Updated on: 16/08/2010
Miami University team to train local doctors
Dr Hussein Hayati is a liver, pancreas and organ transplantation specialist. Along with his team of surgeons and hospital officials, he is working on starting liver transplantation in Kuwait; a process he says is much needed in the country.
Fortunately, he and his team are on the verge of finalizing an agreement with an American team from the university of Miami and a liver transplant unit has been established at the Amiri Hospital currently catering to cancer surgeries and surgical diseases related to the liver, pancreas and the biliary system. These surgeries have also only begun to be performed in Kuwait.
“Kuwait is in need of liver transplantation and we have the facilities to establish this system and if we work hard on deceased donation, we can do 15 to 20 if not more liver transplantation a year. This may reduce the number of people going outside and reduce the costs. A liver transplantation can cost a person a minimum of one million dollars abroad. Liver transplantation will be free of charge here; the expenses will be for the investigations only,” said Dr Hayati.
He added that liver transplantation, procedures are necessary as currently doctors are loosing patients who could have been saved, especially young patients who are nationals and non-nationals.
Q: What does liver transplantation consist of?
A: Liver transplantation is like any other organ transplantation,transferring an organ or organ tissue from a donor to a recipient. It is done in two ways, either you take the liver from a deceased person or brain-dead person or you take it from a living donor who could be a relative or someone with matching criteria.
The diseased liver of the recipient could also be replaced by a piece of liver from the donor. We connect this piece of liver to the recipient and with time the liver grows into almost the size of the liver that he or she needs.
Q: What is the criteria for being a recipient or a donor?
A: Liver transplant is done on those who have liver cirrhosis or liver failure. Liver cirrhosis is the end result for any chronic disease that affects the liver. The most common liver diseases are viruses; we have Hepatitis C and Hepatitis B. They cause chronic illnesses and inflammation which will result is cirrhosis, which means the liver tissue will be replaced by fibrous tissue that is inactive.
There are other causes of chronic liver illness such as alcohol consumption, which is the second common cause for liver failure in the world. Then we have hereditary causes and congenital causes. Either you have enzymatic deficiencies or metabolism problems which these days affect children. However, the most common causes are Hepatitis and alcohol.
Q: What are the most commonly used techniques for liver transplantation?
A: Liver transplantation is done surgically, either transplanting a complete liver or a piece of liver. The techniques for both surgeries are the common. However, if you take the liver from a liver donor it is more time consuming and needs a lot of work because you will end up with two rooms, one for the donor and one for the recipient.
The donor will be under anesthesia and a team will work on him or her to take a piece of liver. Sometimes you need a small piece and sometimes you need a bigger piece. The bigger piece is taken from the right lobe of the liver in adults. In pediatrics, we can take segments. The liver has eight segments and these segments are divided into two lobes anatomically.
That’s why I mentioned piece of liver, cause it could be for a child, they take a segment or two segments of the liver. But if it is an adult, they take either the left or right side, but usually the right side.
The techniques of surgery are slightly different when a piece of liver from a live donor is taken because surgeons will be dealing with smaller liver tissue as well as smaller vessels and ducts that need to be connected. It is more time consuming, if liver is taken from a live donor.
Q: How successful is the live donor liver transplant surgery? How long does it take the recipient and the donor to recover?
A: Usually fit donors with no medical problems are chosen for the surgery, so that you don’t end up with problems during the anesthesia or after the surgery. Their hospital sty is usually five to seven days and then they are discharged. After that it takes three months for the liver to reform and grow to normal size, plus or minus ten percent, and it will appear that no surgery was ever performed.
The situation for the recipient is different and he will take more time to recover because the recipient has taken in a foreign organ to his system or body. He will end up taking medication to reduce his immunity, called immuno-suppressive medication. He will be taking four kinds of medication and then he will be discharged with three kinds which are, with time, withdrawn slowly. If the transplant is from a live donor, the liver will also grow to about normal size.
If a whole liver is transplanted, the recovery time and medications will be the same but the surgery itself is less complicated. The surgeon will be dealing with large structures, bigger vessels and ducts that drain the biliary system, so it is easier to connect the organ to the body.
The life expectancy of a liver transplant recipient depends on the cause of the liver cirrhosis or liver failure. It is divided into viral and non-viral. Viral diseases are Hepatitis B and Hepatitis C. Non-viral causes are alcohol, hereditary problems, congenital problems or enzymatic deficiencies, which is a congenital problem.
Recipients with non-viral liver failure have the best outcome than recipients with viral problems. That is because viruses can come back again when immunity is low and cause damage to the transplanted liver. That is why with the non-viral, we are talking about 95 percent, one year survival and we call it graft survival. It can reach to almost 80 percent, five year survival and ten years you can go to 70 percent.
Recipients with viral disease also divided into two categories; the ones with Hepatitis B and the ones with Hepatitis C. Hepatitis C is the worst because we do not have the proper anti-viral to counteract the effects of the virus.
After the first year of the transplant, there is a 60 percent chance the virus will reoccur. But the amount of damage varies, for some people within three months the liver is completely damaged and they need a re-transplantation. Some people can last for three, four or five years even without any problem.
On the contrary, we have certain antibodies and anti-viral for Hepatitis B. That is why the outcome for Hepatitis B is much better than Hepatitis C. The recurrence of Hepatitis B after transplantation in the transplanted liver is 11 percent. There used to be an 80 percent chance of recurrence, but due to the discover of the anti-viral and antibodies that are included in the treatment regiment, it lowered the chance of recurrence.
Q: Has liver transplantation ever been done in Kuwait?
A: Liver transplantation has not been done yet in Kuwait. We are on the verge of finalizing an agreement with an American team at the University of Miami. We already approached the team and they have visited Kuwait, but we are just waiting for the final agreement.
The team evaluated the facilities in Kuwait and has pointed out that we should start a liver transplant and liver surgery unit at the Amiri Hospital because, according to their evaluation, the Amiri Hospital has the best facilities such as a new ICU and new operating room to avoid infections in these kinds of cases.
Also, we have Al-Thunayan Gestural and Intestinal Center nearby so if we need intervention by endoscopies it is available.
It has been agreed upon by the heads of departments to locate that unite there and the services have already been opened up, but right now we are only doing specialized cancer surgery and operating on surgical diseases related to the liver, pancreas and the biliary system.
These surgeries have only begun to be performed in Kuwait. We have started doing them around a year ago but now we have a specialized place and a team and we are training the ICU and nursing staff to get used to these kinds of cases. We are getting transfers so far from three or four hospitals, excluding Mubarak Hospital.
We are performing one surgery a week because it is not a very common problem but the problem is still there and we are still new and people are still getting used to us. For example, we don’t get transfers for private hospitals, so we need to build a good reputation.
We have the support of the Ministry of Health because we have ministerial decree to establish the unit and to establish the referral system from other hospitals to this unit. So all these specialty surgeries related to the liver, pancreas and the biliary system are done in our unit.
Q: When do you expect liver transplantation to begin in Kuwait?
A: It depends when we get the agreement. There are certain financial issues not finalized yet, but hopefully by the end of this year or early next year.
Q: How necessary is liver transplantation in Kuwait?
A: It is very necessary and we need it. We are loosing patients and especially young patients who are nationals and non-nationals. The non-nationals have Hepatitis C more frequently and the nationals get Hepatitis B often and there are some cases of cirrhosis of an unknown origin, but it is non-viral and non-alcoholic, it can happen like that because there is an entity called idiopathic, we don’t know the cause. There is a small percentage of alcohol related cases as well.
Kuwait is in need of liver transplantation and we have the facilities to establish this system and if we work hard on deceased donation, we can do 15 to 20 if not more transplantation a year. This may reduce the number of people going outside and this may also reduce the cost. A liver transplantation can cost a person a minimum of one million dollars abroad. Liver transplantation will be free of charge here; the expenses will be for the investigations only.
If the services are provided here, it will reduce the costs and it will be much more effective because we are losing young patients. Recently, only in the l last month, we lost an 18-year-old girl to chemical hepatitis. She took more herbal medication and she developed liver failure. She was put into intensive care and we rushed to send her abroad but we didn’t have enough time. She passed away before we were able to send her abroad.
If we had the liver transplant service here, we could have managed to rescue her. There were also similar cases like this one, we have another 28-year-old lady last year, a mother with three children, who took a medication for TB and had a bad reaction that ended with liver failure. We couldn’t save her live.
So the service has to be established and the MoH is working hard on that. They realized that we needed this. They have the expertise in all different specialties but it is just a matter or organization, plus they wanted an outside experienced team to come here so they will gain the trust of the people.
To be honest, there is a lack of trust in the medical services in Kuwait because of awareness problems and political issues. That is why the Minister of Health Dr Hilal Al-Sayer, made an excellent move by bringing in teams for the chest hospital, the cancer center and the transplant center because these are the three main areas we have not built upon in Kuwait. He provided the teams here so that there will be no excuse for going abroad.
Q: Do you have compiled donor list for liver transplantation?
A: We don’t have a donor list; we should have a recipient list according to blood group because evaluating a person consumes a lot of time and money. We cannot do that unless we reach an agreement and have a starting date. If this process takes longer, I have to evaluate the patient again because his status will change with time.
So if we reach an agreement and decide on a starting date, then we can arrange a list of people who are fit for transplants two months prior by contacting all the centers in Kuwait that deal with liver cirrhosis.
We already have 5,000 people with donation cards and their names are registered in Kuwait Society of Organ Transplantation but we are still working on the deceased donation list.
Any program in the world starts with deceased donation, because it is less complicated than living donation. You have to establish a good deceased donation program before you start a living donor program in case the living donors develop problems themselves or living donor transplantation surgeries go wrong.
Dr Mostafa Al-Mousawi is the head of the organ procurement department which started working toward this program in June and is developing a good system. Now we get a good number of reports from the ICUs, it is just that we need to convince the families to donate.
For example, someone who has had an accident and he is comatose in the ICU. We cannot take consent from him; we have to take consent from his family who may even not be in the country.
So the system is being established, it has been there for a long time and is the best system in the Gulf, but we had some drawbacks due to problems with the transplant coordinators. That is why we are sort of re-evaluating the system and the MOH promised to give us more facilities and to establish more teams.
The American team for liver transplantation will include not only surgeons, but physicians, anesthetists, radiologists and coordinators as well who will train out local coordinators. We will have an agreement to send our Kuwaiti coordinators to Miami to be trained and the non-Kuwaitis will be trained here by the Miami team.
So we will have coordinators with different nationalities to communicate with the families from all over the world, such as Egypt, Syria, India and Bangladesh.
Q: Have there been any unique surgeries done so far for the first time in the Gulf?
A: All what we are doing now is new in the Arabian Gulf and we did one case which was not done before in the ME, but these are not done frequently. We do surgeries for cancer of the liver, pancreas, gal bladder and biliary system or tumor and benign conditions that need surgery.
So far we did eight big surgeries since we started in June. We get referrals from different hospitals and some don’t need surgical intervention for the time being.
The case that we did that was unique is called ‘Synchronous Resection’ where we performed two surgeries at the same time on one patient. This patient had cancer of the colon that has spread to the liver. These surgeries are not frequently done because you need special situations and a dedicated and educated patient that can be aware of the risks.
You also need a two-team approach, a team that can handle the colon cancer and a team which can handle the liver, which was our team. When we evaluated the patient, who is 43 years old, we discovered that she had colon cancer and at the same time she had a big metastatic spread of the tumour to the liver. We decided to do the surgery and the patient had a smooth recovery and she was discharged home by day eight.
It is not the surgeries that matter it is the services that you have around. We had excellent ICU care at the Amiri Hospital, the team was superb. The nursing staff in the operating room was excellent as well. You cannot work alone; you need other services to support you and the patient. I hope in the future we get more referrals from different hospitals.
By: Nihal Sharaf
Source
August 16, 2010
Curing the incurable becomes a reality
Monday, 16 August 2010 15:00 Dr Nick Walsh .
“You’re negative,” I said and handed her the results. The smile turns to relief, then elation.
Years of living with the virus, six months of difficult treatment, then a six-month wait to see if the virus was completely eradicated.
She strode out of the consultation room and down the corridor clutching the vital result, with a spring in her step and renewed vitality. Along with the hepatitis C virus, the disease was now gone, as was the stigma. Normal life once again.
We live in world full of viruses – some well known, others not, still others awaiting discovery. They range from the irritating common cold to the devastating sociocultural phenomenon that is the human immuno-deficiency virus, or HIV.
The elusive nature of viruses have long defied medical science, none more so than viral hepatitis, which affects nearly half of the world’s population.
More than 500 million people are currently infected with some form of hepatitis.
Compare that with the 42 million worldwide now living with HIV – long considered a more lethal epidemic – and one can begin to grasp the scope and impact of hepatitis.
In addition to causing liver disease, hepatitis is also the most common cause of liver cancer. The virus falls into a series of alphabetical categories, with hepatitis A and B the most common, and treatable, forms.
Hepatitis C was discovered in 1989, and had been referred to prior to its identification simply as non-A, non-B hepatitis.
It is the most elusive and often deadly form of hepatitis, afflicting nearly 170 million people globally and claiming the lives of half a million people each year.
And until the late 1990s, there was no real hope of a cure. Progress has been steady since that time, and in 2010 we can almost refer to hepatitis C as a curable disease.
Just last year, the medical community watched transfixed as the latest drug trials for hepatitis C reported a 75 percent cure rate for a disease that has for so long defied treatment.
Hepatitis C, or HCV, behaves much like HIV by constantly changing to evade attack by the body’s immune system.
Interestingly, the body can clear the virus itself in about 25 percent of cases. This success rate depends on a number of factors, in particular a strong immune system. And unfortunately, up to 75 percent of those exposed to HCV see initial infection become chronic.
The time lag between initial infection and liver failure can be up to 25 years, so HCV remains largely a silent epidemic.
Most infections occur in the developing world, whereas treatment – often costing upwards of US$15,000 or more – is available mostly to people living in the developed world.
Fortunately, treatment for hepatitis C is available in Phnom Penh, and a number of people have already been cured. But the cost puts treatment out of reach for the more than half a million Cambodians living with the virus.
Successful trials have been achieved with a triple regimen of pegylated interferon, which boosts the immune system, and the antiviral drugs ribavirin and telaprevir. This cocktail saw a cure rate of 75 percent in trials reported recently in the New England Journal of Medicine.
A new antiviral drug, boceprevir, has also produced similar results.
Key to successful treatment is to attack the virus at multiple points in its life cycle in order to give the body’s immune system a better chance of destroying it.
The battle to eradicate hepatitis C is fierce, and it has attracted considerable investment by the pharmaceutical sector.
Not surprising, as 4 million Americans and a similar number of Europeans – as well as millions across developing Asia – are potential candidates for treatment.
Medical researchers are looking for the holy grail, a combination of tablets much like treatment for HIV, as well as a shortened treatment cycle, dropping from the current six to 12 months down to three or less.
Cost remains a crucial factor if the developing world is to benefit from recent and forthcoming breakthroughs.
However, greater awareness of the threat of hepatitis C, and now its potential cure, is vital, and community activists have begun the difficult task of spreading the word.
So the once incurable hepatitis C virus has become less elusive and in some cases curable, but like so many other things it depends on where and under what circumstances you live.
In the end, it will be the strength of the community voice to spur continued research and access to treatment that will ultimately help confine hepatitis C to history and save countless lives in the process.
Normal life once again.
Source
“You’re negative,” I said and handed her the results. The smile turns to relief, then elation.
Years of living with the virus, six months of difficult treatment, then a six-month wait to see if the virus was completely eradicated.
She strode out of the consultation room and down the corridor clutching the vital result, with a spring in her step and renewed vitality. Along with the hepatitis C virus, the disease was now gone, as was the stigma. Normal life once again.
We live in world full of viruses – some well known, others not, still others awaiting discovery. They range from the irritating common cold to the devastating sociocultural phenomenon that is the human immuno-deficiency virus, or HIV.
The elusive nature of viruses have long defied medical science, none more so than viral hepatitis, which affects nearly half of the world’s population.
More than 500 million people are currently infected with some form of hepatitis.
Compare that with the 42 million worldwide now living with HIV – long considered a more lethal epidemic – and one can begin to grasp the scope and impact of hepatitis.
In addition to causing liver disease, hepatitis is also the most common cause of liver cancer. The virus falls into a series of alphabetical categories, with hepatitis A and B the most common, and treatable, forms.
Hepatitis C was discovered in 1989, and had been referred to prior to its identification simply as non-A, non-B hepatitis.
