 7.6 years.

All of the patients were tested for HCV RNA at HCC diagnosis, and all were negative.

Among patients who did not achieve SVR or who were untreated, the risk for HCC was higher. The risk for any liver-related complication, liver-related death or overall death was lower among patients who achieved SVR. These differences were similar after controlling for alcohol use, age, sex and diabetes.

“Patients who have liver cirrhosis prior to the eradication of HCV should continue to undergo surveillance with ultrasound regularly for early detection of hepatocellular carcinoma,” Aleman said.

Soo Aleman, MD, PhD, can be reached at Department of Gastroenterology and Hepatology, and Infectious Diseases, Karolinska University Hospital at Karolinska Institute, 171 76 Stockholm, Sweden; email: soo.aleman@ki.se.

Disclosure: Aleman reports financial relationships with Gilead, Janssen, MSD and Roche.

Screening For Liver Cancer

According to WHO  in 25 % of liver cancer patients, the underlying cause is hepatitis C. Long-term management of chronic hepatitis C infection for patients with cirrhosis include routine screening for liver cancer. These tests might mean an ultrasound twice a year, and twice-yearly measurements of  alpha-fetoprotein (AFP) levels in the blood, which is a liver-cancer marker.

Get Tested

If any of the risk factors mentioned in this article pertain to you, I urge you to please consider the CDC's recommendation and get tested once for hepatitis C. If the test is positive additional testing is needed.

According to the CDC Telebriefing on Hepatitis C testing held this month;

Today's data show that even among young people who get tested positive, only about half had follow-up tests to see if they were still infected. That's what you need to get appropriate care and treatment. Right now there are better Hepatitis C treatments available than ever and there are more treatments coming in the coming year. So confirming that someone is more infected is more important than ever. Not everyone with Hepatitis C will need treatment, but everyone with Hepatitis C should be linked to care so that they can monitor how their liver is doing, determine when and if treatment is warranted, avoid things like excess alcohol which can damage their liver, and avoid medications that could also damage their liver as well as getting vaccinated against hepatitis b to protect their liver. Liver disease is something which is causing an increasing number of deaths, and many of those deaths could be prevented with the current treatments and with preventive actions that people can take if, but only if, they know that they're infected. Today CDC is also issuing updated guidance for doctors and other health care providers about how to test for Hepatitis C and how to provide follow-up.

Need To Talk To Someone ?

Help is available, recently "Project Inform" announced the launch of a new national helpline, 877-HELP-4-HEP (877-435-7443), run by and for people affected by hepatitis C.

AbbVie's Investigational noninterferon HCV treatment effective across patient groups

Frederick A. Nunes, MD, Associate Professor of Medicine, Penn Medicine. Discussing his presentation at Digestive Disease Week 2013 in Orlando, Fla.: #514; Interferon‐free Regimens of ABT‐450/r, ABT‐267, ABT‐333, and Ribavirin Achieve High Sustained Virologic Response 4 Weeks Post‐Treatment (SVR4) Rates in Patients With Chronic HCV Genotype 1 Regardless of Race, Ethnicity, or Other Baseline characteristics.
Source - Healio

View Slides @ NATAP
DDW
Response to 3 DAAs + RBV by Patient Characteristics: INTERFERON-FREE REGIMENS OF ABT-450/r, ABT-267, ABT-333, AND RIBAVIRIN ACHIEVE HIGH SUSTAINED VIROLOGIC RESPONSE 12 WEEKS POST-TREATMENT (SVR12) RATES IN PATIENTS WITH CHRONIC HCV GENOTYPE 1 REGARDLESS OF RACE, ETHNICITY, OR OTHER BASELINE CHARACTERISTICS

May 6
AbbVie's Investigational Hepatitis C Virus Regimen Gets Breakthrough-Therapy Designation

May 24

Digestive Disease Week
Investigational noninterferon HCV treatment effective across patient groups

By: SHARON WORCESTER, Internal Medicine News Digital Network



Dr. Frederick Nunes

ORLANDO – Both 12- and 24-week regimens of an investigational interferon-free therapy for hepatitis C were associated with high sustained virological response rates at 12 weeks post treatment in a phase II study of patients with hepatitis C virus genotype 1 who had baseline characteristics associated with poor response to interferon-based therapies.

The findings of this subgroup analysis of the randomized, open-label, multicenter Aviator trial demonstrate that the high response rates recently reported for the entire cohort also apply to patients with older age, black race, Hispanic/Latino ethnicity, interleukin (IL)-28B non-cc genotype, and higher body mass index (BMI), Dr. Frederick Nunes reported at the annual Digestive Disease Week.

