September 14, 2012

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HIV is shown attaching to and infecting a T4 cell. The virus then inserts its own genetic material into the T4 cell's host DNA. The infected host cell then manufactures copies of the HIV. (Credit: iStockphoto/Medical Art Inc.)

ScienceDaily (Sep. 2, 2012) — For years, doctors treating those with HIV have recognized a relationship between how faithfully patients take the drugs they prescribe, and how likely the virus is to develop drug resistance. More recently, research has shown that the relationship between adherence to a drug regimen and resistance is different for each of the drugs that make up the "cocktail" used to control the disease.

New research conducted by Harvard scientists could help explain why those differences exist, and may help doctors quickly and cheaply design new combinations of drugs that are less likely to result in resistance.

As described in a September 2 paper in Nature Medicine, a team of researchers led by Martin Nowak, Professor of Mathematics and of Biology and Director of the Program for Evolutionary Dynamics, have developed a technique medical researchers can use to model the effects of various treatments, and predict whether they will cause the virus to develop resistance.

"What we demonstrate in this paper is a prototype for predicting, through modeling, whether a patient at a given adherence level is likely to develop resistance to treatment," Alison Hill, a PhD student in Biophysics and co-first author of the paper, said. "Compared to the time and expense of a clinical trial, this method offers a relatively easy way to make these predictions. And, as we show in the paper, our results match with what doctors are seeing in clinical settings."

The hope, said Nowak, is that the new technique will take some of the guesswork out of what is now largely a trial-and-error process.

"This is a mathematical tool that will help design clinical trials," he said. "Right now, researchers are using trial and error to develop these combination therapies. Our approach uses the mathematical understanding of evolution to make the process more akin to engineering."

Creating a model that can make such predictions accurately, however, requires huge amounts of data.

To get that data, Hill and Daniel Scholes Rosenbloom, a PhD student in Organismic and Evolutionary Biology and the paper's other first author, turned to Johns Hopkins University Medical School, where Professor of Medicine and of Molecular Biology and Genetics Robert F. Siliciano was working with PhD student Alireza Rabi (also co-first author) to study how the HIV virus reacted to varying drug dosages.

Such data proved critical to the model that Hill, Rabi and Rosenbloom eventually designed, because the level of the drug in patients -- even those that adhere to their treatment perfectly -- naturally varies. When drug levels are low -- as they are between doses, or if a dose is missed -- the virus is better able to replicate and grow. Higher drug levels, by contrast, may keep the virus in check, but they also increase the risk of mutant strains of the virus emerging, leading to drug resistance.

Armed with the data from Johns Hopkins, Hill, Rabi and Rosenbloom created a computer model that could predict whether and how much the virus, or a drug-resistant strain, was growing based on how strictly patients stuck to their drug regimen.

"Our model is essentially a simulation of what goes on during treatment," Rosenbloom said. "We created a number of simulated patients, each of whom had different characteristics, and then we said, 'Let's imagine these patients have 60 percent adherence to their treatment -- they take 60 percent of the pills they're supposed to.' Our model can tell us what their drug concentration is over time, and based on that, we can say whether the virus is growing or shrinking, and whether they're likely to develop resistance."

The model's predictions, Rosenbloom explained, can then serve as a guide to researchers as they work to design new drug cocktails to combat HIV.

While their model does hold out hope for simplifying the process of designing drug "cocktails," Hill and Rosenbloom said they plan to continue to refine the model to take additional factors -- such as multiple mutant-resistant strains of the virus and varying drug concentrations in other parts of the body -- into effect.

"The prototype we have so far looks at concentrations of drugs in blood plasma," Rosenbloom explained. "But a number of drugs don't penetrate other parts of the body, like the brains or the gut, with the same efficiency, so it's important to model these other areas where the concentrations of drugs might not be as high."

Ultimately, though, both say their model can offer new hope to patients by helping doctors design better, cheaper and more efficient treatments.

"Over the past 10 years, the number of HIV-infected people receiving drug treatment has increased immensely," Hill said. "Figuring out what the best ways are to treat people in terms of cost effectiveness, adherence and the chance of developing resistance is going to become even more important."

Story Source:

The above story is reprinted from materials provided by Harvard University, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Daniel I S Rosenbloom, Alison L Hill, S Alireza Rabi, Robert F Siliciano, Martin A Nowak. Antiretroviral dynamics determines HIV evolution and predicts therapy outcome. Nature Medicine, 2012; DOI: 10.1038/nm.2892

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Hepatitis C: A public health problem with a solution

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As part of World Hepatitis Day, people all around the world struck the "hear no evil, see no evil, speak no evil" pose to highlight the fact that hepatitis C is relatively invisible in the public consciousness. Translated, the shirt reads "Am I Number 12?", a reference to the fact that 1 in 12 people worldwide is living with either chronic hepatitis B or C.

Posted on Friday, September 14, 2012

July 28 marked the World Health Organization’s World Hepatitis Day, and the message is simple: early detection of the hepatitis C virus (HCV) saves lives. All individuals have a role to play if we are to curb the burden of this disease in Canada.

Hepatitis C is a virus that infects the liver and causes damage slowly over many years, or even decades. Symptoms are rarely seen until liver damage is severe, and therefore, most infected people are often unaware of their status. Left untreated, it can lead to liver cirrhosis, liver failure, or even liver cancer. However, unlike many viral infections, hepatitis C is curable.

In the U.S., deaths due to HCV have now surpassed those caused by HIV, and this trend is likely to continue. Here in Canada, according to the Public Health Agency, there are more than 250,000 people infected with HCV, with 13 new cases each day. In fact, this estimate is likely low; as many individuals are unaware they are infected.

This is not an academic problem. A recent study found that hepatitis C causes more years of lost life and illness than any other infectious disease in Ontario (including HIV, influenza and pneumonia). However, because it is a slow and largely silent killer, hepatitis C often attracts less attention than other infections.

The virus is spread primarily through blood-to-blood contact. Current injection drug use and blood transfusions performed before 1990 are important routes of infection, although tattooing, and recreational cocaine or heroin use also put you at risk for hepatitis C. This means that even if you used these drugs, only once, or many years ago, you may be infected.

In many parts of the world, HCV was, and sometimes still is, spread through re-use of needles for medical procedures. The virus can also rarely be transmitted sexually or from mother to child. Foreign-born Canadians may have acquired hepatitis C before coming to Canada but are only now feeling the effects of the disease.

In the U.S., Baby Boomers account for 80 per cent of people with hepatitis C. Many have no idea they have the disease. For these reasons the U.S. Centers for Disease Control and Prevention recently recommended universal screening (through a simple blood test) of anyone born between 1945 and 1965.