It is the most elusive and often deadly form of hepatitis, afflicting nearly 170 million people globally and claiming the lives of half a million people each year.
And until the late 1990s, there was no real hope of a cure. Progress has been steady since that time, and in 2010 we can almost refer to hepatitis C as a curable disease.
Just last year, the medical community watched transfixed as the latest drug trials for hepatitis C reported a 75 percent cure rate for a disease that has for so long defied treatment.
Hepatitis C, or HCV, behaves much like HIV by constantly changing to evade attack by the body’s immune system.
Interestingly, the body can clear the virus itself in about 25 percent of cases. This success rate depends on a number of factors, in particular a strong immune system. And unfortunately, up to 75 percent of those exposed to HCV see initial infection become chronic.
The time lag between initial infection and liver failure can be up to 25 years, so HCV remains largely a silent epidemic.
Most infections occur in the developing world, whereas treatment – often costing upwards of US$15,000 or more – is available mostly to people living in the developed world.
Fortunately, treatment for hepatitis C is available in Phnom Penh, and a number of people have already been cured. But the cost puts treatment out of reach for the more than half a million Cambodians living with the virus.
Successful trials have been achieved with a triple regimen of pegylated interferon, which boosts the immune system, and the antiviral drugs ribavirin and telaprevir. This cocktail saw a cure rate of 75 percent in trials reported recently in the New England Journal of Medicine.
A new antiviral drug, boceprevir, has also produced similar results.
Key to successful treatment is to attack the virus at multiple points in its life cycle in order to give the body’s immune system a better chance of destroying it.
The battle to eradicate hepatitis C is fierce, and it has attracted considerable investment by the pharmaceutical sector.
Not surprising, as 4 million Americans and a similar number of Europeans – as well as millions across developing Asia – are potential candidates for treatment.
Medical researchers are looking for the holy grail, a combination of tablets much like treatment for HIV, as well as a shortened treatment cycle, dropping from the current six to 12 months down to three or less.
Cost remains a crucial factor if the developing world is to benefit from recent and forthcoming breakthroughs.
However, greater awareness of the threat of hepatitis C, and now its potential cure, is vital, and community activists have begun the difficult task of spreading the word.
So the once incurable hepatitis C virus has become less elusive and in some cases curable, but like so many other things it depends on where and under what circumstances you live.
In the end, it will be the strength of the community voice to spur continued research and access to treatment that will ultimately help confine hepatitis C to history and save countless lives in the process.
Normal life once again.
Source
Tackling cancer among poor doesn't have to cost dear
By Kate Kelland
LONDON
Sun Aug 15, 2010 7:04pm EDT
LONDON (Reuters) - The growing burden of cancer in developing countries could be reduced without expensive drugs and equipment, scientists said Monday, but it requires a global effort similar to the fight against HIV/AIDS.
In a study in the Lancet, scientists from the United States, who have formed a Global Task Force on Expanded Access to Cancer Care and Control in Developing Countries (GTF.CCC), said cancer is now a leading cause of death in poor nations but is often neglected in health authorities' prevention and treatment plans.
While only about 5 percent of global resources for cancer are spent in developing countries, the burden of the disease is far greater there than in rich nations, with up to 80 percent of cancer deaths each year occurring in poorer nations.
"Cancer is no longer primarily the burden of high-income countries," the scientists, led by Felicia Knaul of the Harvard Global Equity Initiative, wrote in the study. "The time has come to challenge and disprove the widespread assumption that cancer will remain untreated in poor countries."
They said many cancers that make up the greatest burden in low- and middle-income countries, such as breast cancer, could be treated with drugs that are off-patent and can be manufactured generically at affordable prices.
They cited the breast cancer drug tamoxifen as one example and said that in Malawi, Cameroon and Ghana the total cost of generic chemotherapy drugs with a 50 percent cure rate for a type of cancer called Burkitt's lymphoma could be as low as $50 per patient.
"These drugs should be a focus of cancer treatment programs, rather than expensive on-patent drugs," they wrote.
According to GTF.CCC, rates of cancer in low- and middle-income countries have increased dramatically from 1970, when they accounted for 15 percent of newly reported cancers, to 2008 when that figure rose to 56 percent. The proportion is expected to rise to 70 percent in 2030.
More efforts against smoking, a major risk factor for many cancers which threatens to cause a surge in cancer deaths in Africa in the next decade, would be one relatively cheap way of making an impact, they said, as would increasing awareness about the importance of early cancer detection and screening.
Another intervention with huge potential, they said, would be vaccination against human papillomavirus (HPV), to help prevent cervical cancer, and against hepatitis B virus (HBV), to help prevent liver cancer.
GlaxoSmithKline and Merck & Co make vaccines against HPV and many drugmakers have HBV vaccines but these are often too expensive to be included in the health programs of low- and middle-income countries, the scientists said.
The group criticized what it described as "the public health community's assumption" that cancer could not be treated in poor countries and compared it to "similarly unfounded arguments from more than a decade ago" about treatment for HIV and AIDS.
Major advances in prevention, health services and efforts to bring down drug prices have dramatically increased the number of people in poor countries who have access to HIV treatment.
Knaul's team said like HIV and AIDS, cancer was now "an urgent health and ethical priority" in developing countries.
(Editing by Janet Lawrence)
Source
LONDON
Sun Aug 15, 2010 7:04pm EDT
LONDON (Reuters) - The growing burden of cancer in developing countries could be reduced without expensive drugs and equipment, scientists said Monday, but it requires a global effort similar to the fight against HIV/AIDS.
In a study in the Lancet, scientists from the United States, who have formed a Global Task Force on Expanded Access to Cancer Care and Control in Developing Countries (GTF.CCC), said cancer is now a leading cause of death in poor nations but is often neglected in health authorities' prevention and treatment plans.
While only about 5 percent of global resources for cancer are spent in developing countries, the burden of the disease is far greater there than in rich nations, with up to 80 percent of cancer deaths each year occurring in poorer nations.
"Cancer is no longer primarily the burden of high-income countries," the scientists, led by Felicia Knaul of the Harvard Global Equity Initiative, wrote in the study. "The time has come to challenge and disprove the widespread assumption that cancer will remain untreated in poor countries."
They said many cancers that make up the greatest burden in low- and middle-income countries, such as breast cancer, could be treated with drugs that are off-patent and can be manufactured generically at affordable prices.
They cited the breast cancer drug tamoxifen as one example and said that in Malawi, Cameroon and Ghana the total cost of generic chemotherapy drugs with a 50 percent cure rate for a type of cancer called Burkitt's lymphoma could be as low as $50 per patient.
"These drugs should be a focus of cancer treatment programs, rather than expensive on-patent drugs," they wrote.
According to GTF.CCC, rates of cancer in low- and middle-income countries have increased dramatically from 1970, when they accounted for 15 percent of newly reported cancers, to 2008 when that figure rose to 56 percent. The proportion is expected to rise to 70 percent in 2030.
More efforts against smoking, a major risk factor for many cancers which threatens to cause a surge in cancer deaths in Africa in the next decade, would be one relatively cheap way of making an impact, they said, as would increasing awareness about the importance of early cancer detection and screening.
Another intervention with huge potential, they said, would be vaccination against human papillomavirus (HPV), to help prevent cervical cancer, and against hepatitis B virus (HBV), to help prevent liver cancer.
GlaxoSmithKline and Merck & Co make vaccines against HPV and many drugmakers have HBV vaccines but these are often too expensive to be included in the health programs of low- and middle-income countries, the scientists said.
The group criticized what it described as "the public health community's assumption" that cancer could not be treated in poor countries and compared it to "similarly unfounded arguments from more than a decade ago" about treatment for HIV and AIDS.
Major advances in prevention, health services and efforts to bring down drug prices have dramatically increased the number of people in poor countries who have access to HIV treatment.
Knaul's team said like HIV and AIDS, cancer was now "an urgent health and ethical priority" in developing countries.
(Editing by Janet Lawrence)
Source
August 15, 2010
The promise of an unlimited supply for transfusions
Steve Connor: The promise of an unlimited supply for transfusions
By Steve Connor
Monday, 16 August 2010
More than two million units of blood – some 250,000 gallons – are handled by the transfusion service each year. Yet shortages can and do happen, especially around holiday periods and special events, such as the recent World Cup, when many donors stayed at home.
But one of the greatest problems facing the transfusion service is the growing menace of new infectious agents which can pass undetected into the blood supply. Hepatitis C, HIV and more recently the infectious "prion" behind Creutzfeldt-Jacob disease have all emerged in the population before there was a reliable blood test to screen donated blood.
The issue of emerging infections is likely to get worse with greater international travel and the continued encroachment of humans on the wild places where many of these animal-borne diseases lurk in their natural reservoirs. West Nile virus, for example, is passed on by mosquitoes, but in 2002 the first cases in the US occurred as a result of transmission from infected blood donors.
Developing safe, synthetic alternatives to blood is not, therefore, of simple academic interest. The central function of red blood cells is to carry oxygen around the body and for many decades scientists have laboured over potential alternatives to living red blood cells, from oxygen-carrying chemicals known as perfluorocarbons to the use of the natural oxygen-carrying pigment, haemoglobin.
None of these approaches has really proved a success. However, the manufacture of "synthetic" red blood cells derived from embryonic stem cells makes perfect logical sense. The red blood cell is the vehicle the body uses to oxygenate the tissues and everything we know of embryonic stem cells suggests they can be made to produce red cells. Stem cells from four-day-old spare IVF embryos are also likely to be free of infectious diseases.
Scientists have shown already that mature red blood cells can be made from the adult blood stem cells found in the bone marrow, although these stem cells have limited ability to replicate. Stem cells derived from embryos, however, can multiply ad infinitum, meaning that in theory just one "universal donor" of blood type "O-negative" could supply the country's entire needs.
Source
By Steve Connor
Monday, 16 August 2010
More than two million units of blood – some 250,000 gallons – are handled by the transfusion service each year. Yet shortages can and do happen, especially around holiday periods and special events, such as the recent World Cup, when many donors stayed at home.
But one of the greatest problems facing the transfusion service is the growing menace of new infectious agents which can pass undetected into the blood supply. Hepatitis C, HIV and more recently the infectious "prion" behind Creutzfeldt-Jacob disease have all emerged in the population before there was a reliable blood test to screen donated blood.
The issue of emerging infections is likely to get worse with greater international travel and the continued encroachment of humans on the wild places where many of these animal-borne diseases lurk in their natural reservoirs. West Nile virus, for example, is passed on by mosquitoes, but in 2002 the first cases in the US occurred as a result of transmission from infected blood donors.
Developing safe, synthetic alternatives to blood is not, therefore, of simple academic interest. The central function of red blood cells is to carry oxygen around the body and for many decades scientists have laboured over potential alternatives to living red blood cells, from oxygen-carrying chemicals known as perfluorocarbons to the use of the natural oxygen-carrying pigment, haemoglobin.
None of these approaches has really proved a success. However, the manufacture of "synthetic" red blood cells derived from embryonic stem cells makes perfect logical sense. The red blood cell is the vehicle the body uses to oxygenate the tissues and everything we know of embryonic stem cells suggests they can be made to produce red cells. Stem cells from four-day-old spare IVF embryos are also likely to be free of infectious diseases.
Scientists have shown already that mature red blood cells can be made from the adult blood stem cells found in the bone marrow, although these stem cells have limited ability to replicate. Stem cells derived from embryos, however, can multiply ad infinitum, meaning that in theory just one "universal donor" of blood type "O-negative" could supply the country's entire needs.
Source
Liver Cancer - Related to Hepatitis B Carrier State?
August 15, 2010
Liver cancer refers to either primary liver cancer, that is cancer originating from the liver cells or supporting cells in the liver, or secondary liver cancer, that is cancer that has spread to the liver from the surrounding organs, usually via the blood that drains those organs and flow through the liver. In this article we shall confine ourselves to primary liver cancer, also referred to as hepatocellular carcinoma.
Liver cancer is one of the more commonly occurring cancers in the world, being the fifth most common cancer in men and the eighth most common cancer in women. The total number of new cases diagnosed is estimated to be about 500,000 every year. Men seem to be twice as likely as women to get liver cancer.
What could cause this problem?
The incidence of liver cancer seems to be higher in certain countries. Studies appear to indicate a positive relationship between the incidence of liver cancer and that of hepatitis B virus carrier states as well as hepatitis C virus infections. The risk of a hepatitis B carrier developing liver cancer is about 60 times higher than that of a non hepatitis B carrier. This risk appears to be even higher than the risk of a smoker developing lung cancer (about 20 to 25 times).
What countries have a higher incidence of hepatitis B carrier states? It is observed that certain countries seem to have a much higher incidence of hepatitis B carriers. One case in point is Taiwan, where it is noted that an abnormally high 20% of pregnant mothers were discovered to be carriers of hepatitis B. This compares significantly to the incidence of 1% in the United States. Similar studies show a higher incidence of hepatitis B carrier rates in South-East Asian countries, between 10% to 15%. This has led to the belief that Oriental persons are genetically less able to overcome the hepatitis B virus. This observation is supported by another observation, that the conversion rate to immunization with hepatitis B vaccine is lower in Chinese as compared with other races.
Studies also show that the incidence of new cases of primary liver cancer has decreased significantly in those countries where there has been a deliberate effort to immunize persons to hepatitis B with hepatitis B vaccine. This is one of the rare situations where there is a demonstrable cause/effect relationship, and where there is definite proof that a particular cancer can be prevented, by both vaccination and by screening of blood and blood products for hepatitis B and C viruses.
Other risk factors or suspected causes of liver cancer need to be mentioned here. They are:
Liver Cirrhosis. A situation of scarring of the liver due to chronic damage as a result commonly of heavy drinking. There is a slight increase of risk of liver cancer developing.
Inherited causes. Persons with hemochromatosis, a genetic problem of excess iron deposits in the body have a higher chance of developing liver cancer.
Aflatoxin. A mold found in bad peanuts and grain is a well known culprit in the causation of liver cancer.
Source
Liver cancer refers to either primary liver cancer, that is cancer originating from the liver cells or supporting cells in the liver, or secondary liver cancer, that is cancer that has spread to the liver from the surrounding organs, usually via the blood that drains those organs and flow through the liver. In this article we shall confine ourselves to primary liver cancer, also referred to as hepatocellular carcinoma.
Liver cancer is one of the more commonly occurring cancers in the world, being the fifth most common cancer in men and the eighth most common cancer in women. The total number of new cases diagnosed is estimated to be about 500,000 every year. Men seem to be twice as likely as women to get liver cancer.
What could cause this problem?
The incidence of liver cancer seems to be higher in certain countries. Studies appear to indicate a positive relationship between the incidence of liver cancer and that of hepatitis B virus carrier states as well as hepatitis C virus infections. The risk of a hepatitis B carrier developing liver cancer is about 60 times higher than that of a non hepatitis B carrier. This risk appears to be even higher than the risk of a smoker developing lung cancer (about 20 to 25 times).
What countries have a higher incidence of hepatitis B carrier states? It is observed that certain countries seem to have a much higher incidence of hepatitis B carriers. One case in point is Taiwan, where it is noted that an abnormally high 20% of pregnant mothers were discovered to be carriers of hepatitis B. This compares significantly to the incidence of 1% in the United States. Similar studies show a higher incidence of hepatitis B carrier rates in South-East Asian countries, between 10% to 15%. This has led to the belief that Oriental persons are genetically less able to overcome the hepatitis B virus. This observation is supported by another observation, that the conversion rate to immunization with hepatitis B vaccine is lower in Chinese as compared with other races.
Studies also show that the incidence of new cases of primary liver cancer has decreased significantly in those countries where there has been a deliberate effort to immunize persons to hepatitis B with hepatitis B vaccine. This is one of the rare situations where there is a demonstrable cause/effect relationship, and where there is definite proof that a particular cancer can be prevented, by both vaccination and by screening of blood and blood products for hepatitis B and C viruses.
Other risk factors or suspected causes of liver cancer need to be mentioned here. They are:
Liver Cirrhosis. A situation of scarring of the liver due to chronic damage as a result commonly of heavy drinking. There is a slight increase of risk of liver cancer developing.
Inherited causes. Persons with hemochromatosis, a genetic problem of excess iron deposits in the body have a higher chance of developing liver cancer.
Aflatoxin. A mold found in bad peanuts and grain is a well known culprit in the causation of liver cancer.