The Aviator trial assessed the safety and efficacy of various dosing regimens and combinations of three AbbVie investigational direct-acting antivirals (DAAs) with or without ribavirin, including the potent hepatitis C virus (HCV) protease inhibitor ABT-450 dosed with 100 mg of ritonavir (ABT-450/r, dosed at 100 or 150 mg daily), the NS5A inhibitor ABT-267 (25 mg daily), and the non-nucleoside NS5B inhibitor ABT-333 (400 mg twice daily). A total of 247 patients were included in the subanalysis, Dr. Nunes reported at the meeting.

The regimen that included all three investigational drugs and ribavirin, known as 3 DAA/RBV, was associated with sustained virological response rates of 99% and 93% at 12 weeks in treatment-naive patients and previous peg-interferon/ribavirin (peg-IFN/RBV) null responders, respectively, said Dr. Nunes, who is clinical associate professor of medicine in the University of Pennsylvania Health System, and section chief of gastroenterology at Pennsylvania Hospital, Philadelphia.

In the current analysis, high sustained virological response rates at 12 weeks (SVR12) were also achieved in the 247 patients with chronic HCV genotype 1, including 159 treatment-naive and 88 previous peg-IFN/RBV null responders, who were assigned to 12 or 24 weeks of 3 DAA/RBV. The virological response rates were 99% and 93% for the treatment-naive 12- and 24-week groups, respectively, and 93% and 98% for the null responder 12- and 24-week groups.

The high responses occurred regardless of treatment duration, age, race, ethnicity, BMI, Homeostatic Model of Assessment–Insulin Resistance (HOMA-IR), IL-28B host genotype, or baseline viral load. The rates did not differ significantly on any comparison made in treatment-naive patients or previous null responders, he said.

In the treatment-naive patients, no breakthroughs occurred, although 1% of those in the 12-week treatment arm relapsed, and 3% of the 24-week treatment group relapsed.

In the null responder group, no relapses occurred, but breakthroughs occurred in 7% of those in the 12-week treatment arm, and in 2% of the 24-week treatment arm, he said.

Treatment was safe and generally well tolerated. Four patients discontinued treatment due to drug-related adverse events, most commonly fatigue (in 32.7% and 23.9% of treatment-naive and null responders, respectively) and headache (31.4% and 30.7%, respectively).

One patient had a serious adverse event (arthralgia) considered to be possibly related to the study drug regimen.

Because ribavirin was included in the treatment regimens, it is impossible to tease out whether the adverse events were associated with that drug or with the investigational DAAs, Dr. Nunes noted.

Patients included in the study were noncirrhotic adults aged 18-70 years with a BMI between 18 and 38 kg/m², and HCV genotype 1.

 

"The overall efficacy was excellent irrespective of the baseline grouping. So black race, Hispanic/Latino ethnicity, age greater than 50, BMI over 30, male gender, HOMA-IR greater than 3, IL-28B non-cc genotype, and viral load greater than 7 logs all had very high SVR12 response rates," Dr. Nunes said.

 

The safety and efficacy of this interferon-free 3 DAA/RBV therapy will be further explored in phase III studies, he said.

 

Dr. Nunes has received grant or research support from Merck, Abbott Laboratories, and Roche Pharma AG.

 

http://www.internalmedicinenews.com/news/conference-news/digestive-disease-week/single-article-2013/investigational-noninterferon-hcv-treatment-effective-across-patient-groups/b3d9ead21f9bc4f7c32f92a1d2bfe0f3.html

Risks small between HCV patients’ use of DAAs, neuropsychiatric events

Risks small between HCV patients’ use of DAAs, neuropsychiatric events

Sockalingam S. BMC Gastroenterol. 2013;doi:10.1186/1471-230X-13-86.

May 24, 2013
The risks for neuropsychiatric adverse events among patients with hepatitis C virus being treated with direct-acting antivirals appear minimal, but the risks for drug-drug interactions are high, according to recent study results.

Researchers conducted a literature search of PubMed from 2000 to April 2013 using the search terms, “hepatitis C” and “boceprevir” or “telaprevir,” along with “mental disorders,” “psychotropic drugs” and “drug interactions.” The analysis was designed to evaluate studies on neuropsychiatric adverse effects as a result of direct-acting antivirals (DAAs) and drug-drug interactions (DDIs) involving psychotropic medications and DAAs among hepatitis C virus (HCV) patients.

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