The good news: hepatitis C is curable. With current treatments, up to 75 per cent of people can be cured; but treatment works best when HCV is diagnosed early. Once hepatitis is gone, the liver slowly improves and for those without cirrhosis, there is minimal risk of any long-term consequences. Unlike hepatitis A and B, there is no vaccine for hepatitis C, but if we treat those infected, we can also prevent transmission of the virus.

Physicians have an important role to play. Most family doctors recognize the signs and symptoms of advanced liver disease, but it is important to identify hepatitis C before they are present. Liver blood tests may remain normal despite persistent hepatitis C infection, which could be slowly damaging the liver. Targeted screening of people with known risk factors is important, but this strategy alone is ineffective.

Risk factors may not be obvious, which is why the U.S. Centers for Disease Control and Prevention recommends screening all Baby Boomers, regardless of their background. We should strongly consider adopting the same policy. If we find hepatitis C we can treat it, preventing liver failure, liver cancer and the need for transplantation. This not only saves lives, but also saves on the associated costs that come with these complications.

Universal testing of Baby Boomers is cost-effective and is sound public policy. We love to criticize American healthcare programs, but this time they got it right, and we should follow their lead.

The message is simple: early awareness of infection with hepatitis C save lives. So go and get tested!

Signed,

Mohamed Abdel-Hakeem, PhD Candidate, Université de Montréal

Mia Biondi, PhD Candidate, McGill University

Robert Kozak, PhD, McGill University

Marion Depla, PhD, Université de Montréal

Jordan Feld, MD, MPH, University of Toronto

Marc Bilodeau, MD, Université de Montréal, Director of the National CIHR Research Training Program in Hepatitis C

Michael Houghton, PhD, University of Alberta

Lorne Tyrrell, MD, PhD, Director of the Li Ka Shing Institute of Virology, University of Alberta

Mark Wainberg, PhD, Director of the McGill University AIDS Centre

Mark Tyndall, MD, ScD, Chief and Chair of the Infectious Diseases Division, University of Ottawa

Rob Myers, MD, MSc, Director of the Viral Hepatitis Clinic, University of Calgary Gerry Mugford, PhD, Memorial University

Naglaa Shoukry, B. Pharm, PhD, Director of the Viral Hepatitis Research Group, Université de Montréal

Thomas Michalak, MD, PhD, Memorial University

Julie Bruneau, MD, MSc, Université de Montréal

Aled Edwards, PhD, University of Toronto

Joyce Wilson, PhD, University of Saskatchewan

Gail Butt, RN, PhD, University of British Columbia

Qiang Liu, PhD, University of Saskatchewan

Eve Roberts, MD, University of Toronto

Louise Balfour, PhD, University of Ottawa

Raymond Tellier, MD, MSc, University of Calgary

Rodney Russell, PhD, Memorial University

Hugo Soudeyns, PhD, Université de Montréal

Marina Klein, MD, MSc, McGill University

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High Dietary Fructose May Impair Liver Function

DURHAM, N.C.—Obese patients with type 2 diabetes who consume higher amounts of fructose display reduced levels of liver adenosine triphosphate (ATP)—a compound involved in the energy transfer between cells, according to a new study published in the journal Hepatology. The findings indicate elevated uric acid levels are associated with more severe hepatic ATP depletion in response to fructose intake.

The study, funded in part by grants from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), also suggests that uric acid levels may serve as a marker for increased fructose consumption and hepatic ATP depletion. Uric acid is produced by the breakdown of purines, natural substances commonly found in foods. According to the researchers, increased dietary fructose can alter the body’s metabolism and energy balance. Energy depletion in the liver may be associated with liver injury in patients with non-alcoholic fatty liver disease (NAFLD) and in those at risk for developing this metabolic condition.

Prior research reports that fructose consumption in the United States has more than doubled in the past 30 years. Studies have shown that Americans’ fructose intake climbed from 15 grams per day in the early 1900s to 55 grams per day in 1994, which experts believe stems from an increase in soft drink consumption.

“There is an alarming trend of increased rates of obesity, type 2 diabetes and NAFLD in the U.S.," said lead author Dr. Manal Abdelmalek from Duke University Medical Center. “Given the concurrent rise in fructose consumption and metabolic diseases, we need to fully understand the impact of a high-fructose diet on liver function and liver disease."

For the present study, 244 obese and diabetic adults from the Look AHEAD Study were evaluated, with dietary fructose consumption estimated by the food frequency questionnaire. Liver ATP and uric acid levels were measured in 105 patients who participated in the Look AHEAD Fatty Liver Ancillary Study. Researchers assessed the change in liver ATP content using an IV fructose challenge in 25 subjects, comparing patients with low fructose consumption (less than 15 grams per day) to those with high fructose consumption (greater than 15 grams per day).

Participants with a high intake of dietary fructose had lower liver ATP levels at baseline and a greater change in ATP content following the fructose challenge than those who consumed a lower amount of fructose. Patients with high uric acid levels (5.5 mg/dL or more) displayed lower ATP stores in response to fructose.

“High fructose consumption and elevated levels of uric acid are associated with more severe depletion of liver ATP. Our findings suggest that increased dietary fructose intake may impair liver ‘energy balance’," Abdelmalek said, adding further research to define the clinical implications of these findings on metabolism and NAFLD is necessary.

Sources:

AlphaGalileo: Increased Dietary Fructose Linked to Elevated Uric Acid Levels and Lower Liver Energy Stores

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Smokers may have more sleep problems: study

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A woman disposes a cigarette in Los Angeles, California, May 31, 2012. Credit: Reuters/Jonathan Alcorn

Thu Sep 13, 2012 9:27pm EDT

(Reuters) - Smokers may get fewer hours of sleep and have less restful slumber than non-smokers, according to a German study that looked at more than two thousand people.

Researchers whose work appeared in the journal Addiction Biology found that of nearly 1,100 smokers surveyed, 17 percent got fewer than six hours of sleep each night and 28 percent reported "disturbed" sleep quality.

That compared with rates of seven percent and 19 percent respectively among more than 1,200 non-smokers who were also surveyed, said lead researcher Stefan Cohrs, of Charite Berlin medical school in Germany.

"This study demonstrates for the first time an elevated prevalence of sleep disturbance in smokers compared with non-smokers in a population without lifetime history of psychiatric disorders even after controlling for potentially relevant risk factors," Cohrs and his colleagues wrote.

The findings cannot prove that smoking directly impairs sleep, since smokers may have other habits that could affect their shut-eye such as staying up late to watch TV or getting little exercise, Cohrs told Reuters Health in an email.

But there is also reason to believe the stimulating effects of nicotine may be to blame.