Source
Peginterferon Plus Ribavirin and Sustained Virological Response in HCV-Related Cirrhosis: Outcomes and Factors Predicting Response
Am J Gastroenterol advance online publication 10 August 2010; doi: 10.1038/ajg.2010.294
Conrado M Fernández-RodrÃguez MD 1, Sonia Alonso MD 1, Stella M Martinez MD 2, Xavier Forns MD 2, Jose M Sanchez-Tapias MD 2, Diego Rincón MD 3, Gil Rodriguez-Caravaca MD 1, Rafael Bárcena MD 4, Miguel A Serra MD 5, Manuel Romero-Gómez MD 6, Inmaculada Fernandez MD 7, Javier Garcia-Samaniego MD 8, Javier Fuente MD 9, Ricard Solá MD 10, Ricardo Moreno-Otero MD 11 and Ramón Planas MD 12 on behalf of the Group for the Assessment of Prevention of Cirrhosis Complications and Virological Response (APREVIR)
1 Hospital Universitario Fundación Alcorcón, Madrid, Spain
2 Hospital Clinic I Provincial, Badalona and IDIBAPS, Ciberehd, Badalona, Spain
3 Hospital Universitario Gregorio Marañón Ciberehd, Madrid, Spain
4 Hospital Ramón y Cajal, Madrid, Spain
5 Hospital ClÃnico Universitario, Valencia, Spain
6 Hospital de Valme Ciberehd, Sevilla, Spain
7 Hospital Universitario 12 de Octubre, Madrid, Spain
8 Hospital Carlos III Ciberehd, Madrid, Spain
9 Hospital Miguel Servet, Zaragoza, Spain
10 Hospital del Mar, Badalona, Spain
11 Hospital Universitario de La Princesa, Madrid, Spain
12 Hospital Germans Trias i Pujol, Ciberehd, Badalona, Spain
Correspondence: Conrado M. Fernández-RodrÃguez, MD, Hospital Universitario Fundación Alcorcón, Av Budapest-1, 28922, Madrid, Spain. E-mail: cfernandez@fhalcorcon.es
Received 4 September 2010; Accepted 11 March 2010; Published online 10 August 2010.
OBJECTIVES: Patients with hepatitis C virus (HCV) cirrhosis are difficult to treat and have a high risk of liver decompensation or hepatocellular carcinoma. We sought to identify factors that could predict treatment response.
METHODS: Collaborating centers (n=26) provided data for patients (n=568) with HCV cirrhosis undergoing treatment with peginterferon-α plus ribavirin (RBV). Univariate and multivariate analyses were used to evaluate factors predicting treatment outcomes.
RESULTS: Sustained viral response (SVR) in naive patients was 30.7%, with no significant differences between centers. Median follow-up was 35 months (range: 1–81). Factors predicting SVR were: non-genotype 1 (odds ratio (OR)=4.183; 95% confidence interval (CI): 2.353–7.438) overall dose and ≥80% of the scheduled time of treatment (OR=3.177; 95% CI: 1.752–5.760); serum γ-glutamyl transpeptidase (GGT) <76 IU per ml (OR=4.092; 95% CI: 2.418–6.927); baseline viral load <6 × 105 (OR=2.597; 95% CI: 1.583–4.262); absence of ultrasound signs of portal hypertension (OR=2.067; 95% CI: 1.26–3.39). No patient with a HCV-RNA decline <1 log10 at week 4 achieved SVR. Event-free survival at 5 years was 91% in patients with SVR vs. 59% in non-responders (P<0.001). Overall survival in patients with SVR was 98% vs. 86% in non-responders (P=0.005). Independent factors predicting events were absence of SVR (hazard ratio (HR)=2.66; 95% CI: 1.32–5.54), baseline serum albumin <3.9 g per 100 ml (HR=3.06; 95% CI: 1.81–5.15), presence of esophageal varices on endoscopy (HR=2.489; 95% CI: 1.546–4). Improved outcome was more evident in responders with less advanced disease at baseline.
CONCLUSIONS: SVR can be achieved in approximately one-third of patients with HCV-related cirrhosis. SVR independently reduces the likelihood of clinical decompensation and improves survival.
Source
Conrado M Fernández-RodrÃguez MD 1, Sonia Alonso MD 1, Stella M Martinez MD 2, Xavier Forns MD 2, Jose M Sanchez-Tapias MD 2, Diego Rincón MD 3, Gil Rodriguez-Caravaca MD 1, Rafael Bárcena MD 4, Miguel A Serra MD 5, Manuel Romero-Gómez MD 6, Inmaculada Fernandez MD 7, Javier Garcia-Samaniego MD 8, Javier Fuente MD 9, Ricard Solá MD 10, Ricardo Moreno-Otero MD 11 and Ramón Planas MD 12 on behalf of the Group for the Assessment of Prevention of Cirrhosis Complications and Virological Response (APREVIR)
1 Hospital Universitario Fundación Alcorcón, Madrid, Spain
2 Hospital Clinic I Provincial, Badalona and IDIBAPS, Ciberehd, Badalona, Spain
3 Hospital Universitario Gregorio Marañón Ciberehd, Madrid, Spain
4 Hospital Ramón y Cajal, Madrid, Spain
5 Hospital ClÃnico Universitario, Valencia, Spain
6 Hospital de Valme Ciberehd, Sevilla, Spain
7 Hospital Universitario 12 de Octubre, Madrid, Spain
8 Hospital Carlos III Ciberehd, Madrid, Spain
9 Hospital Miguel Servet, Zaragoza, Spain
10 Hospital del Mar, Badalona, Spain
11 Hospital Universitario de La Princesa, Madrid, Spain
12 Hospital Germans Trias i Pujol, Ciberehd, Badalona, Spain
Correspondence: Conrado M. Fernández-RodrÃguez, MD, Hospital Universitario Fundación Alcorcón, Av Budapest-1, 28922, Madrid, Spain. E-mail: cfernandez@fhalcorcon.es
Received 4 September 2010; Accepted 11 March 2010; Published online 10 August 2010.
OBJECTIVES: Patients with hepatitis C virus (HCV) cirrhosis are difficult to treat and have a high risk of liver decompensation or hepatocellular carcinoma. We sought to identify factors that could predict treatment response.
METHODS: Collaborating centers (n=26) provided data for patients (n=568) with HCV cirrhosis undergoing treatment with peginterferon-α plus ribavirin (RBV). Univariate and multivariate analyses were used to evaluate factors predicting treatment outcomes.
RESULTS: Sustained viral response (SVR) in naive patients was 30.7%, with no significant differences between centers. Median follow-up was 35 months (range: 1–81). Factors predicting SVR were: non-genotype 1 (odds ratio (OR)=4.183; 95% confidence interval (CI): 2.353–7.438) overall dose and ≥80% of the scheduled time of treatment (OR=3.177; 95% CI: 1.752–5.760); serum γ-glutamyl transpeptidase (GGT) <76 IU per ml (OR=4.092; 95% CI: 2.418–6.927); baseline viral load <6 × 105 (OR=2.597; 95% CI: 1.583–4.262); absence of ultrasound signs of portal hypertension (OR=2.067; 95% CI: 1.26–3.39). No patient with a HCV-RNA decline <1 log10 at week 4 achieved SVR. Event-free survival at 5 years was 91% in patients with SVR vs. 59% in non-responders (P<0.001). Overall survival in patients with SVR was 98% vs. 86% in non-responders (P=0.005). Independent factors predicting events were absence of SVR (hazard ratio (HR)=2.66; 95% CI: 1.32–5.54), baseline serum albumin <3.9 g per 100 ml (HR=3.06; 95% CI: 1.81–5.15), presence of esophageal varices on endoscopy (HR=2.489; 95% CI: 1.546–4). Improved outcome was more evident in responders with less advanced disease at baseline.
CONCLUSIONS: SVR can be achieved in approximately one-third of patients with HCV-related cirrhosis. SVR independently reduces the likelihood of clinical decompensation and improves survival.
Source
Cancer’s little helpers
Home / August 28th, 2010; Vol.178 #5 / Feature
Tiny pieces of RNA may turn cells to the dark side
By Tina Hesman Saey
August 28th, 2010; Vol.178 #5 (p. 18)
When tiny hairpin-shaped molecules act up, they don’t rebel loner-style like James Dean. Instead they take on the persona of Darth Vader, crushing proteins under their command and turning acquaintances to the dark side as well. In this case, though, the fight is for control not of the universe, but of the body. And a dark-side victory could end in cancer.
No one would have predicted a decade ago that these microRNAs, as the hairpins are called, were involved in cancer, because no one even knew that they existed in people. Mere snippets of RNA — DNA’s underappreciated cousin — these micromolecules are about 22 chemical letters long. But their size belies their power.
When on their best behavior, the molecules are competent and capable managers of the protein-building process that keeps a cell humming in perfect harmony. But when microRNAs go rogue, the results can be disastrous.
New research is revealing just how important these newly discovered molecules are. An imbalance of microRNAs can cause cancer by encouraging runaway cell growth or by dampening a cell’s defenses, and can also make the disease more stubborn. But just as Darth Vader never completely lost the young Jedi Anakin Skywalker within him, even bad microRNAs may have good in them yet. Some scientists think that therapies aimed at soothing riled-up microRNAs may help cure the very cancers that the molecules help cause.
Most of the discoveries linking microRNAs and cancer have come in the past five years. “This is extremely rapid progression,” says Curtis Harris, chief of the human carcinogenesis lab at the National Cancer Institute, based in Bethesda, Md.
Micro middle managers
The realization that such small molecules could play a big role in disease was late in coming, says Carlo Croce of Ohio State University in Columbus. “In the beginning there was no interest in microRNAs at all,” he says.
The first microRNA was discovered in 1993 in roundworms. It took another seven years before the next microRNA was found in the same organism. Though both of those microRNAs help control worm development, most scientists regarded them as biological curiosities.
But then researchers found microRNAs at work in fruit flies, people and other organisms. Those discoveries suggested that microRNAs might be important regulatory molecules for all animals, not just flukes of worm biology.
MicroRNAs work in middle management in most plant and animal cells, scientists now know. The molecules help regulate the protein-manufacturing process by essentially issuing permits decreeing when and where proteins may be built. By riding piggyback on messenger RNAs, which are copies of the protein-building blueprints contained within DNA, microRNAs prevent the instructions from reaching protein-building machinery inside cells.
While it may sound nefarious, microRNAs’ interference with protein production helps a cell maintain balance. MicroRNAs ensure that cells save energy by not making unnecessary proteins and help prevent levels of potentially harmful proteins, such as those that initiate the self-destruct program known as apoptosis, from reaching critical mass.
Each type of microRNA in a cell may potentially pair with hundreds of different types of messenger RNA, says Isidore Rigoutsos, a computational and molecular biologist at Thomas Jefferson University in Philadelphia. And each messenger RNA may have many different microRNAs piling on its back.
“It’s safe to say that microRNAs are important,” Rigoutsos says. “The difficulty is saying what are the limits of importance, and they keep being expanded more and more and more.”
Cancer connection
Croce’s lab was among the first to illustrate just how big a role the little molecules could play in people. His group showed that genes encoding microRNAs frequently go missing in tumor cells. In particular, two microRNAs, miR-15 and miR-16, are missing or found at lower than normal levels in 68 percent of chronic lymphocytic leukemia cases.
Cancer biologists usually lump microRNAs into two groups: those that protect against cancer and those that promote it (though the distinction isn’t perfect). Cancer cells tend to have lower levels of most microRNAs but have an oversupply of a few others.
In the protective corner are microRNAs such as miR-15 and miR-16. One of the many proteins regulated by those two microRNAs is BCL2, which keeps cells from pushing the self-destruct button. Cells commit suicide when they become too damaged to operate properly — an important self-defense mechanism for an organism that doesn’t want to walk around with malfunctioning cells. So cells need just the right amount of BCL2 to keep from killing themselves unnecessarily, but not so much of it that they can never die.
The microRNAs pair with messenger RNA to strike the right balance of BCL2. But when miR-15 and miR-16 levels are knocked down — which can happen if a copy of a gene is lost or if something goes wrong during microRNA manufacturing — cells make far too much BCL2, essentially disabling the self-destruct mechanism and making cells immortal. Immortality is one hallmark of cancer.
At the opposite end of the spectrum is one of the baddest microRNA bad boys, miR-21. Elevated levels cause cancer in mice, researchers from Yale University reported online August 8 in Nature. And higher than normal levels have been linked to at least 13 major types of cancer in people and to poor prognoses for people with colon, lung, breast, pancreatic or head and neck cancers, Harris says (SN: 2/2/08, p. 70).
High levels of miR-21 can slow an important cellular security system involving a protein named p53, researchers from the University of California, Santa Barbara have found. This protein performs multiple protective services, including spurring repair of damaged DNA, halting growth until damage is repaired or ending it all if repair isn’t possible (SN: 12/6/08, p. 22). Last year researchers reported in Nature that p53 helps slice microRNAs into their mature form. Too much miR-21 can strip cells of their p53 defenses, leading to cancer.
Though miR-21 has stood out among the troublemakers, Croce’s team has shown that this microRNA and others don’t work alone. The molecular managers are master networkers. In 50 different normal human tissues, microRNAs collaborate to direct cellular activities, Croce and colleagues reported online May 3 in Genome Research. The networks consist of microRNAs that help direct production of proteins, some of which, in turn, control production of other microRNAs, and so on.
But time and again, in 51 different types of cancer, Croce’s team found that the microRNAs’ teamwork had broken down. The cohesive networks disintegrated into rogue hubs of activity. These anarchist factions throw a wrench into the well-oiled machinery that usually keeps a cell healthy.
It’s a rather small wrench, though. MicroRNAs wield their power subtly, tweaking and massaging protein levels up or down a wee bit here and there instead of stopping production altogether.
“A microRNA doesn’t function like an ‘off’ switch,” says cancer biologist Dihua Yu of the University of Texas MD Anderson Cancer Center in Houston.
Even a little bump or dip in protein levels, maybe by just 5 to 10 percent, is enough to send a cell careening down the path to cancer, Croce says.
One of the most delicately balanced cancer-associated proteins is PTEN. It reins in cell growth to prevent wild replication, as seen in cancer. In the parlance of cancer research, PTEN is known as a tumor suppressor, and it works best when there is just the right amount of it.
Losing one copy of the gene for PTEN — essentially cutting protein levels in half — is enough to turn a cell cancerous, previous studies have shown. Other research has demonstrated that microRNAs, including miR-21, help govern production of PTEN. And a study reported June 24 in Nature found that a messenger RNA doppelgänger of PTEN found in healthy cells distracts PTEN-stifling microRNAs, allowing more of the protein to be made. If the twin is missing, the weight of microRNAs on messenger RNA’s back can crush protein production.
New research from Yu’s lab also suggests that reducing the amount of PTEN protein in a tumor cell even slightly is not a good idea. Higher levels of miR-21 slow down PTEN production and make breast cancer cells resistant to an anticancer agent called Herceptin, Yu and colleague Sumaiyah Rehman reported in April in Washington, D.C., at the annual meeting of the American Association for Cancer Research.
Dicer danger
PTEN isn’t the only protein that can make cancer worse. A new study shows that small changes in the amount of a protein involved in producing microRNAs can determine whether tumors stay put or spread to the rest of the body.
That discovery grew from efforts to figure out why most microRNAs are at lower levels in cancer cells but some microRNAs are overproduced. “We were intrigued by this paradox,” says Stefano Piccolo, a cellular and molecular biologist at the University of Padua in Italy.
The resolution came from an unexpected source, a protein that helps slice larger RNAs into microRNAs. This protein, Dicer, is a key component of the microRNA manufacturing machinery. Cutting levels of Dicer in half spurs on cancer because less of it leads to less microRNA, which can mean increased production of proteins that drive rapid growth. Still, cancer cells need some Dicer to survive and reproduce, since Dicer helps make microRNAs that regulate production of proteins.
So cancer cells need to control Dicer levels the way a student sets the volume on an iPod to provide background study music. The volume shouldn’t be too quiet or too loud. “You need to find that perfect middle,” Piccolo says.
Cells dial in just the right amount of Dicer by using a family of microRNAs, miR-103.1, miR-103.2 and miR-107, Piccolo and his colleagues reported in the June 25 Cell. Those three microRNAs, which occur at high levels in some cancer cells, latch on to messenger RNAs encoding Dicer and ratchet down its production, meaning less of other microRNAs get made. But Dicer levels never drop to nothing, because the same microRNAs rely on the protein to snip them free from larger pieces of RNA.