"If you smoke and you do suffer from sleep problems, it is another good reason to quit smoking," Cohrs said.

Poor sleep quality may not only make your waking hours tougher. Some studies have also linked habitually poor sleep to health problems like obesity, diabetes and heart disease.

The study included 1,071 smokers and 1,243 non-smokers who were free of mental health disorders, since those conditions may make a person both more likely to smoke and more vulnerable to sleep problems.

The researchers used a questionnaire that gauges sleep quality. Overall, more than one-quarter of smokers had a score than landed them in the category of "disturbed" sleep, meaning they had a high probability of insomnia.

Many things can affect sleep quality, and Cohrs's team was able to account for factors such as age, weight, and alcohol abuse. Yet smoking was still linked to poorer sleep quality.

It's still possible there are other things about smokers that impair their sleep, but Cohrs said he thinks the most likely culprit is nicotine - and the prospect of better sleep could provide smokers with an additional reason to quit. SOURCE: bit.ly/TOrYk0

(Reporting from New York by Amy Norton at Reuters Health; editing by Elaine Lies)

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Finding the Pathways to Drug-induced Liver Injury

Urs Boelsterli, left,  Winfried Krueger, and Theodore Rasmussen in a stem cell research lab at the Physics/Biology Building on Aug.29, 2012. (Peter Morenus/UConn Photo)

Urs Boelsterli, left, Winfried Krueger, and Theodore Rasmussen in a stem cell research lab at the Biology/Physics Building. (Peter Morenus/UConn Photo)

September 12, 2012 By: Colin Poitras

Antibiotics are the first line of defense against many infections. But for some individuals, treatment with certain antibiotics can bring on a new set of health problems, including serious liver damage.

Why some individuals are vulnerable to this potentially life-threatening drug reaction while others are not remains unclear.

Now, with the support of a three-year, $1.29 million grant from Connecticut’s Stem Cell Research Program, a team of University of Connecticut scientists is looking deeper into the problem, investigating whether genes play a role in determining a person’s susceptibility to drug-induced liver injury. Ultimately, the researchers hope to develop a reliable genetic test can be used to identify individuals most at risk.

The collaborative grant was one of the first handed out by the state of Connecticut for stem cell research targeting a specific disease.

Drug-induced liver injury is an important public health issue affecting thousands of people around the world annually. It is particularly insidious, as it can develop suddenly after weeks or months of drug treatment.

“It’s a significant clinical problem with high morbidity and mortality and nobody knows why this happens,” says Urs A. Boelsterli, an expert in mechanistic toxicology and one of three researchers in UConn’s School of Pharmacy working on the project. Theodore Rasmussen, a stem cell specialist and associate professor of pharmacology and toxicology, and Winfried Krueger, a genetics specialist and associate research professor in the School of Pharmacy, round out the research team. Paul Watkins, director of the Hamner-University of North Carolina Institute for Drug Safety Sciences, is providing the team with patient skin and blood samples that will be used for the development of the stem cells critical to the research.

One of the antibiotics the research team is focusing on is isoniazid, which is used worldwide to treat tuberculosis and causes drug-induced liver injury in about 1 percent of all people who take the drug.

The researchers are currently developing a line of induced pluripotent stem cells or iPS cells, that are derived from skin and blood cells and can be turned into liver cells called hepatocytes. Using stem cells fashioned from cells obtained from both healthy individuals and those with liver injury allows the researchers to overcome one of the primary obstacles to their work – the lack of available material for testing. Donated liver biopsies are rare, and ethically, the researchers cannot ask for liver biopsy samples from a living person.

In the past, most research in this area has involved the use of animal models and limited clinical trials. But the toxicology tests are not optimal, as mice may not react to some drugs in the same way as humans and – because they are raised for testing – mice can lack the broad genetic variations needed to truly study a drug’s effects in the human population as a whole. In vitro studies for drug toxicity, such as the one being performed at UConn, are a new and promising step toward greater understanding.

“We take skin cells or blood cells, which are both very medically accessible, and we reprogram them into iPS cells that can be made into hepatocytes,” says Rasmussen, who is affiliated with the Department of Pharmaceutical Sciences and UConn’s Stem Cell Institute. “These are like pharmaceutically-naïve hepatocytes because they have never been exposed to pharmaceuticals in the liver. But what they do have is each individual’s unique genome. If we use them in tests and get a different response from an individual with liver injury and one without, then it is very likely that genetics plays a role rather than environment because we have pretty much taken environment out of the equation.”

When this point is reached, Krueger will then follow up by developing a genome expression profile for the proteins suspected of being involved in the disease to see which particular subset of regulated genes and pathways may be linked to susceptibility for drug-induced liver injury.

“Once those genes are identified, that would be a tremendous advance in the field because right now there is no indication of which target genes are participating in this disease,” Krueger says.

Adds Rasmussen, “Eventually, we’d like to develop a genetic test that would essentially show an individual’s risk profile before you give them a drug.”

More than a thousand different drugs can cause liver disease in patients. Most individuals can take a drug and not have a serious reaction. But because such a large number of people use these medications, even a small percentage of users who experience health problems is a concern.

“For most drug development companies, liver injury is the most important toxicological problem right now,” says Boelsterli, the Boehringer Ingelheim Endowed Chair in UConn’s School of Pharmacy. “Not only does it kill drugs in development, but companies may not find out until later clinical trials or when a drug is already on the market that it can produce idiosyncratic liver injury and the drug has to be pulled. Companies can lose millions of dollars in development costs. The situation is especially tragic if a drug has been proven to be a good one that fights a disease.”

Krueger says the group’s research will help drug developers identify at-risk populations early on.

“When companies develop a new drug, they don’t always know what all the risk factors are in the population because it is so novel,” he says. “But if you have a bank of hepatocytes against which you can test a drug, then you have a filter in place and can identify a certain subset of patients who may be at risk if they use the drug. That may allow you to still keep the drug on the market, as long as it includes a warning for the particular population at risk.”

Rasmussen says this kind of disease-specific stem cell research is a platform for personalized medicine.

Adds Boelsterli, “With Induced Pluripotent Stem Cells, we can look at patient-specific genomes and incorporate that information into drug screening that was never before possible. Being able to look at such a broad spectrum of genetic variation in the context of drug toxicology is really quite novel.”

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WASHINGTON, Sept. 13, 2012 /PRNewswire-USNewswire/ -- AIDS-related deaths among all state and federal prisoners dropped from 24 deaths per 100,000 inmates in 2001 to five per 100,000 in 2010, according to a report by the Justice Department's Bureau of Justice Statistics (BJS). In 2010, 72 inmates in state prisons and seven in federal prisons died from AIDS-related causes.