Piccolo’s finding neatly solves the paradox of why most microRNA levels can be low in cancer cells while some are high, but his study didn’t stop there. The research also provides further evidence that low Dicer levels make cancer more dangerous.
In the study, Piccolo’s team discovered that some aggressive tumors had higher than normal levels of the microRNAs that regulate Dicer, and thus less of the protein. More of these microRNAs were also associated with breast cancer’s spread and poor prognosis in patients.
Additional experiments with tumor cells growing in lab dishes showed that the cells usually tend to cluster. But when Dicer levels are lowered to about 50 to 60 percent of normal, or levels of miR-107 are increased, cells begin migrating across the dish. Dips in Dicer levels make cells mobile, the team suggests. Less Dicer may mean less of other microRNAs that hold back production of proteins that are responsible for getting cells in gear. With fewer inhibitory microRNAs around, go-proteins can be made and cells get a move on.
Tumor cells may be taking advantage of one of Dicer’s jobs in normal cells — helping cells move around. “Cancer doesn’t invent anything,” Piccolo says.
Tiny treatment options
Getting a clue that a microRNA is involved in a problem also gives researchers a potential solution. In experiments with mice, inhibiting miR-21 made resistant tumor cells more susceptible to Herceptin, Rehman reported at the cancer research meeting.
Increasing susceptibility to anticancer drugs is just one way that microRNAs could be useful in the clinic, says oncologist Muller Fabbri of Ohio State.
Specific microRNA levels rise or fall in different tumor types, creating a signature for that type of cancer, studies have shown. Such signatures could help correctly diagnose cancer in people whose tumors have migrated. Often pathologists can examine a brain tumor and determine that it arose from breast cancer cells, but sometimes cancer cells conceal their real birthplace. Characteristic patterns of microRNA could help identify where tumor cells originated in the 8 to 10 percent of cases when “even the pathologist doesn’t have a clue,” Fabbri says. Examining the pattern of microRNA levels in a patient’s tumor may also help doctors identify aggressive forms (SN: 2/2/08, p. 70).
In diseases such as liver cancer, researchers may be able to replace missing microRNAs or boost levels to stop the cancer, a team reported last year in Cell. And in cancers in which levels of certain microRNAs are too high, researchers can deploy decoy molecules to pull microRNAs from their targets. A team reported in January in Science that the strategy appears to work for treating hepatitis C infection in monkeys (SN: 1/2/10, p. 14).
Croce thinks that targeting several microRNAs in anarchist networks may help treat cancer with little chance of resistance developing. But such therapies are still years away. “We have to show that it is really true,” he says, “not just in experiments with mice, but in clinical trials.”
For now, no microRNA therapies are available for cancer, but researchers are watching trials of the anti-microRNA therapy against hepatitis C in people.
“The rapidity of what’s going on is what gives some of us optimism that this could have value,” Harris says. “Relatively shortly, we’re going to know the degree of importance of microRNAs.”
Source
Tiny pieces of RNA may turn cells to the dark side
By Tina Hesman Saey
August 28th, 2010; Vol.178 #5 (p. 18)
When tiny hairpin-shaped molecules act up, they don’t rebel loner-style like James Dean. Instead they take on the persona of Darth Vader, crushing proteins under their command and turning acquaintances to the dark side as well. In this case, though, the fight is for control not of the universe, but of the body. And a dark-side victory could end in cancer.
No one would have predicted a decade ago that these microRNAs, as the hairpins are called, were involved in cancer, because no one even knew that they existed in people. Mere snippets of RNA — DNA’s underappreciated cousin — these micromolecules are about 22 chemical letters long. But their size belies their power.
When on their best behavior, the molecules are competent and capable managers of the protein-building process that keeps a cell humming in perfect harmony. But when microRNAs go rogue, the results can be disastrous.
New research is revealing just how important these newly discovered molecules are. An imbalance of microRNAs can cause cancer by encouraging runaway cell growth or by dampening a cell’s defenses, and can also make the disease more stubborn. But just as Darth Vader never completely lost the young Jedi Anakin Skywalker within him, even bad microRNAs may have good in them yet. Some scientists think that therapies aimed at soothing riled-up microRNAs may help cure the very cancers that the molecules help cause.
Most of the discoveries linking microRNAs and cancer have come in the past five years. “This is extremely rapid progression,” says Curtis Harris, chief of the human carcinogenesis lab at the National Cancer Institute, based in Bethesda, Md.
Micro middle managers
The realization that such small molecules could play a big role in disease was late in coming, says Carlo Croce of Ohio State University in Columbus. “In the beginning there was no interest in microRNAs at all,” he says.
The first microRNA was discovered in 1993 in roundworms. It took another seven years before the next microRNA was found in the same organism. Though both of those microRNAs help control worm development, most scientists regarded them as biological curiosities.
But then researchers found microRNAs at work in fruit flies, people and other organisms. Those discoveries suggested that microRNAs might be important regulatory molecules for all animals, not just flukes of worm biology.
MicroRNAs work in middle management in most plant and animal cells, scientists now know. The molecules help regulate the protein-manufacturing process by essentially issuing permits decreeing when and where proteins may be built. By riding piggyback on messenger RNAs, which are copies of the protein-building blueprints contained within DNA, microRNAs prevent the instructions from reaching protein-building machinery inside cells.
While it may sound nefarious, microRNAs’ interference with protein production helps a cell maintain balance. MicroRNAs ensure that cells save energy by not making unnecessary proteins and help prevent levels of potentially harmful proteins, such as those that initiate the self-destruct program known as apoptosis, from reaching critical mass.
Each type of microRNA in a cell may potentially pair with hundreds of different types of messenger RNA, says Isidore Rigoutsos, a computational and molecular biologist at Thomas Jefferson University in Philadelphia. And each messenger RNA may have many different microRNAs piling on its back.
“It’s safe to say that microRNAs are important,” Rigoutsos says. “The difficulty is saying what are the limits of importance, and they keep being expanded more and more and more.”
Cancer connection
Croce’s lab was among the first to illustrate just how big a role the little molecules could play in people. His group showed that genes encoding microRNAs frequently go missing in tumor cells. In particular, two microRNAs, miR-15 and miR-16, are missing or found at lower than normal levels in 68 percent of chronic lymphocytic leukemia cases.
Cancer biologists usually lump microRNAs into two groups: those that protect against cancer and those that promote it (though the distinction isn’t perfect). Cancer cells tend to have lower levels of most microRNAs but have an oversupply of a few others.
In the protective corner are microRNAs such as miR-15 and miR-16. One of the many proteins regulated by those two microRNAs is BCL2, which keeps cells from pushing the self-destruct button. Cells commit suicide when they become too damaged to operate properly — an important self-defense mechanism for an organism that doesn’t want to walk around with malfunctioning cells. So cells need just the right amount of BCL2 to keep from killing themselves unnecessarily, but not so much of it that they can never die.
The microRNAs pair with messenger RNA to strike the right balance of BCL2. But when miR-15 and miR-16 levels are knocked down — which can happen if a copy of a gene is lost or if something goes wrong during microRNA manufacturing — cells make far too much BCL2, essentially disabling the self-destruct mechanism and making cells immortal. Immortality is one hallmark of cancer.
At the opposite end of the spectrum is one of the baddest microRNA bad boys, miR-21. Elevated levels cause cancer in mice, researchers from Yale University reported online August 8 in Nature. And higher than normal levels have been linked to at least 13 major types of cancer in people and to poor prognoses for people with colon, lung, breast, pancreatic or head and neck cancers, Harris says (SN: 2/2/08, p. 70).
High levels of miR-21 can slow an important cellular security system involving a protein named p53, researchers from the University of California, Santa Barbara have found. This protein performs multiple protective services, including spurring repair of damaged DNA, halting growth until damage is repaired or ending it all if repair isn’t possible (SN: 12/6/08, p. 22). Last year researchers reported in Nature that p53 helps slice microRNAs into their mature form. Too much miR-21 can strip cells of their p53 defenses, leading to cancer.
Though miR-21 has stood out among the troublemakers, Croce’s team has shown that this microRNA and others don’t work alone. The molecular managers are master networkers. In 50 different normal human tissues, microRNAs collaborate to direct cellular activities, Croce and colleagues reported online May 3 in Genome Research. The networks consist of microRNAs that help direct production of proteins, some of which, in turn, control production of other microRNAs, and so on.
But time and again, in 51 different types of cancer, Croce’s team found that the microRNAs’ teamwork had broken down. The cohesive networks disintegrated into rogue hubs of activity. These anarchist factions throw a wrench into the well-oiled machinery that usually keeps a cell healthy.
It’s a rather small wrench, though. MicroRNAs wield their power subtly, tweaking and massaging protein levels up or down a wee bit here and there instead of stopping production altogether.
“A microRNA doesn’t function like an ‘off’ switch,” says cancer biologist Dihua Yu of the University of Texas MD Anderson Cancer Center in Houston.
Even a little bump or dip in protein levels, maybe by just 5 to 10 percent, is enough to send a cell careening down the path to cancer, Croce says.
One of the most delicately balanced cancer-associated proteins is PTEN. It reins in cell growth to prevent wild replication, as seen in cancer. In the parlance of cancer research, PTEN is known as a tumor suppressor, and it works best when there is just the right amount of it.
Losing one copy of the gene for PTEN — essentially cutting protein levels in half — is enough to turn a cell cancerous, previous studies have shown. Other research has demonstrated that microRNAs, including miR-21, help govern production of PTEN. And a study reported June 24 in Nature found that a messenger RNA doppelgänger of PTEN found in healthy cells distracts PTEN-stifling microRNAs, allowing more of the protein to be made. If the twin is missing, the weight of microRNAs on messenger RNA’s back can crush protein production.
New research from Yu’s lab also suggests that reducing the amount of PTEN protein in a tumor cell even slightly is not a good idea. Higher levels of miR-21 slow down PTEN production and make breast cancer cells resistant to an anticancer agent called Herceptin, Yu and colleague Sumaiyah Rehman reported in April in Washington, D.C., at the annual meeting of the American Association for Cancer Research.
Dicer danger
PTEN isn’t the only protein that can make cancer worse. A new study shows that small changes in the amount of a protein involved in producing microRNAs can determine whether tumors stay put or spread to the rest of the body.
That discovery grew from efforts to figure out why most microRNAs are at lower levels in cancer cells but some microRNAs are overproduced. “We were intrigued by this paradox,” says Stefano Piccolo, a cellular and molecular biologist at the University of Padua in Italy.
The resolution came from an unexpected source, a protein that helps slice larger RNAs into microRNAs. This protein, Dicer, is a key component of the microRNA manufacturing machinery. Cutting levels of Dicer in half spurs on cancer because less of it leads to less microRNA, which can mean increased production of proteins that drive rapid growth. Still, cancer cells need some Dicer to survive and reproduce, since Dicer helps make microRNAs that regulate production of proteins.
So cancer cells need to control Dicer levels the way a student sets the volume on an iPod to provide background study music. The volume shouldn’t be too quiet or too loud. “You need to find that perfect middle,” Piccolo says.
Cells dial in just the right amount of Dicer by using a family of microRNAs, miR-103.1, miR-103.2 and miR-107, Piccolo and his colleagues reported in the June 25 Cell. Those three microRNAs, which occur at high levels in some cancer cells, latch on to messenger RNAs encoding Dicer and ratchet down its production, meaning less of other microRNAs get made. But Dicer levels never drop to nothing, because the same microRNAs rely on the protein to snip them free from larger pieces of RNA.
Piccolo’s finding neatly solves the paradox of why most microRNA levels can be low in cancer cells while some are high, but his study didn’t stop there. The research also provides further evidence that low Dicer levels make cancer more dangerous.
In the study, Piccolo’s team discovered that some aggressive tumors had higher than normal levels of the microRNAs that regulate Dicer, and thus less of the protein. More of these microRNAs were also associated with breast cancer’s spread and poor prognosis in patients.
Additional experiments with tumor cells growing in lab dishes showed that the cells usually tend to cluster. But when Dicer levels are lowered to about 50 to 60 percent of normal, or levels of miR-107 are increased, cells begin migrating across the dish. Dips in Dicer levels make cells mobile, the team suggests. Less Dicer may mean less of other microRNAs that hold back production of proteins that are responsible for getting cells in gear. With fewer inhibitory microRNAs around, go-proteins can be made and cells get a move on.
Tumor cells may be taking advantage of one of Dicer’s jobs in normal cells — helping cells move around. “Cancer doesn’t invent anything,” Piccolo says.
Tiny treatment options
Getting a clue that a microRNA is involved in a problem also gives researchers a potential solution. In experiments with mice, inhibiting miR-21 made resistant tumor cells more susceptible to Herceptin, Rehman reported at the cancer research meeting.
Increasing susceptibility to anticancer drugs is just one way that microRNAs could be useful in the clinic, says oncologist Muller Fabbri of Ohio State.
Specific microRNA levels rise or fall in different tumor types, creating a signature for that type of cancer, studies have shown. Such signatures could help correctly diagnose cancer in people whose tumors have migrated. Often pathologists can examine a brain tumor and determine that it arose from breast cancer cells, but sometimes cancer cells conceal their real birthplace. Characteristic patterns of microRNA could help identify where tumor cells originated in the 8 to 10 percent of cases when “even the pathologist doesn’t have a clue,” Fabbri says. Examining the pattern of microRNA levels in a patient’s tumor may also help doctors identify aggressive forms (SN: 2/2/08, p. 70).
In diseases such as liver cancer, researchers may be able to replace missing microRNAs or boost levels to stop the cancer, a team reported last year in Cell. And in cancers in which levels of certain microRNAs are too high, researchers can deploy decoy molecules to pull microRNAs from their targets. A team reported in January in Science that the strategy appears to work for treating hepatitis C infection in monkeys (SN: 1/2/10, p. 14).
Croce thinks that targeting several microRNAs in anarchist networks may help treat cancer with little chance of resistance developing. But such therapies are still years away. “We have to show that it is really true,” he says, “not just in experiments with mice, but in clinical trials.”
For now, no microRNA therapies are available for cancer, but researchers are watching trials of the anti-microRNA therapy against hepatitis C in people.
“The rapidity of what’s going on is what gives some of us optimism that this could have value,” Harris says. “Relatively shortly, we’re going to know the degree of importance of microRNAs.”
Source
Alpha-fetoprotein above normal levels as a risk factor for the development of hepatocellular carcinoma in patients infected with hepatitis C virus
Journal of Gastroenterology
DOI: 10.1007/s00535-010-0293-6
Masakuni Tateyama, Hiroshi Yatsuhashi, Naota Taura, Yasuhide Motoyoshi, Shinya Nagaoka, Kenji Yanagi, Seigo Abiru, Koji Yano, Atsumasa Komori and Kiyoshi Migita, et al.
Abstract
Background
Noninvasive risk factors are required for predicting the development of hepatocellular carcinoma (HCC) not only in patients with cirrhosis but also in those with chronic hepatitis who are infected with hepatitis C virus (HCV).
Methods
A total of 707 patients with chronic HCV infection without other risks were evaluated for the predictive value of noninvasive risk factors for HCC, including age, sex, viral load, genotype, fibrosis stage, aspartate and alanine aminotransferase levels, bilirubin, albumin, platelet count, and alpha-fetoprotein (AFP) at entry to the study, as well as interferon (IFN) therapy they received.
Results
The ten-year cumulative incidence rates of HCC for patients with fibrosis stages F0/F1, F2, F3, and F4 were 2.5, 12.8, 19.3, and 55.9%, respectively. Multivariate analysis identified age ≥57 years [hazard ratio (HR) 2.026, P = 0.004], fibrosis stage F4 (HR 3.957, P < 0.001), and AFP 6–20 ng/mL (HR 1.942, P = 0.030) and ≥20 ng/mL (HR 3.884, P < 0.001), as well as the response to IFN [relative risk (RR) 0.099, P < 0.001], as independent risk factors for the development of HCC. The ten-year cumulative incidence rates of HCC in the patients with AFP levels of <6, 6–20, and ≥20 ng/mL at entry were 6.0, 24.6, and 47.3%, respectively.
Conclusions
Not only high (>20 ng/mL), but also even slightly elevated (6–20 ng/mL) AFP levels, could serve as a risk factor for HCC to complement the fibrosis stage. In contrast, AFP levels <6 ng/mL indicate a low risk of HCC development in patients infected with HCV, irrespective of the fibrosis stage.