The rate of AIDS-related deaths among all state and federal prison inmates declined on average about 16 percent each year from 2001 through 2010. Among all inmates with HIV/AIDS, the AIDS-related death rate dropped on average about 13 percent each year, from 134 deaths per 10,000 inmates with HIV/AIDS in 2001 to 38 per 10,000 in 2010.

In 2010, the estimated rate of HIV/AIDS among state and federal prisoners dropped to 146 cases per 10,000 inmates from 194 cases per 10,000 in 2001. This was an average decline of about three percent each year, consistent with the decline across states with small, medium and large prison inmate populations.

Based on the latest available data, the rate of AIDS-related deaths among persons ages 15 to 54 in the U.S. general population was seven deaths per 100,000 in 2009, which was slightly higher than the rate of six deaths per 100,000 inmates for AIDS-related deaths in state prisons for the same age group.

The number of male inmates in state or federal prisons who had HIV/AIDS declined from 19,027 at year end 2009 to 18,337 at year end 2010, while the number of females who had HIV/AIDS decreased from 1,853 to 1,756 over the one-year period.

The decrease in HIV/AIDS deaths among state prisoners was driven mainly by declines among males, black non-Hispanics, and inmates age 35 or older. The number of AIDS-related deaths among male state prisoners declined from 89 deaths in 2009 to 69 in 2010. Among black non-Hispanic state prisoners, it dropped sharply from 70 to 43 deaths, and among state prisoners age 35 or older the number dropped from 87 to 60 deaths. These declines in HIV/AIDS deaths were offset by slight increases among white non-Hispanic state prisoners (from 15 to 23 deaths) and prisoners under age 35 (from seven to 12 deaths).

California, Florida, New York and Texas housed 51 percent of state prisoners with HIV/AIDS, but held 37 percent of all state prisoners in custody. As a percentage of their custody population, New York state prisons had the highest percentage of HIV/AIDS inmates (5.5 percent), followed by Louisiana (3.5 percent), and Maryland and Florida (3.2 percent each).

The findings in this report are based on information from BJS's National Prisoner Statistics Program (which annually collects information from the 50 state departments of corrections and the Federal Bureau of Prisons on prisoner counts, characteristics, admissions and releases), and from BJS's Deaths in Custody Reporting Program (which collects individual-level data on causes of inmate deaths and characteristics of inmates who died).

The report, HIV in Prisons, 2001-2010 (NCJ 238877), was written by BJS statistician Laura M. Maruschak. The report, related documents and additional information about the Bureau of Justice Statistics' statistical publications and programs can be found on the BJS website at http://www.bjs.gov/.

The Office of Justice Programs (OJP), headed by Acting Assistant Attorney General Mary Lou Leary, provides federal leadership in developing the nation's capacity to prevent and control crime, administer justice, and assist victims. OJP has six components: the Bureau of Justice Assistance; the Bureau of Justice Statistics; the National Institute of Justice; the Office of Juvenile Justice and Delinquency Prevention; the Office for Victims of Crime; and the Office of Sex Offender Sentencing, Monitoring, Apprehending, Registering, and Tracking. More information about OJP can be found at http://www.ojp.gov.

SOURCE U.S. Department of Justice - Bureau of Justice Statistics

RELATED LINKS
http://www.bjs.gov

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New hope for Hepatitis C patients

Thursday, September 13, 2012 - 12:10

by Bernama

Location: KUALA LUMPUR

HEPATITIS disease, an inflammation of the liver which is most commonly caused by a viral infection, has a long gruesome history in mankind.

Be it hepatitis A, B, C, D or E, all are fatal diseases and have killed more people than malaria, dengue and HIV/AIDS combined together in the past decade. According to the World Health Organisation (WHO), there are about 12–15 million acute cases of hepatitis A worldwide with 3,000 deaths occurring annually.

In addition, there are about two billion people infected with hepatitis B worldwide, with about 360 million living with chronic infection and 600,000 dying because of it.

About 130–170 million people are chronically infected with hepatitis C and more than 350,000 people die from the virus-related liver diseases worldwide each year.

Over 50 per cent more infectious than HIV

To make it worse, hepatitis B virus (HBV) and hepatitis C virus (HCV) are more infectious than HIV.

"HBV is up to 100 per cent more infectious than HIV while the HCV is about 50 times more infectious,” said a spoke person from healthcare product manufacturer Roche Malaysia Sdn Bhd.

"Both viruses are stronger than the HIV and could withstand environmental exposure up to seven hours. HIV is weaker and would cease to exist within a short time of exposure," she said.
Nevertheless, similar to HIV, both viruses are easily transmitted through blood.

"They could also be transmitted through injection of recreational drugs, tattooing, acupuncture, unprotected sex, body piercing, kidney dialysis and transmission from mother to child during birth," she said.

It is worrisome that the number of patients of both diseases are higher as compared to the other types of hepatitis diseases in the country, said Professor Dr Rosmawati Mohamed, a Consultant Hepatologist (Liver Specialist) at the University of Malaya Medical Centre (UMMC), here.

Medication and treatment

She pointed out that the lifelong disease is somehow unnoticeable in some of the patients, because most of them never really experience major problems, until they are older.

"There are those who get the disease as early as five years old, but it only comes to their notice after 20 years," she said.

But they can thank their lucky stars now. The disease, which was considered incurable till sometime back, is now curable, she said, adding that in the past nine years, a curable drug or medication has been found and can cure hepatitis C patients.

"There was a study conducted on about seven thousand hepatitis C patients, before this, who were treated with the drug over a six-year period.”

"After the treatment, the virus could no longer be detected in them, and it stays undetectable even after five years" she said.

"A new drug has also been discovered a month ago for hepatitis C patients that could boost the rate of their recuperation," she said.

It is an outstanding discovery for hepatitis C patients, even though curable drugs for other types of hepatitis are still not discovered.

Nevertheless, all types of hepatitis could be controlled through regular treatments which are available in all of the hospitals nationwide.

However, she said early screening is needed and a consultation with doctors is required beforehand to ensure that the disease would not go under the radar and patients receive ongoing treatment.

Thus, she advised the public to go for early screening if they are experiencing any of the diseases' symptoms.

“Not to worry, the treatment is available nationwide in all general hospitals and there are adequate specialist doctors to cater to the needs of patients," ensured

Symptoms

Dr Rosmawati later pointed out that in general, there are four common symptoms of the hepatitis diseases. Among others, she said the four would be jaundice, loss of appetite, fatigue and muscle aches.

"Jaundice would be a classic symptom of hepatitis, whereby it happens due to the accumulation of a chemical called bilirubin in the body's tissues. The liver usually processes this chemical as a waste product, but when the liver is damaged it's unable to do its normal job and the chemical accumulates in the blood and starts to leak out into the body tissue.
"When enough of this chemical accumulates it's possible to see yellow tinge in the skin, urine and especially, around the whites of the eyes," she said.

Other than that, Dr Rosmawati, also the Chairperson of the Malaysian Campaign on World Hepatitis Day 2012, said patients would also experience loss of appetite, where sometimes it lasts for a very short time before being replaced by nausea and vomiting.

The patient would also feel debilitating effects of tiredness due to liver damages and also muscle and joint aches which could last from days to weeks, she said.

The symptoms might be minor, but she added that 25 per cent of adults who are chronically infected with HBV from childhood will develop liver cancer and for those with HCV, up to 70 per cent of chronically-infected persons will develop liver disease, 20 per cent develop cirrhosis and up to five per cent die from it.

Lack of awareness

The lack of awareness among the people, which is not at a conforming level today, puts the disease at higher risk of being registered as an epidemic.

According to the Health Minister of Malaysia, Datuk Seri Liow Tiong Lai, in five years before last year, the prevalence of hepatitis disease in the country, particularly type B and C, is estimated to be around three to six per 100,000 people.

A total of 640 hepatitis B and 724 hepatitis C patients were recorded in 2010, whilst the number almost doubled last year with 1,250 for hepatitis B and 1,047 for hepatitis C.
Liow said the number had only increased almost two-fold due to the free-screening programmes held by the ministry in 2010, and the number is expected to increase further if the health screening is taken up by more people with the disease's symptoms.

Liow also pointed out that the disease has managed to stay out of the ministry's radar for far too long and has been neglected, even though the notification of it is mandatory under the 'Prevention and Control of Infectious Disease Act 1988.

World Hepatitis Day Malaysia 2012

Seeing the lack of awareness about these diseases among the public, especially of hepatitis B and C, Dr Rosmawati and her colleagues started an awareness campaign on their own in 2010, alongside World Hepatitis Day which was assigned by WHO every July 28.

"The main objective of the campaign was to remedy the situation," she said. Other than enhancing hepatitis awareness, the campaign with the theme of 'It's closer than you think' was also focusing on early diagnosis, prevention and treatment of hepatitis C.

"For this year, a three-day campaign was held at One Utama Shopping Complex together with 20 hospitals nationwide participating in the campaign, which provide free hepatitis screenings," she said.

But for those who missed it, Dr Rosmawati said the UMMC is still offering free hepatitis screening all year, for those who are at high-risk.

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A Day with HIV

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By Gay TodaySeptember 13, 2012

Each day across the globe almost 7,000 people, including 900 children, will contract HIV, joining an estimated 34.2 million people already living with HIV. During any 24 hours more than 4,600 people around the world will die of an AIDS-related cause.

But on one day, Friday, September 21, people everywhere, both HIV positive and negative, can share an image of coping and care through the lens of a camera.

On that day, Positively Aware (www.positivelyaware.com ), is asking people to take a digital photograph to record a moment of their day that will focus the world’s attention on the daily trials and triumphs of people living with HIV. For the third year A Day with HIV (www.adaywithhiv.com ) will help remove the stigma of HIV and to advance an international community of care through this collective photographic portrait.

On Friday, September 21 anyone can record a special image, a time with friends and family, at work or play, or any moment in the day that helps people better understand how HIV impacts people, loved ones, colleagues and communities. Photos need to be submitted by Tuesday, September 25 on the A Day with HIV web site. People can follow A Day with HIV’s Facebook page (www.facebook.com/ADayWithHIV )) or on Twitter @A_Day_With_HIV (https://twitter.com/a_day_with_hiv) to see updates and selected photographs, and to share the site and its vision with friends to help spread the word.

Here is the link to the full press release about A Day with HIV.

http://www.adaywithhiv.com/images/2012/gallery/mediaKit/ADWHIV_press_release_2012-08-27.pdf

Kim Novino
Bridgeman Communications
(for A Day With HIV)
P: 508-695-9192
E: kim@bridgeman.com

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PRESS RELEASE

Sept. 14, 2012, 9:00 a.m. EDT

Preeminent Liver Expert Dr. Baburao Koneru to Serve as Principal Investigator

PARAMUS, N.J., Sep 14, 2012 (BUSINESS WIRE) -- Proteonomix, Inc. (otc/bb:PROT), a biotechnology company focused on developing therapeutics based upon the use of human cells and their derivatives, today announced it has entered into an agreement with Piscataway, N.J.-based University of Medicine and Dentistry of New Jersey (UMDNJ) to conducted a Phase 1 clinical trial with its proprietary, patent-pending mobilization technology UMK-121 in patients with end-stage liver disease (ESLD). The Company also announced that Chief Executive Officer Michael Cohen made a presentation at the National Investment Banking Association's (NIBA) 123rd Investment Conference yesterday at the New York Marriott Downtown in New York City.

The single-center Phase 1 clinical trial, Mobilization of Stem Cells with UMK 121 in Patients with Cirrhosis, will enroll 15 patients with ESLD. The trial will study the safety of mobilization of stem cells in this patient population, as well as the effects of mobilization of stems cells from bone marrow to the peripheral circulation on liver function. Baburao Koneru, M.D., Professor and Chief of the Division of Transplant and Hepatobiliary Surgery at New Jersey Medical School, will serve as the trial's principal investigator.

"We are extremely pleased to announce that our trial will be conducted at this highly respected institution under the direction of Dr. Koneru, who is a renowned expert in the field of liver function," said Mr. Cohen. "Our presentation to the investment professionals attending the NIBA conference provided an opportunity to discuss the potential of UMK-121 in ESLD as we make preparations to commence this clinical trial, which we hope to initiate in the coming months."

UMK-121 combines two existing FDA-approved drugs with the intention of mobilizing mesenchymal stem cells from bone marrow to the peripheral circulation. This proprietary drug combination is designed to reduce inflammation and increase angiogenesis to restore liver function, potentially extending the life of ESLD patients awaiting liver transplant.

About the University of Medicine and Dentistry of New Jersey

The University of Medicine and Dentistry of New Jersey (UMDNJ) is New Jersey's only health sciences university with more than 6,000 students on five campuses attending three medical schools, the State's only dental school, a graduate school of biomedical sciences, a school of health related professions, a school of nursing and New Jersey's only school of public health. UMDNJ operates University Hospital, a Level I Trauma Center in Newark, and University Behavioral HealthCare, which provides a continuum of healthcare services with multiple locations throughout the State.