Keywords Alpha-fetoprotein - Hepatitis C virus - Hepatocellular carcinoma
Source
DOI: 10.1007/s00535-010-0293-6
Masakuni Tateyama, Hiroshi Yatsuhashi, Naota Taura, Yasuhide Motoyoshi, Shinya Nagaoka, Kenji Yanagi, Seigo Abiru, Koji Yano, Atsumasa Komori and Kiyoshi Migita, et al.
Abstract
Background
Noninvasive risk factors are required for predicting the development of hepatocellular carcinoma (HCC) not only in patients with cirrhosis but also in those with chronic hepatitis who are infected with hepatitis C virus (HCV).
Methods
A total of 707 patients with chronic HCV infection without other risks were evaluated for the predictive value of noninvasive risk factors for HCC, including age, sex, viral load, genotype, fibrosis stage, aspartate and alanine aminotransferase levels, bilirubin, albumin, platelet count, and alpha-fetoprotein (AFP) at entry to the study, as well as interferon (IFN) therapy they received.
Results
The ten-year cumulative incidence rates of HCC for patients with fibrosis stages F0/F1, F2, F3, and F4 were 2.5, 12.8, 19.3, and 55.9%, respectively. Multivariate analysis identified age ≥57 years [hazard ratio (HR) 2.026, P = 0.004], fibrosis stage F4 (HR 3.957, P < 0.001), and AFP 6–20 ng/mL (HR 1.942, P = 0.030) and ≥20 ng/mL (HR 3.884, P < 0.001), as well as the response to IFN [relative risk (RR) 0.099, P < 0.001], as independent risk factors for the development of HCC. The ten-year cumulative incidence rates of HCC in the patients with AFP levels of <6, 6–20, and ≥20 ng/mL at entry were 6.0, 24.6, and 47.3%, respectively.
Conclusions
Not only high (>20 ng/mL), but also even slightly elevated (6–20 ng/mL) AFP levels, could serve as a risk factor for HCC to complement the fibrosis stage. In contrast, AFP levels <6 ng/mL indicate a low risk of HCC development in patients infected with HCV, irrespective of the fibrosis stage.
Keywords Alpha-fetoprotein - Hepatitis C virus - Hepatocellular carcinoma
Source
Hep C lawsuit asserts 1991 incident at Texas hospital should have increased caution
By Felisa Cardona
The Denver Post
Posted: 08/15/2010 01:00:00 AM MDT
Eighteen years before surgery scrub technician Kristen Parker infected 18 patients at Rose Medical Center with hepatitis C, another employee infected patients the same way at a Texas hospital later owned by one of the owners of Rose.
A lawsuit filed in Denver District Court states that Hospital Corporation of America, which partly owns Rose Medical Center, should have been more careful with the way drugs were stored and secured after its earlier lawsuit.
Parker, 27, is serving 30 years in federal prison after she injected herself with the painkiller fentanyl that was meant for surgery patients. She then filled the syringes with saline and placed them back on carts, resulting in the patients being injected with the infected needles during surgery.
The latest lawsuit, filed Aug. 3, claims anesthesiologists left the drugs in unlocked surgery rooms — in violation of hospital policy and state and federal statutes.
"Every single surgery room at Rose had controlled substances that were intended for vulnerable surgery patients lying around for drug addicts like Parker to divert, use and fill with saline," said patients' attorney Hollynd Hoskins.
Five lawsuits are pending against Rose Medical Center, and one has been settled, said Cara Harshberger, spokeswoman for the hospital.
The first case set for trial is in June before Denver District Judge Herbert Stern.
The latest suit was filed by Hoskins on behalf of a Denver mother of three who is using the initials L.K. because she does not want her medical condition made public.
For six minutes, a syringe filled with the painkiller fentanyl sat unsecured in a surgery room before L.K.'s procedure on Feb. 13, 2009. The lawsuit says that is when Parker stole the drug and left the infected needle behind.
The anesthesiologist, Dr. Herbert N. Chado, named as a defendant in the lawsuit, unknowingly injected L.K. with the contaminated needle, and months later, the woman learned that she was infected with hepatitis C.
L.K. underwent interferon treatment and, at first, responded to the medication, but the virus has since come back.
In 1994, the Colorado Board of Medical Examiners placed Chado on five years of probation for abusing the drug Sufenta, an opiate. Chado, who pursued treatment, did not practice medicine from 1993 to 2001, state records show.
Chado did not return a call seeking comment about the lawsuit.
Minutes before L.K. was infected, Chado failed to lock the surgery room and didn't have the fentanyl in his sight, the suit says.
"We have had and continue to have rigorous controls in place to ensure medication security," Harshberger said. "This includes having pass- code-protected computerized medication systems in each operating room, with methodical auditing of the usage of that equipment, providing ongoing education for staff and physicians regarding medication security, and exploring options for packaging of medication."
In 1991, scrub tech David Wayne Thomas stole fentanyl from the now-defunct Mid-Cities Surgi-Center in Bedford, Texas.
The hospital was owned by Medical Care America at the time of the incident but was acquired by Hospital Corporation of America in 1994, Harshberger said.
Thomas, who was infected with hepatitis C, pleaded guilty to stealing the drugs and served three years of an eight-year sentence, according to a 1995 Fort Worth Star-Telegram article. It is not clear whether Thomas knew he was infected with the virus, as Parker did, when he was contaminating the needles.
Civil lawsuits were brought by 48 patients against Hospital Corporation of America and the anesthesiologists who were responsible for securing the medication. The cases were settled.
Legal experts told the newspaper the settlements could have surpassed $100 million.
Harshberger said Rose remains committed to helping patients, including paying for the testing and treatment of those affected by Parker's actions.
"The criminal actions of this former employee put our patients at risk, and for that we were truly saddened and angered," she said.
Felisa Cardona: 303-954-1219 or fcardona@denverpost.com
Source
The Denver Post
Posted: 08/15/2010 01:00:00 AM MDT
Eighteen years before surgery scrub technician Kristen Parker infected 18 patients at Rose Medical Center with hepatitis C, another employee infected patients the same way at a Texas hospital later owned by one of the owners of Rose.
A lawsuit filed in Denver District Court states that Hospital Corporation of America, which partly owns Rose Medical Center, should have been more careful with the way drugs were stored and secured after its earlier lawsuit.
Parker, 27, is serving 30 years in federal prison after she injected herself with the painkiller fentanyl that was meant for surgery patients. She then filled the syringes with saline and placed them back on carts, resulting in the patients being injected with the infected needles during surgery.
The latest lawsuit, filed Aug. 3, claims anesthesiologists left the drugs in unlocked surgery rooms — in violation of hospital policy and state and federal statutes.
"Every single surgery room at Rose had controlled substances that were intended for vulnerable surgery patients lying around for drug addicts like Parker to divert, use and fill with saline," said patients' attorney Hollynd Hoskins.
Five lawsuits are pending against Rose Medical Center, and one has been settled, said Cara Harshberger, spokeswoman for the hospital.
The first case set for trial is in June before Denver District Judge Herbert Stern.
The latest suit was filed by Hoskins on behalf of a Denver mother of three who is using the initials L.K. because she does not want her medical condition made public.
For six minutes, a syringe filled with the painkiller fentanyl sat unsecured in a surgery room before L.K.'s procedure on Feb. 13, 2009. The lawsuit says that is when Parker stole the drug and left the infected needle behind.
The anesthesiologist, Dr. Herbert N. Chado, named as a defendant in the lawsuit, unknowingly injected L.K. with the contaminated needle, and months later, the woman learned that she was infected with hepatitis C.
L.K. underwent interferon treatment and, at first, responded to the medication, but the virus has since come back.
In 1994, the Colorado Board of Medical Examiners placed Chado on five years of probation for abusing the drug Sufenta, an opiate. Chado, who pursued treatment, did not practice medicine from 1993 to 2001, state records show.
Chado did not return a call seeking comment about the lawsuit.
Minutes before L.K. was infected, Chado failed to lock the surgery room and didn't have the fentanyl in his sight, the suit says.
"We have had and continue to have rigorous controls in place to ensure medication security," Harshberger said. "This includes having pass- code-protected computerized medication systems in each operating room, with methodical auditing of the usage of that equipment, providing ongoing education for staff and physicians regarding medication security, and exploring options for packaging of medication."
In 1991, scrub tech David Wayne Thomas stole fentanyl from the now-defunct Mid-Cities Surgi-Center in Bedford, Texas.
The hospital was owned by Medical Care America at the time of the incident but was acquired by Hospital Corporation of America in 1994, Harshberger said.
Thomas, who was infected with hepatitis C, pleaded guilty to stealing the drugs and served three years of an eight-year sentence, according to a 1995 Fort Worth Star-Telegram article. It is not clear whether Thomas knew he was infected with the virus, as Parker did, when he was contaminating the needles.
Civil lawsuits were brought by 48 patients against Hospital Corporation of America and the anesthesiologists who were responsible for securing the medication. The cases were settled.
Legal experts told the newspaper the settlements could have surpassed $100 million.
Harshberger said Rose remains committed to helping patients, including paying for the testing and treatment of those affected by Parker's actions.
"The criminal actions of this former employee put our patients at risk, and for that we were truly saddened and angered," she said.
Felisa Cardona: 303-954-1219 or fcardona@denverpost.com
Source
Death at his back
As his body succumbs to hepatitis C, inmate spends last days trying to warn others
11:33 PM CDT on Saturday, August 14, 2010
By Donna Fielder / Staff Writer
This is a cautionary tale from a dead man walking.
Michael Mabry doesn’t have a lot to be proud of.
He’s been in and out of prison all his adult life. He’s been a speed fiend and a cokehead most of that time. He’s been busted for drugs and burglarizing buildings and tried two jailbreaks, and he has a criminal record in three states. He has eight children “scattered around,” he says, but he’s mostly alone now.
He’s a dead man, he says.
He won’t leave the infirmary at the Denton County Jail alive. Hepatitis C attacked his liver before he knew anything was wrong. By the time it was diagnosed, he was in the final stages of cirrhosis of the liver, and there’s nothing anyone can do for him, in jail or not.
So the 49-year-old Denton man sits on his cot in a medical cell, with a commode in the open a couple of feet away and the only decoration a roll of toilet paper and some graffiti scratched on the wall, and he thinks about his life and what he’s done wrong. He wonders what he could do to maybe get one small mark on the right side of his sheet.
“I don’t think I’ve done anything to warrant going to hell,” he says. “But you never know. It sure wouldn’t hurt to get a few points in with the Man up there.”
He doesn’t have much time. He’s a con man, he admits. But he can’t con his way out of the trouble he’s in.
The only thing Mabry can offer is his life experience and its consequences as a warning to others. He got hepatitis C from jailhouse tattoos, he says. Everybody in prison gets tats; many contract hepatitis C from the methods they use.
But it’s the youngsters he’d like to help now, he said. Tattoos also are popular with the general population. Most adults go to tattoo parlors that are licensed by the state and have strict guidelines to hold down the chance of contracting a disease from infected implements. But those younger than 18 must have parental permission to legally obtain a tattoo. Many young people turn to more informal — and more dangerous — methods of inking up.
Gang wannabes use homemade devices to ink in their gang affiliations. Other kids get a friend to help them render forever their girlfriends’ names or symbols that have meaning to them. If they knew, Mabry says, if they understood that dirty needles, shared tattoo devices made of paper clips, safety pins — the myriad other unhealthy, sharp things — can kill them, maybe they wouldn’t get started down that road.
According to medical information provided by a website devoted to hepatitis, 4 million Americans now have hepatitis C.
It is more prevalent in Europe, but it emerged in the U.S. in the 1960s, related to blood transfusions and intravenous drug use. A reliable test for it was developed in the 1990s, and it was revealed to be a much larger problem than anyone knew. It causes cirrhosis of the liver and liver cancer.
When casual users share a needle to inject drugs or an instrument to inject ink under the skin, blood can be transmitted from one person to another. Hepatitis C is one of the diseases that can be transmitted in blood. It attacks the liver — and left untreated, destroys it.
The liver has many functions, including filtering harmful substances from the blood, breaking down fats, storing vitamins and producing urea. The body cannot survive without it. Cirrhosis inflames the liver and ultimately causes it to fail. Caught early, the symptoms can be treated. But it is incurable.
Jailhouse prevalence of hepatitis C
Doug Sanders supervises the medical staff at the jail. He believes that Mabry is within weeks of death. Since Mabry’s disease is only communicable by bodily fluid exchange, there’s no reason to isolate him, he said. The staff manages his medication to try to keep him comfortable.
Since Mabry also injected drugs, he could have contracted hepatitis from a dirty needle. But he is convinced it was a tattoo needle, and since he has so many tattoos, it is reasonable to think that he is right, Sanders said.
“It’s alarming. It’s extremely prevalent in jail populations. You might think the HIV virus would be more prevalent, but the greatest risk exposure in jails and prisons nationwide is hepatitis C.”
Jail administrators try hard to keep inmates from finding ways to make jailhouse tattoos, Sanders said. Guards seize anything that could be used to make them.
“We are absolutely discouraging it. We confiscate it. But they have so many ways of engineering a machine. They find ways around it,” he said.
Mabry’s isn’t the first advanced case that the jail medical staff have treated. They are preparing him as best they can for the suffering he’s about to endure, Sanders said. “He has some very difficult days ahead.”
A dim future
Death is becoming real for Mabry. He spends a lot of time talking to chaplain Bobby Ayers. He’s working on a bill he’d like to become a law. He knows he’s not going to finish it, so he offers advice.
“Kids are knuckleheaded, you know,” Mabry says. “If I could save one kid ...”
Perched on his cot, his longish black hair slicked down, his orange jumpsuit covering the numerous tats on his back, chest and legs, he thinks about that for a minute.
“It ain’t just the needle you get it from. It’s the ink they reuse,” he said. “You know, I studied the law and I beat it one time. I slicked out of a charge I did on a technicality. They wrote on my paperwork that I’m a master manipulator of the law. I studied this disease. I’m not stupid. I studied to find a way to beat it, but you can’t.”
He pulls up his shirt to display drug- and gang-related tattoos. He has a bandito tat on his chest, a large dagger with a snake wrapped around it — he says it’s related to Rex Cauble and the Cowboy Mafia — on one leg, and a fairly good rendering of the Grim Reaper on his back.
“He’s coming for me, by God,” he said. “It’s day by day now.”
Mabry demonstrates how a tattoo machine can be made with things not considered contraband in the jail and some that are. A decent jailhouse tattoo machine can be constructed with a ballpoint pen, a paper clip, some string and the tiny motor from a Walkman, he says. Ashes and shampoo can be combined to make ink.
Walkman tape players are no longer available at the county jail. Mabry said an inmate can always figure out another way.
“We say you can put one prisoner on one roof with a match and another one on another roof a mile away with a cigarette, and before you know it both of them have half a match and half a cigarette and they’re both smoking,” he said.
Mabry says his liver no longer functions. It swelled, he said, until it broke his ribs. He said he’s had eight heart attacks since he was diagnosed less than a year ago, and his aorta burst because his veins and arteries thinned out. He also has diabetes. He’s in pain, which the medical personnel in the infirmary try to lessen with drugs. He’s a poster boy for staying away from casual tattoos. If you have to get them, go to a licensed tattoo shop, he says. They have rules to keep things clean.
Mabry often loses his train of thought. He rambles and forgets.
“The worst part of this disease is your brain goes,” he said. “They tell me that when it gets that far, it’s the best thing for me. But I don’t want my brain to go and just be lying here.”
He thinks a minute and then laughs.
“I have a million dollars worth of medical bills right now. But they ain’t never gonna get it. Maybe somebody will read this story and it will save them. It’d be good if I could at least do that.”
DONNA FIELDER can be reached at 940-566-6885. Her e-mail address is dfielder@dentonrc.com.
Source
11:33 PM CDT on Saturday, August 14, 2010
By Donna Fielder / Staff Writer
This is a cautionary tale from a dead man walking.
Michael Mabry doesn’t have a lot to be proud of.
He’s been in and out of prison all his adult life. He’s been a speed fiend and a cokehead most of that time. He’s been busted for drugs and burglarizing buildings and tried two jailbreaks, and he has a criminal record in three states. He has eight children “scattered around,” he says, but he’s mostly alone now.
He’s a dead man, he says.
He won’t leave the infirmary at the Denton County Jail alive. Hepatitis C attacked his liver before he knew anything was wrong. By the time it was diagnosed, he was in the final stages of cirrhosis of the liver, and there’s nothing anyone can do for him, in jail or not.