About National Investment Banking Association (NIBA)

NIBA is the only national not-for-profit trade association of regional and independent brokerages, investment banking firms, institutional investors and related capital market service providers. Since its inception, NIBA member firms have successfully completed more than 1,000 equity offerings totaling approximately $10 billion in new capital. The member firms of NIBA represent more than 8,000 registered representatives with an estimated $78 billion in assets under management, and are responsible for 90% of all Initial Public Offerings under $20 million. For more information, please visit www.nibanet.org .

About Proteonomix, Inc.

Proteonomix is a biotechnology company focused on developing therapeutics based upon the use of human cells and their derivatives. The Proteonomix family of companies includes Proteoderm, StromaCel, PRTMI and THOR Biopharma. Proteoderm is a wholly owned subsidiary that has developed an anti-aging line of skin care products. StromaCel develops therapeutic modalities for the treatment of cardiovascular disease and plans to file an IND application for treatment of patients who have suffered post-myocardial infarction. Proteonomix Regenerative Translational Medicine Institute, Inc. (PRTMI) intends to focus on the translation of promising research in stem cell biology and cellular therapy to clinical applications of regenerative medicine. Additional information is available at www.proteonomix.com and www.proteoderm.com .

Certain statements contained herein are "forward-looking statements" (as defined in the Private Securities Litigation Reform Act of 1995). Proteonomix, Inc. cautions that statements made in this press release constitute forward-looking statements and makes no guarantee of future performance. Actual results or developments may differ materially from projections. Forward-looking statements are based on estimates and opinions of management at the time statements are made.

SOURCE: Proteonomix, Inc.

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HIV vaccine trials struggle to enrol women

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Researchers want more women to enrol in HIV/AIDS vaccine trials. Jenny Matthews / Panos Pictures

Lack of testing could make potential HIV vaccine less effective for women, say researchers.

Esther Nakkazi

13 September 2012

An article by SciDev.Net

[BOSTON] A low number of women participating in clinical trials of HIV/AIDS vaccines in developing countries is continuing to frustrate scientists' efforts to tell whether they are effective in protecting women.

On average, only about a fifth of the participants in phase I and II HIV vaccine trials in most sites in Africa are women, yet they bear a bigger burden of the epidemic, the AIDS Vaccine 2012 conference heard this week in Boston, United States (9–12 September).

"We could end up with a vaccine that we can only say elicits a good immune response in men," said Hannah Kibuuka, director of the Makerere University Walter Reed Project (MUWRP), an HIV vaccine development group in Uganda. "We will not know if it works equally well in women."

More women than men are infected with HIV, they have a higher viral load and their immune response could be different.

Merlin Robb, clinical deputy director of the US Military HIV Research Program, said that although African women attend screening, they tend not to enrol in trials.

One reason, he said, is that trials require women to use contraceptives and not fall pregnant, but most women eligible for trials are usually within the reproductive age.

They may also be more influenced than men by their peers, and many live in societies where they have to seek consent from their partners and parents to take part in a trial, Robb said.

Danielle Poole, a researcher who has worked on human papillomavirus (HPV) vaccine trials in Mali, added evidence about barriers to consent. Most of the women, even adults, said they had to get consent from their parents or parents, and most were not willing to participate in HPV trials.

"If it were an HIV vaccine site, I would imagine it would be very similar because both are sexually transmitted diseases," Poole said.

The high number of necessary visits to health centres by women participating in trials may also be an obstacle. For instance, women who participated in the CAPRISA 004 microbicide trial in South Africa had to make 22 visits to the site, and undergo seven internal examinations, in 18 months, researchers said.

The conference was attended by more than 1,100 researchers, funders and policymakers and included more than 440 presentations on the latest in HIV vaccine research.

Nature doi:10.1038/nature.2012.11415

This article was originally published by SciDev.Net on 12 September 2012.

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Hep C concerns for HIV positive men

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Posted on 14 September 2012

An Australian expert has called for an urgent rethink on the relationship between HIV and Hepatitis C (HCV) as emerging evidence shows hepatitis C can be sexually transmitted between HIV-positive men.

It is estimated up to 30 percent of HIV positive men will also have HCV.

Royal Melbourne and Alfred hospitals Associate Professor Joe Sasadeusz said sexual transmission of HCV in HIV-positive men who have sex with men had been increasingly reported in several case series during the past decade.

He urged education for at-risk communities and the development and promotion of effective prevention strategies.

While sharing injecting drug equipment is the main cause of transmission, HCV transmission in the absence of injecting drug use was an emerging problem for HIV-positive men who had sex with men.

“There is an urgent need for education of the at-risk community and to develop and promote effective prevention strategies to this population,” he said.

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What to do with a positive hep C test

Lynn Rapsilber, MSN, ANP-BC, APRN

September 13, 2012

According to the CDC, there are approximately 180 million hepatitis C antibody-positive individuals worldwide, 4.1 million of which reside in the United States. With 3 to 4 million new cases diagnosed per year, hepatitis C is among the fastest growing illnesses.

There are more than 7 million carriers of the hepatitis C virus (HCV) and 2.7 million chronically infected individuals. Approximately 12,000 people die from hepatitis C every year. The highest prevalence of the disease is among those aged 30 to 54 years.

Hepatitis C is often not recognized until asymptomatic persons are identified as HCV-positive. Blood testing, first made available in 1992, is the only way to determine that an individual has hepatitis C. The treatment goal is viral eradication. If eradication cannot be accomplished, clinicians must slow disease progression, improve histology, decrease the risk of hepatocelluar carcinoma and improve quality of life.

Who is at risk?

Hepatitis C (Flaviviridae hepacivirus) is a small, enveloped, single-stranded RNA virus. This virus mutates rapidly, so changes in the envelope proteins may help it invade the immune system. The virus does not incorporate itself into the host DNA, resulting in the ability to cure the infection indefinitely.

Acute hepatitis C refers to the first six months after infection. Between 60% and 70% of individuals infected with HCV develop no symptoms during this acute phase. In the minority of patients, acute-phase symptoms may be mild and nonspecific. Approximately 55% to 85% of acute hepatitis C patients will remain infected. Signs and symptoms of acute hepatitis C infection include fatigue, fever, dark urine, clay-colored stools, abdominal pain, loss of appetite, nausea, vomiting, joint pain and jaundice.

Hepatitis C can also be chronic and cause chronic liver disease that ranges from mild to severe, including cirrhosis and liver cancer. Liver disease associated with chronic hepatitis C is usually insidious and progresses slowly without any signs or symptoms for several decades.

HCV can be transmitted through a variety of ways, including:

  • Transfusions and organ transplants before 1992
  • IV drug use
  • Intranasal cocaine use
  • Sharing personal items with an infected person (e.g., razors, shavers, and toothbrushes)
  • Tattooing and body piercing
  • High-risk sexual activity
  • Clotting factors before 1987
  • Occupational exposures (health-care professionals)
  • Mother-to-infant transmission (rare but still considered a risk).

Testing and screening

HCV antibody testing is sensitive and inexpensive. Anti-HCV screening assays include the enzyme immunoassay (EIA) or the enhanced chemiluminescence immunoassay (CIA). Positive results are reportable and should be confirmed with a repeat test. The recombinant immnunoblot assay (RIBA), a more specific serologic anti-HCV assay, is no longer used. Once the antibody test is positive, HCV-polymerase chain reaction (PCR) RNA test measures how much HCV is in the bloodstream.

The American Association for the Study of Liver Disease (AASLD) recommends that all persons be screened for behaviors that place them at risk for hepatitis C infection as part of comprehensive health screening. Universal testing is not required at this time. The groups that are most strongly recommended for testing include:

  • Recent and current injection drug users (even if they have only used once)
  • HIV-infected individuals
  • Hemodialysis recipients
  • Hemophilia patients who received clotting factor concentrates before 1987
  • Patients with unexplained elevated liver abnormalities
  • Recipients of organ transplant or transplantation before July 1992
  • Children born to women infected with hepatitis C
  • Health-care workers who have had a needle exposure
  • Current sexual partners of individuals with hepatitis C
  • Persons who have used illicit noninjectible drugs (e.g., intranasal cocaine).

In addition to the viral load measurement or the PCR RNA testing, genotyping should also be performed. Of the six genotypes, genotypes 1, 2 and 3 are the most common in the United States.

Consequences of hepatitis C

Some of the consequences of chronic hepatitis C include hepatic fibrosis, cirrhosis, hepatocellular carcinoma, end-stage liver disease requiring transplantation and various extra-hepatic manifestations.

Hepatitis C causes inflammation of the tissue, resulting in fibrosis, which leads to scarring. This affects liver function, which further progresses the scarring to cirrhosis, eventually leading to liver failure and ultimately transplant. About 30% of those with hepatitis C will experience liver scarring leading to potential cirrhosis. Hepatocellular carcinoma occurs in about 3% of the population infected with hepatitis C. This incidence has increased over the past two decades and is identified through imaging studies or jaundice and in elevated alpha-fetoprotein levels in the blood. Surgical resection or ablative procedures increase the chance for cure.

Extra-hepatic manifestations of hepatitis C include:

  • Hematologic (anemia, and lymphoma)
  • Dermatologic (lichen planus and vasculitis)
  • Renal (glomular nephritis and nephritic syndrome)
  • Endocrine (hypothyroidism and diabetes)
  • Neuropsychiatric disease
  • Ocular (corneal ulcer and uveitis)
  • Vascular (polyarteritis nodosa and necrotizing vasculitis)
  • Neuromuscular (arthralgias and arthritis)
  • Autoimmune (CREST syndrome).

Transmission

Avoiding transmission to others is one of the best ways to contain the spread of the infection. Advise individuals with hepatitis C to: avoid sharing toothbrushes, shaving equipment, razors, nail files, and clippers; avoid tattoos and body piercings; do not donate blood, organ tissue or semen; cover bleeding wounds to prevent contact with others; discontinue illicit drug use; do not share needles. Because of the low sexual transmission rate, barrier protection is not needed in monogamous relationships; otherwise, safe sex practices are warranted.

Alcohol and hepatitis C

The effects in alcohol and hepatitis C are well documented. Alcohol consumption of greater than 50 g per day clearly increases the progression of hepatitis C fibrosis. Daily consumption of less than 50 g appears to increase hepatitis C PCR RNA viral load levels.

Treatment eligibility

The AASLD recommends that all patients with chronic hepatitis C be considered candidates for treatment. Review all risks and benefits with the patient. Treatment is based on histology, symptoms, probability of viral eradication, and progression of disease -- not just the alanine aminotransferase levels. Treatment is contraindicated in patients with:

  • Major uncontrolled depression
  • Solid organ transplant (e.g., renal, heart, or lung)
  • Autoimmune hepatitis and other autoimmune conditions that could be worsened by treatment
  • Undiagnosed and untreated thyroid disease
  • Pregnancy unwillingness to comply with contraception
  • Severe hypertension, congestive heart failure, coronary artery disease, diabetes, and chronic obstructive pulmonary disease that is not well controlled

Hypersensitivity to any of the treatment medications (i.e., peginterferon alfa-2a [Pegasys] and alfa-2b [PEG-Intron], ribavirin [Copegus, Rebetol, RibaTab, Ribasphere], telaprevir [Incivek], Boceprevir [Victrelis]).

Work-up

The initial work-up of hepatitis C should include a complete medical, family, and social history; depression scale; and laboratory testing (Table 1). With the advent of the protease inhibitors (PIs), liver biopsy is not required; however, if a patient is considering treatment and unsure whether or to proceed, a biopsy can document what liver damage has occurred and determine the grade of inflammation and the stage of liver fibrosis.

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Dental work must be completed prior to treatment. Vaccination for hepatitis A and B should be initiated and should not delay the start of treatment.

Predictors of treatment response include age (younger individuals have greater likelihood of response), sex (both males and females are at the same rate of treatment response), race (blacks respond less favorably to treatment than whites), and weight (higher BMI, insulin resistance, and fatty liver can hinder the ability to process medications that can help treatment response). Severe depression and anxiety and continued drug and alcohol use will impact the ability of the medications to be effective in cure. HIV-positive individuals who are co-infected with hepatitis C respond less favorably to treatment.

Treatment response

Treatment response for hepatitis C is measured by viral response. Rapid viral responders have no measurable virus at four weeks. Early viral responders have a >2 log drop at four weeks and no measureable virus at 12 weeks. Slow viral responders are not negative at week 12 but turn negative at week 24. Null responders have <2 log drop in viral load. Sustained viral response is no measurable virus six months after treatment and is considered a cure.

Genotype used to be a factor in treatment response, but with the development of the new PIs, genotype 1 responses are equal to or comparable to genotype 2 and 3. The higher the viral load the greater the virus to be killed, which can impede response.

Adherence to treatment is favorable when there is a good patient/provider relationship; adequate support systems in place; compliance with follow-up instructions, appointments, and lab draws; belief on the part of the patient that treatment will be beneficial; completion of the treatment; and a thorough explanation of the costs associated with treatment (i.e., insurance co-payments, medications, prior authorization).