So the 49-year-old Denton man sits on his cot in a medical cell, with a commode in the open a couple of feet away and the only decoration a roll of toilet paper and some graffiti scratched on the wall, and he thinks about his life and what he’s done wrong. He wonders what he could do to maybe get one small mark on the right side of his sheet.
“I don’t think I’ve done anything to warrant going to hell,” he says. “But you never know. It sure wouldn’t hurt to get a few points in with the Man up there.”
He doesn’t have much time. He’s a con man, he admits. But he can’t con his way out of the trouble he’s in.
The only thing Mabry can offer is his life experience and its consequences as a warning to others. He got hepatitis C from jailhouse tattoos, he says. Everybody in prison gets tats; many contract hepatitis C from the methods they use.
But it’s the youngsters he’d like to help now, he said. Tattoos also are popular with the general population. Most adults go to tattoo parlors that are licensed by the state and have strict guidelines to hold down the chance of contracting a disease from infected implements. But those younger than 18 must have parental permission to legally obtain a tattoo. Many young people turn to more informal — and more dangerous — methods of inking up.
Gang wannabes use homemade devices to ink in their gang affiliations. Other kids get a friend to help them render forever their girlfriends’ names or symbols that have meaning to them. If they knew, Mabry says, if they understood that dirty needles, shared tattoo devices made of paper clips, safety pins — the myriad other unhealthy, sharp things — can kill them, maybe they wouldn’t get started down that road.
According to medical information provided by a website devoted to hepatitis, 4 million Americans now have hepatitis C.
It is more prevalent in Europe, but it emerged in the U.S. in the 1960s, related to blood transfusions and intravenous drug use. A reliable test for it was developed in the 1990s, and it was revealed to be a much larger problem than anyone knew. It causes cirrhosis of the liver and liver cancer.
When casual users share a needle to inject drugs or an instrument to inject ink under the skin, blood can be transmitted from one person to another. Hepatitis C is one of the diseases that can be transmitted in blood. It attacks the liver — and left untreated, destroys it.
The liver has many functions, including filtering harmful substances from the blood, breaking down fats, storing vitamins and producing urea. The body cannot survive without it. Cirrhosis inflames the liver and ultimately causes it to fail. Caught early, the symptoms can be treated. But it is incurable.
Jailhouse prevalence of hepatitis C
Doug Sanders supervises the medical staff at the jail. He believes that Mabry is within weeks of death. Since Mabry’s disease is only communicable by bodily fluid exchange, there’s no reason to isolate him, he said. The staff manages his medication to try to keep him comfortable.
Since Mabry also injected drugs, he could have contracted hepatitis from a dirty needle. But he is convinced it was a tattoo needle, and since he has so many tattoos, it is reasonable to think that he is right, Sanders said.
“It’s alarming. It’s extremely prevalent in jail populations. You might think the HIV virus would be more prevalent, but the greatest risk exposure in jails and prisons nationwide is hepatitis C.”
Jail administrators try hard to keep inmates from finding ways to make jailhouse tattoos, Sanders said. Guards seize anything that could be used to make them.
“We are absolutely discouraging it. We confiscate it. But they have so many ways of engineering a machine. They find ways around it,” he said.
Mabry’s isn’t the first advanced case that the jail medical staff have treated. They are preparing him as best they can for the suffering he’s about to endure, Sanders said. “He has some very difficult days ahead.”
A dim future
Death is becoming real for Mabry. He spends a lot of time talking to chaplain Bobby Ayers. He’s working on a bill he’d like to become a law. He knows he’s not going to finish it, so he offers advice.
“Kids are knuckleheaded, you know,” Mabry says. “If I could save one kid ...”
Perched on his cot, his longish black hair slicked down, his orange jumpsuit covering the numerous tats on his back, chest and legs, he thinks about that for a minute.
“It ain’t just the needle you get it from. It’s the ink they reuse,” he said. “You know, I studied the law and I beat it one time. I slicked out of a charge I did on a technicality. They wrote on my paperwork that I’m a master manipulator of the law. I studied this disease. I’m not stupid. I studied to find a way to beat it, but you can’t.”
He pulls up his shirt to display drug- and gang-related tattoos. He has a bandito tat on his chest, a large dagger with a snake wrapped around it — he says it’s related to Rex Cauble and the Cowboy Mafia — on one leg, and a fairly good rendering of the Grim Reaper on his back.
“He’s coming for me, by God,” he said. “It’s day by day now.”
Mabry demonstrates how a tattoo machine can be made with things not considered contraband in the jail and some that are. A decent jailhouse tattoo machine can be constructed with a ballpoint pen, a paper clip, some string and the tiny motor from a Walkman, he says. Ashes and shampoo can be combined to make ink.
Walkman tape players are no longer available at the county jail. Mabry said an inmate can always figure out another way.
“We say you can put one prisoner on one roof with a match and another one on another roof a mile away with a cigarette, and before you know it both of them have half a match and half a cigarette and they’re both smoking,” he said.
Mabry says his liver no longer functions. It swelled, he said, until it broke his ribs. He said he’s had eight heart attacks since he was diagnosed less than a year ago, and his aorta burst because his veins and arteries thinned out. He also has diabetes. He’s in pain, which the medical personnel in the infirmary try to lessen with drugs. He’s a poster boy for staying away from casual tattoos. If you have to get them, go to a licensed tattoo shop, he says. They have rules to keep things clean.
Mabry often loses his train of thought. He rambles and forgets.
“The worst part of this disease is your brain goes,” he said. “They tell me that when it gets that far, it’s the best thing for me. But I don’t want my brain to go and just be lying here.”
He thinks a minute and then laughs.
“I have a million dollars worth of medical bills right now. But they ain’t never gonna get it. Maybe somebody will read this story and it will save them. It’d be good if I could at least do that.”
DONNA FIELDER can be reached at 940-566-6885. Her e-mail address is dfielder@dentonrc.com.
Source
Physicians Concerned About Nationwide Drug Shortages
Reported by: Kevin Reece - KHOU TV
HOUSTON - A watchdog group calls the current state of drug shortages in this country “alarming” and doctors in the Texas Medical Center agree the problem is more severe this summer than in years past.
Jonathan O’Malley, 18, is a leukemia patient at MD Anderson. Earlier this year he received a cord blood transplant and doctors are managing his recovery and the variety of health issues his fight includes. Among the litany of problems chemotherapy has already brought him, he's developed an infection. It’s called cytomegalovirus or CMV. The recommended treatment and final line of defense for Jonathan is an anti-viral drug called Foscarnet.
But on the blog kept by Jonathan's parents, we noticed this disturbing sentence from his mom: "There is a nationwide shortage of this drug and they have absolutely none available...this could be life or death for so many cancer patients," Melanie O’Malley wrote.
At Texas Children's Hospital we found a doctor who agreed.
“For these patients these drugs are life-saving and absolutely vital,” said Dr. Robert Krance, a stem cell and gene therapy expert. Two of his stem cell transplant patients also rely on Foscarnet to keep infections in check.
"And when you don't have suitable alternatives you really have patients at risk for having complications and even fatal complications if you can't work around that,” Krance said.
So why is Foscarnet suddenly in short supply? That's a difficult answer to get.
It was originally made by two companies: Astra Zeneca and Hospira. Astra Zeneca stopped making the drug last year. And now Hospira has temporarily halted production altogether.
The company, headquartered in Lake Forest, Illinois would only tell us by email that: “We expect to be back on the market in the fourth quarter (the quarter starting Oct. 1 and running through Dec. 31).” A report by the American Society of Health-Systems Pharmacists last month stated that “Hospira has Foscarnet presentations on hold due to product testing out of specification.”
"We really don't get a very clear reason why it happens so you're always left somewhat in the dark,” said Krance.
And it's not the only drug in short supply. The American Society of Health System Pharmacists currently lists shortages for more than 140 drugs and drug products including the likes of Hepatitis A Vaccine, morphine injections, and measles, mumps, and rubella vaccine.
The institute for Safe Medication Practices called the shortages "alarming," "unprecedented" and "grim."
"I think a lot of that is financial pressure,” said Wendy Smith RPH, PharmD, a pharmacist at MD Anderson. “There's not a lot of excess drugs sitting on the shelf at any one place."
Smith agrees the shortages are more severe this summer. But said managing sparse drug supplies are a daily part of doing business.
The Food and Drug Administration blames shortages on the business decisions of drug companies, occasional problems with manufacturing, or, in the case of Foscarnet, only one company finds it profitable to produce.
“We may not ever know why a particular product was shorted out,” added Smith.”So it's frustrating for a lot of people."
"We try to preserve product for patients who need it the most and try to withstand and wait until things on the production is able to be picked up,” said Smith.
As for Jonathan, we are told he has enough of the drugs he needs at least for now. Although Krance says he wishes it wasn’t an issue at all.
“When drugs are no longer available to a patient who needs it desperately, it's often too late,” said Krance
Source
The Race Is On For Hepatitis C Treatment
On Friday August 13, 2010, 6:57 pm EDT
How's this for a biopharmaceutical market opportunity? Prospective patients in need: 170 million. That's 3% of the world's population.
The disease is hepatitis C, a contagious, slow-developing, blood-borne disease that can make 80% of those infected vulnerable to severe liver problems, including cirrhosis and cancer.
Hepatitis C wasn't even identified until 1987. A blood test for it became available in 1992.
Now a score of companies are racing to bring new treatments on stream. Out front are Merck (NYSE:MRK - News) with boceprevir, and a partnership of Vertex Pharmaceuticals (NMS:VRTX) and Johnson & Johnson (NYSE:JNJ - News) with telaprevir.
The market will be pretty much evenly split between the two, says Damien Conover, a strategist and senior pharmaceutical analyst at rating firm Morningstar. Telaprevir may have a slight edge, he says.
Both drugs are protease inhibitors, which prevent a virus from replicating itself. While they treat the same disease, they are different in both results and side effects.
Used on patients who have had no previous treatment, boceprevir and telaprevir beat down the hepatitis C virus to undetectable levels in 66% and 75% of patients respectively, Conover says.
Both drugs are likely to go to the Food and Drug Administration for a verdict by the end of the year. That means both could reach the market next year.
"Right now it's hard to tell who's in the lead," Conover said.
Meanwhile, Merck and Vertex-J&J appear to be competing for headlines.
A week ago, the British-based Lancet medical journal carried a Merck-funded study showing that boceprevir brought the virus down to undetectable levels in 66% of patients over 48 weeks of treatment in combination with drugs in use now.
The next day, Aug. 10, Vertex reported study results showing that some patients did so well after a 24-week course of telaprevir (plus the current drugs in use) that they got no added benefit from a 48-week course of treatment. The message: Telaprevir does the job in half the time.
Merck acquired boceprevir with its $41 billion purchase of Schering-Plough in 2009. Vertex developed telaprevir with money from J&J in return for marketing rights.
Whether one or both of the drugs get FDA approval, the hepatitis market is about to undergo a "major paradigm shift," said Steven Silver, an analyst at Standard & Poor's.
"We've gone many years without a new drug on the landscape," he said.
It's hard to know which drug will do better in real life and in the market because they have not been tested head-to-head.
That's a long-standing problem in the drug-development industry. Prospective new products are tested either against a placebo (sugar pills) or, as in the cases of boceprevir and telaprevir, against the current standard of care.
For hepatitis C, that standard is a combination of interferon and ribavirin. It's a hit-or-miss treatment.
In simple terms, ribavirin is an antiviral medication that stops the virus that causes hepatitis C from spreading. Interferon prevents viral replication in surrounding cells.
According to the National Center for Biotechnology Information, it's not known if treatment with ribavirin and interferon actually cures hepatitis C infection, prevents liver damage caused by hepatitis C or keeps hepatitis C from spreading to other people.
The standard hepatitis C treatment results in a reduction of the virus to undetectable levels in fewer than half of cases, according to WebMD (NMS:WBMD).
Boceprevir and telaprevir are protease inhibitors. In brief, they attack the hepatitis C virus itself, WebMD says.
Without head-to-head tests, with the same dosing regimen and with the same kind of patient population, it's hard for investors to figure out whether boceprevir or telaprevir will be the greater success, assuming both get FDA approval, Conover says.
But head-to-head studies "are often not in the best interest of the company," he said.
They can show one drug so superior as to make the other unmarketable. "Head-to-head studies can backfire," Conover said.
According to Silver, the investment community "is trying to ballpark the information released to date."
He sees Vertex prevailing with telaprevir: "It's poised to be the market leader."
Data collected on real world use of these drugs are still some years off.
The market will be watching boceprevir and telaprevir for the next three or four years, Silver says.
An important factor will be the success rate of the drugs on people who have previously failed to respond to the standard of care.
That's not how clinical trials are run. They are usually conducted with patients who have not had therapy, the so-called treatment-naive. Using treatment-naive patients creates a baseline but does not approximate real-life conditions.
Most people with a disease have tried one or more drugs, ratcheting up from least to most powerful and expensive.
Another real-life issue will be the side effects. Newly diagnosed patients may find the side effects of either drug, plus interferon and ribavirin, intolerable.
The most common telaprevir side effect is a rash, Stevens says.
Boceprevir's predominant side effect is anemia. That raises the prospect that another drug will need to be added to the regimen, perhaps Epogen, the anemia-fighting biologic from Amgen (NMS:AMGN).
It's available as a generic in Europe, but remains branded in the U.S.
Another reason to think telaprevir has the inside track is the likelihood that it will require a shorter period of treatment, Silver says.
"At the end of the day, this race will be data-driven," he said.
While there's been no head-to-head trial, the existing data should become available for close comparison at a meeting of the American Association for the Study of Liver Diseases in Boston starting Oct. 28.
By most counts, the global market for hepatitis C products is now $4 billion a year. According to a report from the commercial analysis firm Research & Markets, that should rise to $8.5 billion by 2016.
The reasons for the growth: the increasing number of cases and the new drugs in the pipeline that will make treatment more accessible and tolerable.
Source
How's this for a biopharmaceutical market opportunity? Prospective patients in need: 170 million. That's 3% of the world's population.
The disease is hepatitis C, a contagious, slow-developing, blood-borne disease that can make 80% of those infected vulnerable to severe liver problems, including cirrhosis and cancer.
Hepatitis C wasn't even identified until 1987. A blood test for it became available in 1992.
Now a score of companies are racing to bring new treatments on stream. Out front are Merck (NYSE:MRK - News) with boceprevir, and a partnership of Vertex Pharmaceuticals (NMS:VRTX) and Johnson & Johnson (NYSE:JNJ - News) with telaprevir.
The market will be pretty much evenly split between the two, says Damien Conover, a strategist and senior pharmaceutical analyst at rating firm Morningstar. Telaprevir may have a slight edge, he says.
Both drugs are protease inhibitors, which prevent a virus from replicating itself. While they treat the same disease, they are different in both results and side effects.
Used on patients who have had no previous treatment, boceprevir and telaprevir beat down the hepatitis C virus to undetectable levels in 66% and 75% of patients respectively, Conover says.
Both drugs are likely to go to the Food and Drug Administration for a verdict by the end of the year. That means both could reach the market next year.
"Right now it's hard to tell who's in the lead," Conover said.
Meanwhile, Merck and Vertex-J&J appear to be competing for headlines.
A week ago, the British-based Lancet medical journal carried a Merck-funded study showing that boceprevir brought the virus down to undetectable levels in 66% of patients over 48 weeks of treatment in combination with drugs in use now.
The next day, Aug. 10, Vertex reported study results showing that some patients did so well after a 24-week course of telaprevir (plus the current drugs in use) that they got no added benefit from a 48-week course of treatment. The message: Telaprevir does the job in half the time.
Merck acquired boceprevir with its $41 billion purchase of Schering-Plough in 2009. Vertex developed telaprevir with money from J&J in return for marketing rights.
Whether one or both of the drugs get FDA approval, the hepatitis market is about to undergo a "major paradigm shift," said Steven Silver, an analyst at Standard & Poor's.
"We've gone many years without a new drug on the landscape," he said.
It's hard to know which drug will do better in real life and in the market because they have not been tested head-to-head.
That's a long-standing problem in the drug-development industry. Prospective new products are tested either against a placebo (sugar pills) or, as in the cases of boceprevir and telaprevir, against the current standard of care.
For hepatitis C, that standard is a combination of interferon and ribavirin. It's a hit-or-miss treatment.
In simple terms, ribavirin is an antiviral medication that stops the virus that causes hepatitis C from spreading. Interferon prevents viral replication in surrounding cells.