Treatment recommendations

The current treatment recommendations for hepatitis C are based on genotype. Individuals with genotype 2 HCV receive peginterferon and ribavirin. Peginterferon helps fight the virus in two ways: (1) it helps healthy cells defend themselves against the virus; and (2) it strengthens the immune response, which helps the T and B cells fight off the virus. Peginterferon alfa-2a and alfa-2b are administered as subcutaneous weekly injections.

Side effects of treatment include flulike symptoms, fatigue, headache, arthralgias and myalgias, fever and chills. Other potential symptoms include anemia, diarrhea, nausea, worsening depression, mood instability, injection-site reaction, weight change, alopecia and increased susceptibility to infections and insomnia.

Ribavirin is an antiviral that interferes with RNA metabolism and slows the growth of the virus when used together with peginterferon. Ribavirin is administered orally b.i.d. Side effects include nausea; hemolytic anemia; MI with anemia; and such pulmonary symptoms as dyspnea, infiltrate and pneumonitis. Ribavirin is teratogenic and can cause birth defects or death of an unborn child. Female partners and female partners of individuals being treated with ribavirin should not become pregnant during treatment or for six months after treatment has stopped.

Protease inhibitors

PIs represent the new class of hepatitis C treatment and give new hope for individuals infected with genotype 1 HCV. Eligibility includes those who are treatment-naïve, partial responders, relapsers and null responders. PIs are given in conjunction with peginterferon and ribavirin. The response rates are quite phenomenal: 80% in treatment-naïve individuals; 75%-85% in relapsers; 50% in partial responders; and even 30% in null responders. There are two PIs available at this time.

Boceprevir. This medication is given orally 800 mg (four 200-mg tablets) t.i.d., every eight hours with food. Treatment is initiated with a four-week lead-in period of peginterferon and ribavirin alone; the triple therapy with boceprivir begins at week 5.

Duration of boceprevir for treatment-naïve individuals depends on response. If a negative HCV PCR RNA is achieved at week 4, week 8, and week 12, treatments can cease at 28 weeks. Response-guided treatment (RGT) continues depending on whether the patient is below 100 IUs of viral load measurement at specific intervals. A treatment-naive patient detected at eight weeks and negative at 12 weeks will complete boceprivir at week 36 but continue the peginterferon and ribavirin for a total of 48 weeks.

Previous partial responders and relapsers get the four-week lead in of peginterferon and ribavirin, followed by triple therapy for at least 36 weeks if negative viral-load measurements are found at four, eight, 12, 24 and 36 weeks. A patient who had measurable viral load at week 8 but was below 100 IU/mL would continue treatment for a total of 36 weeks and then dual therapy with peginterferon and ribavirin for 48 weeks.

Null responders and all cirrhotic patients get a four-week lead-in, followed by triple therapy with boceprivir, peginterferon and ribavirin for a total of 44 weeks. Any time the viral load measurement is above 100 IU/mL, the treatment is discontinued.

Telaprevir. This medication is given orally 750 mg (two 375-mg tablets) t.i.d. every eight hours with a high-fat 20-gram snack. RGT for telaprevir includes starting with triple therapy. Therapy for treatment-naïve and previous relapsers includes all three medications up front (telaprevir, peginterferon and ribavirin) for a period of 12 weeks. Depending on response, the treatment can end as early as 24 weeks or may continue for up to 36 weeks. Patients with cirrhosis may benefit from a full 48-week course.

For a previous partial responder or null responder, prescribe triple therapy (telaprevir, peginterferon and ribavirin) for 12 weeks, followed by 36 weeks of peginterferon and ribavirin alone. If viral load is nondetected at week 4 and week 12, discontinue the telaprevir and continue the peginterferon and ribavirin for a total response-week duration of 24 weeks. If the viral load is detectable but below 1,000 IU/mL at week 4 and week 12, continue the treatment to week 12, and then order an additional 36 weeks of dual therapy with peginterferon and ribavirin for a total treatment duration of 48 weeks. If at any time the viral load measurement goes above 1,000 IU/mL, at week 4, week 12, or detectable at week 24, the therapy is discontinued.

Managing side effects

Educate patients on the importance of adequate hydration and maximizing nutrition and energy-conservation strategies. If possible, clinicians should work with patient's employer to see about decreasing 12-hour shifts to eight hours to maximize energy conservation.

It is imperative that patients undergoing treatment for hepatitis C be able to continue to work, as this provide a distraction from the side effects of the medication. Counseling, patient support groups, or referral for professional help should also be considered.

Advise patients to use moisturizer to prevent rashes and dry skin. Alopecia can be minimized through less-frequent hair manipulation. Antiemetics for nausea, hematologic support for anemia and premedication with nonsteroidal anti-inflammatory drugs and alternating with acetaminophen for flulike symptoms is recommended.

During treatment monitoring, have patient visit every other week for side-effect management, counseling, and review of lab data. Viral load measurements throughout the course of treatment as described by the PI treatment algorithms are recommended and should be adhered to for the futility rules.

Above all, no PI should be stopped once it is started. The chance of developing resistance to these medications rapidly increases with the omission of even one dose. It is essential that all patients take peginterferon and ribavirin with these medications as well, and they are not interchangeable. Always stop the PI if the viral load measurement continues to increase.

Patient selection for antiviral therapy

For successful outcomes, it is imperative that clinicians spend the time up front to counsel and teach the patients and their families or supportive others. Explain that commitment requires the full duration of the treatment. Have patients sign a consent form agreeing to frequent blood testing, scheduled office visits, pregnancy prevention, and abstention from alcohol and drug use.

There is significant risk for medication reactions with PIs. A throughout medication review must be obtained before starting these drugs. Several medications are contraindicated, including simvastatin (Zocor), St. John's wort, and sildenafil (Viagra). Other medications require cautious use, including amlodipine (Norvasc), clarithromycin (Biaxin), methadone and zolpidem (Ambien). Please see the Victrelis and Incivek pagackage inserts for a complete list of potential drug interactions.

The goal with any of the treatments described is to support the patient through the process, foster a partnership in this unique opportunity to cure, and provide congratulations on the successes along the way.

Lynn Rapsilber, MSN, ANP-BC, APRN, is a nurse practitioner with Litchfield County Gastroenterology in Torrington, Conn.

References

  1. Ghany MG, Strader DB, Thomas DL, et al. Diagnosis, management, and treatment of hepatitis C: an update. Hepatology. 2009;49:1335-1374.
  2. Strader DB, Wright T, Thomas DL, et al. Diagnosis, management, and treatment of hepatitis C. Hepatology. 2004;39:1147-1171.
  3. Victrelis (boceprevir) Package Insert. Merck & Co., Inc.; 2011.
  4. Incivek (telaprevir) Package Insert. Vertex Pharmaceuticals; 2011.

    All electronic documents accessed September 13, 2012.

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