According to the National Center for Biotechnology Information, it's not known if treatment with ribavirin and interferon actually cures hepatitis C infection, prevents liver damage caused by hepatitis C or keeps hepatitis C from spreading to other people.
The standard hepatitis C treatment results in a reduction of the virus to undetectable levels in fewer than half of cases, according to WebMD (NMS:WBMD).
Boceprevir and telaprevir are protease inhibitors. In brief, they attack the hepatitis C virus itself, WebMD says.
Without head-to-head tests, with the same dosing regimen and with the same kind of patient population, it's hard for investors to figure out whether boceprevir or telaprevir will be the greater success, assuming both get FDA approval, Conover says.
But head-to-head studies "are often not in the best interest of the company," he said.
They can show one drug so superior as to make the other unmarketable. "Head-to-head studies can backfire," Conover said.
According to Silver, the investment community "is trying to ballpark the information released to date."
He sees Vertex prevailing with telaprevir: "It's poised to be the market leader."
Data collected on real world use of these drugs are still some years off.
The market will be watching boceprevir and telaprevir for the next three or four years, Silver says.
An important factor will be the success rate of the drugs on people who have previously failed to respond to the standard of care.
That's not how clinical trials are run. They are usually conducted with patients who have not had therapy, the so-called treatment-naive. Using treatment-naive patients creates a baseline but does not approximate real-life conditions.
Most people with a disease have tried one or more drugs, ratcheting up from least to most powerful and expensive.
Another real-life issue will be the side effects. Newly diagnosed patients may find the side effects of either drug, plus interferon and ribavirin, intolerable.
The most common telaprevir side effect is a rash, Stevens says.
Boceprevir's predominant side effect is anemia. That raises the prospect that another drug will need to be added to the regimen, perhaps Epogen, the anemia-fighting biologic from Amgen (NMS:AMGN).
It's available as a generic in Europe, but remains branded in the U.S.
Another reason to think telaprevir has the inside track is the likelihood that it will require a shorter period of treatment, Silver says.
"At the end of the day, this race will be data-driven," he said.
While there's been no head-to-head trial, the existing data should become available for close comparison at a meeting of the American Association for the Study of Liver Diseases in Boston starting Oct. 28.
By most counts, the global market for hepatitis C products is now $4 billion a year. According to a report from the commercial analysis firm Research & Markets, that should rise to $8.5 billion by 2016.
The reasons for the growth: the increasing number of cases and the new drugs in the pipeline that will make treatment more accessible and tolerable.
Source
August 14, 2010
Less-Invasive Biopsies More Common
By Michael Smith, North American Correspondent, MedPage Today
Published: August 13, 2010
Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine,
Harvard Medical School, Boston and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner Earn CME/CE credit for reading medical news.
The number of biopsies using less-invasive percutaneous methods nearly doubled over a decade, according to researchers.
And, because of the shift to image-guided procedures, radiologists are now performing half of all procedures, and 70% of lymph node biopsies, according to Sharon Kwan, MD, of the University of California San Francisco, and colleagues.
But practice patterns are still evolving and in some areas, nonradiologists are increasing their share of biopsies, Kwan and colleagues reported online in Radiology.
The first percutaneous needle biopsy of the liver was reported in 1932, but the advent of new imaging techniques in recent years suggests that image-guided percutaneous procedures -- performed by radiologists -- would have largely replaced more invasive procedures.
To investigate the issue, Kwan and colleagues analyzed Medicare claims data from 1997 through 2008, which showed that biopsies using all procedures rose from 1,380 to 1,945 procedures per 100,000 Medicare enrollees between 1997 and 2008.
That change represents a compound annual growth rate of 3%, the researchers reported.
During the study period, they found, percutaneous needle biopsies did increase -- from 59% to 67% of all biopsies (with the exception of breast biopsies, where a coding change in 2001 affected the reported distribution of open versus percutaneous procedures).
The use of percutaneous needle biopsies rose from 295,836 in 1997 to 573,397 in 2008 -- equivalent to an increase from 953 to 1,645 biopsies per 100,000 Medicare enrollees, for a compound annual growth rate of 5%.
On the other hand, the researchers reported, biopsies performed with nonpercutaneous approaches had a compound annual growth rate of minus 3% over the same time period.
But the choice of method varied widely with anatomic site, they found. On one hand, percutaneous needle biopsies were the dominant choice for kidney and liver, representing 96% and 90%, respectively, of all biopsies in these sites in 2008.
On the other hand, percutaneous needle biopsies were the minority in the superficial lymph nodes and musculoskeletal soft tissues, at 46% and 30%, respectively, they reported.
Most Current Procedural Terminology codes don't distinguish between percutaneous procedures performed with and without image guidance, the researchers noted, but for two areas that do -- percutaneous core biopsies of the breast and fine needle aspirations -- there was an increase in the use of imaging.
For breast biopsies, image guidance rose from 85% in 2002 to 95% in 2008, while for fine needle aspirations, the increase was even greater -- from 54% in 2004 to 77% in 2008, they found.
Over the study period, the top three specialties performing biopsies were radiology, general surgery, and pulmonology. Members of those specialties together performed 75% of all biopsies during the period.
Radiologists' share, however, increased steadily, from 35% in 1997 to 56% in 2008, while general surgeons and pulmonologists saw their shares decrease from 21% to 15% and 10% to 5%, respectively, Kwan and colleagues reported.
The most rapid growth, according to anatomic region, occurred in lymph node biopsies, where radiologists' share increased from 12% to 70%, for a compound annual growth rate of 22%.
Radiologists' share of fine needle aspirations also increased -- from 4% to 44%, for a compound annual growth rate of 37%.
The researchers noted that one limitation of Medicare data is that they mainly involve an elderly population, so the findings may not apply to a younger population.
Also, they reported, the precision of the analysis was limited by the "idiosyncrasies" of Current Procedural Terminology coding, which was used to calculate numbers and types of procedures.
The study was supported by the National Institute of Biomedical Imaging and Bioengineering.
The authors declared they had no financial relationships to disclose.
Primary source: Radiology
Source reference:
Kwan SW, et al "Effect of advanced imaging technology on how biopsies are done and who does them" Radiology 2010; DOI: 10.1148/radiol.10092130.
Source
Published: August 13, 2010
Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine,
Harvard Medical School, Boston and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner Earn CME/CE credit for reading medical news.
The number of biopsies using less-invasive percutaneous methods nearly doubled over a decade, according to researchers.
And, because of the shift to image-guided procedures, radiologists are now performing half of all procedures, and 70% of lymph node biopsies, according to Sharon Kwan, MD, of the University of California San Francisco, and colleagues.
But practice patterns are still evolving and in some areas, nonradiologists are increasing their share of biopsies, Kwan and colleagues reported online in Radiology.
The first percutaneous needle biopsy of the liver was reported in 1932, but the advent of new imaging techniques in recent years suggests that image-guided percutaneous procedures -- performed by radiologists -- would have largely replaced more invasive procedures.
To investigate the issue, Kwan and colleagues analyzed Medicare claims data from 1997 through 2008, which showed that biopsies using all procedures rose from 1,380 to 1,945 procedures per 100,000 Medicare enrollees between 1997 and 2008.
That change represents a compound annual growth rate of 3%, the researchers reported.
During the study period, they found, percutaneous needle biopsies did increase -- from 59% to 67% of all biopsies (with the exception of breast biopsies, where a coding change in 2001 affected the reported distribution of open versus percutaneous procedures).
The use of percutaneous needle biopsies rose from 295,836 in 1997 to 573,397 in 2008 -- equivalent to an increase from 953 to 1,645 biopsies per 100,000 Medicare enrollees, for a compound annual growth rate of 5%.
On the other hand, the researchers reported, biopsies performed with nonpercutaneous approaches had a compound annual growth rate of minus 3% over the same time period.
But the choice of method varied widely with anatomic site, they found. On one hand, percutaneous needle biopsies were the dominant choice for kidney and liver, representing 96% and 90%, respectively, of all biopsies in these sites in 2008.
On the other hand, percutaneous needle biopsies were the minority in the superficial lymph nodes and musculoskeletal soft tissues, at 46% and 30%, respectively, they reported.
Most Current Procedural Terminology codes don't distinguish between percutaneous procedures performed with and without image guidance, the researchers noted, but for two areas that do -- percutaneous core biopsies of the breast and fine needle aspirations -- there was an increase in the use of imaging.
For breast biopsies, image guidance rose from 85% in 2002 to 95% in 2008, while for fine needle aspirations, the increase was even greater -- from 54% in 2004 to 77% in 2008, they found.
Over the study period, the top three specialties performing biopsies were radiology, general surgery, and pulmonology. Members of those specialties together performed 75% of all biopsies during the period.
Radiologists' share, however, increased steadily, from 35% in 1997 to 56% in 2008, while general surgeons and pulmonologists saw their shares decrease from 21% to 15% and 10% to 5%, respectively, Kwan and colleagues reported.
The most rapid growth, according to anatomic region, occurred in lymph node biopsies, where radiologists' share increased from 12% to 70%, for a compound annual growth rate of 22%.
Radiologists' share of fine needle aspirations also increased -- from 4% to 44%, for a compound annual growth rate of 37%.
The researchers noted that one limitation of Medicare data is that they mainly involve an elderly population, so the findings may not apply to a younger population.
Also, they reported, the precision of the analysis was limited by the "idiosyncrasies" of Current Procedural Terminology coding, which was used to calculate numbers and types of procedures.
The study was supported by the National Institute of Biomedical Imaging and Bioengineering.
The authors declared they had no financial relationships to disclose.
Primary source: Radiology
Source reference:
Kwan SW, et al "Effect of advanced imaging technology on how biopsies are done and who does them" Radiology 2010; DOI: 10.1148/radiol.10092130.
Source
Vietnam veteran running out of options
A bronze star awarded to Frank Tate of Drums rests next to a map of where the chemical Agent Orange was applied during the Vietnam war. Tate, who saved another Marine's life during the war, and served in areas where Agent Orange was utilized, has cirrhosis of the liver that the Department of Veterans Affairs will not acknowledge as a disease caused by the foliage-destroying chemical.
By JILL WHALEN (Staff Writer)
Published: August 9, 2010
Frank Tate received the prestigious Bronze Star Medal for dragging two seriously injured Marines across fire-swept terrain in Vietnam as machine gun bullets sailed past him.
More than 30 years later, Tate's own life needs saving.
The Drums man's liver has all but completely failed. His body is filling with fluids, and his skin has already turned yellow - a telltale sign of jaundice.
Doctors told him he needs a liver transplant, said his wife, Carol Tate. But none will attempt the procedure, saying the former Marine's health is too depleted and thus, an operation is too risky.
Frank has seen many doctors, Carol said, and many of them agree: the 59-year-old's liver cirrhosis was caused by his exposure to Agent Orange, the name given to the herbicide used by the United States during the Vietnam War to destroy foliage that provided cover for the enemy.
What's frustrating, Frank said, is that the Department of Veterans Affairs doesn't acknowledge cirrhosis as a disease caused by Agent Orange.
"They won't admit to it," Frank said.
It's a tough pill for the Tates to swallow.
Tate said he lived a healthy life, leaving his Lattimer home in 1968 to serve during the Vietnam War with the Fox Company, 2nd Battalion, 7th Marines, First Marine Division. He was attached to a tank division and later dispatched to serve in the field, and eventually achieved the rank of lance corporal.
It was during the height of a 1969 battle in Vietnam's Que Son Valley that Tate came across two seriously wounded Marines lying in an exposed area, according to the citation accompanying Frank's military medal. He scooped up the first and carried him to a covered area, then dodged enemy fire again to drag the second Marine to a rice paddy dike. He also faced bullets again as he ran to retrieve additional medical supplies for the wounded.
A year after the heroic rescues, the 1968 Hazleton High School graduate returned home.
"Even when I came back from Vietnam, my liver count was always high. I was close to 21. My family doctor at that time - or anyone who sent me for blood work - always said that I have high liver counts," Frank recalled. "It was the only test that did not come back good."
Not a concern
Doctors, however, never seemed to press Frank to go for more tests to determine what was causing high readings of alkaline phosphatase in his liver, he said. With no reason for alarm, Frank and Carol, who have been married 36 years, never pursued the issue, they said.
Frank's health seemed mostly solid until 2000 when he needed a triple bypass. He had been working at the former Allsteel in Valmont Industrial Park for 33 years, where he served as president of the United Auto Workers union.
Then, another difficult blow came in 2007 when tests following gallbladder surgery revealed he had cirrhosis.
"I had no idea I was sick or that I had cirrhosis," he said. "It was as if all of a sudden I needed a liver."
No doctor could pinpoint what caused the disease, Frank explained.
His local doctor, Dr. Eugene Stish, Conyngham, said it's his "personal opinion" that Frank's cirrhosis was caused by Agent Orange exposure. "However, I have absolutely no proof that that is what caused it," he said.
But Stish said Frank did not have any history of alcohol abuse or exposure to other dangerous chemicals - two typical causes of the disease.
Exposure to Agent Orange is "the most logical reason" that Tate developed the disease, Stish said.
Following the diagnosis, Frank recalled each day brought more weakness. He went to Thomas Jefferson University hospitals, Philadelphia, to determine whether he was eligible for a liver transplant.
"I was down there for 11 days," Frank said of his stay earlier this year. "They did all kinds of tests on me."
Carol said it appeared her husband would be approved for a transplant until a last-minute evaluation by an anesthesiologist ruined his chances.
"They didn't think I would survive the operation, or if I did survive the operation, it wouldn't be for very long," Frank said. The unchecked liver disease caused other organs in his body - his heart, lungs and kidneys - to deteriorate and weaken.
During subsequent visits to Geisinger Medical Center, Danville, and Veterans Administration hospitals, the Tates said they were told the same bad news.
Since Frank's diagnosis, the couple have learned others who served in Vietnam have had similar problems.
"A cousin of my wife died of liver disease," Frank said. "He was in Vietnam."
As a young serviceman, Frank said he "wasn't aware" of Agent Orange. But in 1984, he received a letter from the office of Gov. Dick Thornburgh along with a map of where the toxic herbicide was applied. Frank said he served in some of those places.
The letter began with "Dear Pennsylvania Vietnam Veteran" and asked all 200,000 Vietnam-era veterans from the commonwealth to complete a questionnaire with military and health information "related to possible exposure to Agent Orange and other herbicides."
It's the only piece of correspondence Frank has received that hints at possible exposure. Carol noted that while her husband does receive disability benefits from the Veterans Administration, he does not receive Agent Orange compensation.
"The government just seems like it doesn't want to admit anything," she said.
'Thing of the past'
Steve and Lisa Krouse, the neighbors the Tates consider family, have taken the Tates to medical appointments and check on the couple daily.
At least one of the out-of-area doctors who has treated Frank gave the impression the government considers Agent Orange "a thing of the past" and as such, is not investing in research or cures for it, Steve Krouse said.
"They might feel that everyone who was exposed to it is weaning away and they're not putting too much effort into helping the people who were exposed to Agent Orange," Krouse said.
Calls to the Department of Veterans Affairs regarding Agent Orange were not returned to the Standard-Speaker. But a department-released list does not classify cirrhosis as a disease caused by exposure to the chemical.
At this point, the Tates and Krouses say they're hoping for a miracle.
"We're not giving up hope for him," Krouse said. "Western medicine might say he's done. But there is eastern medicine, there are stem cell transplants."
Krouse has been researching possible cures and treatments and said he learned stem cell transplants for those with liver diseases are proving successful in the United Kingdom and Germany.
And, through additional research, he's learned of an ongoing study by the University of California-San Diego and Veterans Affairs-San Diego that is proving it's possible to halt and reverse cirrhosis. There's also a drug being used successfully in a British study that nurses diseased livers back to normal, he said.
Krouse said he would love if Frank could somehow get a stem cell transplant - although it wouldn't be covered by his insurance - or be involved in one of the studies.
"He fought bravely," Krouse said, "and he's still fighting, only this time for his own life, and with only one very strong weapon - hope. And just maybe a little divine intervention too. It is what's keeping him alive right now."
Both Carol and Frank are hoping to find an answer soon, and said they wanted to share Frank's story to see if anyone else can help.
"Right now, you are reaching for time, and the time is going so fast. And I'm scared stiff," Carol said.
Frank can be contacted at greedy@ptd.net.
jwhalen@standardspeaker.com
Source
USM Studies Palm Oil Extract For Chronic Disease
August 10, 2010 16:58 PM
GEORGE TOWN, Aug 10 (Bernama) -- Universiti Sains Malaysia (USM) is in the midst of studying the use of the palm oil extract known as tocotrienol in the treatment of chronic diseases such as non-alcoholic fatty liver disease (NAFLD).
One of the researchers, Prof Lutfi Shuaib said the research started in 2007 and expected to be completed by the year end.
He said that 60 adults with high-cholesterol problems volunteered for the study and received 200mg of tocotrienol for a year.
"Initial finding shows that 50 per cent of the volunteers show positive results.
"The finding will be tabled soon at the meeting of the American Association for the Study of Liver Diseases in Boston, the United States," he said in a briefing for Plantation Industries and Commodities Minister Tan Sri Bernard Dompok.
Lutfi said the study was to prove that tocotrienol as a food supplement could be used to treat the NAFLD.
"Malaysia is the second biggest palm oil producer and tocotrienol production could potentially become an important economic activity," he said.
-- BERNAMA
Source
GEORGE TOWN, Aug 10 (Bernama) -- Universiti Sains Malaysia (USM) is in the midst of studying the use of the palm oil extract known as tocotrienol in the treatment of chronic diseases such as non-alcoholic fatty liver disease (NAFLD).
One of the researchers, Prof Lutfi Shuaib said the research started in 2007 and expected to be completed by the year end.
He said that 60 adults with high-cholesterol problems volunteered for the study and received 200mg of tocotrienol for a year.
"Initial finding shows that 50 per cent of the volunteers show positive results.
"The finding will be tabled soon at the meeting of the American Association for the Study of Liver Diseases in Boston, the United States," he said in a briefing for Plantation Industries and Commodities Minister Tan Sri Bernard Dompok.
Lutfi said the study was to prove that tocotrienol as a food supplement could be used to treat the NAFLD.
"Malaysia is the second biggest palm oil producer and tocotrienol production could potentially become an important economic activity," he said.
-- BERNAMA
Source
No science backs up 'miracle cure'
By JOE SCHWARCZ, Freelance August 14, 2010
Malaria, AIDS, hepatitis, herpes, cancer. Terrible diseases. That's why thousands and thousands of scientists around the world, armed with advanced degrees, are engaged in research projects aimed at finding a cure.
Now, ask yourself this question: What is the chance of a gold prospector, with no training in the health sciences, tackling a problem and finding an answer that has eluded the world's most renowned researchers? Furthermore, it's simple to administer, readily available and destroys the H1N1 virus, clears up acne, eliminates heavy metals and cures the common cold to boot. I can tell you what probability I would attach to this miracle solution performing as claimed. Let me see now, how does "zero" sound?
There's nothing subtle about the name of this purported wonder: "Miracle Mineral Solution (MMS)!" Well, there are no miracles to be had. Or minerals. Admittedly, however, there is a solution. Not a solution to any problem, but a solution in the sense of a substance being dissolved in water. And that substance is sodium chlorite, a common disinfectant and bleaching agent. Its chief promoter, Jim Humble, is either a brilliant inventor, a self-delusional scientifically-bewildered simpleton or a cunning scoundrel. Take your pick. I know which box I would tick off.
In a decidedly non-humble fashion, Humble claims that "this breakthrough can save your life, or the life of a loved one." He then brags that his discovery is "the answer to AIDS, hepatitis A, B and C, malaria, herpes, TB, most cancers and many more of mankind's worse diseases."
Of course you may not have heard of this revolutionary treatment, because it is being hidden from the public by those devilish pharmaceutical companies whose profits would be destroyed if the word got out about all diseases being cured in such a simple fashion.
Let's just trace how this visionary, this wonder worker, this mental colossus, discovered the gift "that would shift the course of human health history forever."
Incidentally, MMS wasn't this amazing philanthropist's first gift to humanity. That was the automatic garage door opener, which humble Humble supposedly invented, although I can't find any documented evidence for this claim.
In any case, the MMS saga begins in the South American jungle where our hero was prospecting for gold when two of his men fell ill with malaria. With no prospects for immediate medical help, Humble had to resort to his razor-sharp wits.
The sodium chlorite solution they had brought along to disinfect water obviously killed bacteria, maybe it would also destroy whatever was causing the malaria. So, he gave the men some of the solution and was stunned to see their symptoms vanish in just four hours. I bet he was!
Now Humble had a new calling: rid the world of malaria.
He started to treat sick South Americans but found that the sodium chlorite solution was only effective 70 per cent of the time. Not good enough for this dazzling mind!
He began to experiment with his concoction and discovered that when mixed with citric acid, the chlorite would be converted to chlorine dioxide, which turned out to be a superior product. Wow!
Before long, Humble claimed to have registered 75,000 successful treatments of malaria with his miracle product.
Strange, but I can't find any of these spectacular results documented in the scientific literature. Wouldn't you think that the discovery of such a simple cure for malaria would merit publication? Surely a Nobel Prize would be in the offing! Ah, I know. It must be those dastardly jealous scientists, or the evil pharmaceutical companies that are preventing publication. Yup. Must be.
As a supporter explains, "Humble had become so famous that two drug companies contacted the Minister of Health (in an unnamed country) and threatened to quit shipping drugs to the local hospitals if she didn't do something about the person claiming to be able to cure malaria."
Those fiendish companies! It's a wonder they have allowed Humble to live.
Actually, maybe they haven't. Attempts to contact him have repeatedly failed. I'm told he is "travelling" the world, busily helping people. Helping them lighten their wallets, I suspect.
If you want to know the details of his discovery -that is "how to manufacture it in your own kitchen, how to use it intravenously, how to cure colds in an hour, how to cure the worst of flu in 12 hours, how to treat cancer, AIDS and hundreds of other problems" -you have to buy his book.
I'm not sure how to describe that epic work, but "comedic" comes to mind.
Discussions about how chlorine dioxide "elongates the electron shell" of pathogens, and how its safety is confirmed by the fact that its "oxidation strength" of 0.95 volts is less than oxygen's 1.30 volts, amount to no more than mindless chemical chatter. I don't buy it. More importantly, Health Canada and the U.S. Food and Drug Administration don't buy it, either. And both urge consumers not to buy any version of Miracle Mineral Supplement.
Not only is there no evidence of efficacy for any condition, there is evidence of possible harm. Nausea, vomiting, and a life-threatening drop in blood pressure have been reported.
Humble actually maintains that nausea is a good thing because it means the body is eliminating toxins, but if bothered, he suggests it can be controlled "by eating cold apple slices that will absorb stomach toxins that have been dumped there." Like I said, comedic.
But what is decidedly not comedic is the advice on some MMS websites that AIDS patients give up their drugs and resort to intravenous MMS.
Jim Humble went out looking for gold and it seems that at least figuratively he has found it. But it is fool's gold.
MMS is not based on any reasonable science, has not been tested in any sort of randomized trials, and amounts to no more than a scheme to capitalize on the gullibility of the scientifically challenged and the desperate.
Promoting the sale of this product is criminal.
Joe Schwarcz is director of McGill University's Office for Science and Society ( http://www.oss.mcgill.ca/).
He can be heard every Sunday from 3-4 p.m. on CJAD radio.
joe.schwarcz@mcgill.ca
© Copyright (c) The Montreal Gazette
Source
Also See: Miracle Mineral Solution (MMS): Product as consumed produces a potent bleach
Malaria, AIDS, hepatitis, herpes, cancer. Terrible diseases. That's why thousands and thousands of scientists around the world, armed with advanced degrees, are engaged in research projects aimed at finding a cure.
Now, ask yourself this question: What is the chance of a gold prospector, with no training in the health sciences, tackling a problem and finding an answer that has eluded the world's most renowned researchers? Furthermore, it's simple to administer, readily available and destroys the H1N1 virus, clears up acne, eliminates heavy metals and cures the common cold to boot. I can tell you what probability I would attach to this miracle solution performing as claimed. Let me see now, how does "zero" sound?
There's nothing subtle about the name of this purported wonder: "Miracle Mineral Solution (MMS)!" Well, there are no miracles to be had. Or minerals. Admittedly, however, there is a solution. Not a solution to any problem, but a solution in the sense of a substance being dissolved in water. And that substance is sodium chlorite, a common disinfectant and bleaching agent. Its chief promoter, Jim Humble, is either a brilliant inventor, a self-delusional scientifically-bewildered simpleton or a cunning scoundrel. Take your pick. I know which box I would tick off.
In a decidedly non-humble fashion, Humble claims that "this breakthrough can save your life, or the life of a loved one." He then brags that his discovery is "the answer to AIDS, hepatitis A, B and C, malaria, herpes, TB, most cancers and many more of mankind's worse diseases."
Of course you may not have heard of this revolutionary treatment, because it is being hidden from the public by those devilish pharmaceutical companies whose profits would be destroyed if the word got out about all diseases being cured in such a simple fashion.
Let's just trace how this visionary, this wonder worker, this mental colossus, discovered the gift "that would shift the course of human health history forever."
Incidentally, MMS wasn't this amazing philanthropist's first gift to humanity. That was the automatic garage door opener, which humble Humble supposedly invented, although I can't find any documented evidence for this claim.
In any case, the MMS saga begins in the South American jungle where our hero was prospecting for gold when two of his men fell ill with malaria. With no prospects for immediate medical help, Humble had to resort to his razor-sharp wits.
The sodium chlorite solution they had brought along to disinfect water obviously killed bacteria, maybe it would also destroy whatever was causing the malaria. So, he gave the men some of the solution and was stunned to see their symptoms vanish in just four hours. I bet he was!
Now Humble had a new calling: rid the world of malaria.
He started to treat sick South Americans but found that the sodium chlorite solution was only effective 70 per cent of the time. Not good enough for this dazzling mind!
He began to experiment with his concoction and discovered that when mixed with citric acid, the chlorite would be converted to chlorine dioxide, which turned out to be a superior product. Wow!
Before long, Humble claimed to have registered 75,000 successful treatments of malaria with his miracle product.
Strange, but I can't find any of these spectacular results documented in the scientific literature. Wouldn't you think that the discovery of such a simple cure for malaria would merit publication? Surely a Nobel Prize would be in the offing! Ah, I know. It must be those dastardly jealous scientists, or the evil pharmaceutical companies that are preventing publication. Yup. Must be.
As a supporter explains, "Humble had become so famous that two drug companies contacted the Minister of Health (in an unnamed country) and threatened to quit shipping drugs to the local hospitals if she didn't do something about the person claiming to be able to cure malaria."
Those fiendish companies! It's a wonder they have allowed Humble to live.
Actually, maybe they haven't. Attempts to contact him have repeatedly failed. I'm told he is "travelling" the world, busily helping people. Helping them lighten their wallets, I suspect.
If you want to know the details of his discovery -that is "how to manufacture it in your own kitchen, how to use it intravenously, how to cure colds in an hour, how to cure the worst of flu in 12 hours, how to treat cancer, AIDS and hundreds of other problems" -you have to buy his book.
I'm not sure how to describe that epic work, but "comedic" comes to mind.
Discussions about how chlorine dioxide "elongates the electron shell" of pathogens, and how its safety is confirmed by the fact that its "oxidation strength" of 0.95 volts is less than oxygen's 1.30 volts, amount to no more than mindless chemical chatter. I don't buy it. More importantly, Health Canada and the U.S. Food and Drug Administration don't buy it, either. And both urge consumers not to buy any version of Miracle Mineral Supplement.
Not only is there no evidence of efficacy for any condition, there is evidence of possible harm. Nausea, vomiting, and a life-threatening drop in blood pressure have been reported.
Humble actually maintains that nausea is a good thing because it means the body is eliminating toxins, but if bothered, he suggests it can be controlled "by eating cold apple slices that will absorb stomach toxins that have been dumped there." Like I said, comedic.
But what is decidedly not comedic is the advice on some MMS websites that AIDS patients give up their drugs and resort to intravenous MMS.
Jim Humble went out looking for gold and it seems that at least figuratively he has found it. But it is fool's gold.
MMS is not based on any reasonable science, has not been tested in any sort of randomized trials, and amounts to no more than a scheme to capitalize on the gullibility of the scientifically challenged and the desperate.
Promoting the sale of this product is criminal.
Joe Schwarcz is director of McGill University's Office for Science and Society ( http://www.oss.mcgill.ca/).
He can be heard every Sunday from 3-4 p.m. on CJAD radio.
joe.schwarcz@mcgill.ca
© Copyright (c) The Montreal Gazette
Source
Also See: Miracle Mineral Solution (MMS): Product as consumed produces a potent bleach
A New Syringe Is First to Have Automatic Spring Mechanism Protecting Nurses
According to TransMedia, A New Syringe Is First to Have Automatic Spring Mechanism Protecting Nurses
A new safety syringe that can save lives is coming soon to a hospital near you. And one U.S. Marine combat veteran who became a nurse after wounded in Vietnam couldn't be happier.
The newly patented safety syringe from Protectus Medical Devices, Inc. (OTCQB: PTMD) will be the first to protect on-the-go healthcare workers from sometimes deadly needlestick accidents that occur all too frequently when giving injections.
And it does it automatically!
"The Protectus Automatic Self-sheathing Safety Syringe will be to nurses what seat belts and air bags are to motorists," said former Marine Marc Barbanell who has been taking the syringe on test drives and finding it incredibly safe. "Even when patients jerk their arm during an injection and send the syringe flying, it can't hurt anyone," said Barbanell, a Silver Star recipient who has since given thousands of injections to private patients.
"If a nurse were to lose control of this syringe or have it knocked out of her hands, she'd automatically be protected as a spring-activated plastic sheath instantly covers the needle, rendering it harmless and incapable of sticking anyone accidentally.
According to most recent statistics, nearly a million needlestick injuries are reported annually among U.S. healthcare workers costing healthcare system over $3 billion a year.
Workers at U.S. hospitals on average incur approximately 30 needlestick injuries per 100 beds annually. Studies show nurses sustain most of these injuries and one in seven U.S. healthcare workers is accidentally stuck by a contaminated sharp every year, while it is believed only one in three needlesticks is even reported.
From these sharps injuries there have been scores of documented cases of HIV seroconversion among healthcare personnel and 2,000 workers a year become infected with hepatitis C, and 400 contract hepatitis B. More than 20 additional types of infectious agents have been transmitted through needlesticks, including tuberculosis, syphilis, malaria, herpes, diphtheria, gonorrhea, typhus, and Rocky Mountain spotted fever.
The CDC estimates more than 80 percent of needlestick injuries can be prevented by the use of safer medical devices, such as the Protectus syringe. Needlesticks occur most in fast-paced, stressful and often understaffed facilities.
Source: TransMedia Group
Source
A new safety syringe that can save lives is coming soon to a hospital near you. And one U.S. Marine combat veteran who became a nurse after wounded in Vietnam couldn't be happier.
The newly patented safety syringe from Protectus Medical Devices, Inc. (OTCQB: PTMD) will be the first to protect on-the-go healthcare workers from sometimes deadly needlestick accidents that occur all too frequently when giving injections.
And it does it automatically!
"The Protectus Automatic Self-sheathing Safety Syringe will be to nurses what seat belts and air bags are to motorists," said former Marine Marc Barbanell who has been taking the syringe on test drives and finding it incredibly safe. "Even when patients jerk their arm during an injection and send the syringe flying, it can't hurt anyone," said Barbanell, a Silver Star recipient who has since given thousands of injections to private patients.
"If a nurse were to lose control of this syringe or have it knocked out of her hands, she'd automatically be protected as a spring-activated plastic sheath instantly covers the needle, rendering it harmless and incapable of sticking anyone accidentally.
According to most recent statistics, nearly a million needlestick injuries are reported annually among U.S. healthcare workers costing healthcare system over $3 billion a year.
Workers at U.S. hospitals on average incur approximately 30 needlestick injuries per 100 beds annually. Studies show nurses sustain most of these injuries and one in seven U.S. healthcare workers is accidentally stuck by a contaminated sharp every year, while it is believed only one in three needlesticks is even reported.
From these sharps injuries there have been scores of documented cases of HIV seroconversion among healthcare personnel and 2,000 workers a year become infected with hepatitis C, and 400 contract hepatitis B. More than 20 additional types of infectious agents have been transmitted through needlesticks, including tuberculosis, syphilis, malaria, herpes, diphtheria, gonorrhea, typhus, and Rocky Mountain spotted fever.
The CDC estimates more than 80 percent of needlestick injuries can be prevented by the use of safer medical devices, such as the Protectus syringe. Needlesticks occur most in fast-paced, stressful and often understaffed facilities.
Source: TransMedia Group
Source
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