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New tests help pinpoint who will SVR before tx.
As I mentioned in a previous post concerning mortality and HCV tests such as the one below can determine with good accuracy who is likely to proceed to cirrhosis. There are other studies on this topic,using different means to accomplish the same goal, especially with G1. These types of diagnostic tests could greatly influence who should or shouldn't pursue treatment at this time. Elimination of the scattershot approach used now for treating to a more targeted one would have profound effects on many aspects of treatment . Most importantly it would result in fewer patients exposed needlessly to IFN/Riba. Anyone who has ever been on tx , or just read about it, can see the great benefit this can have for those with HCV. As an example if we can identify through genetic markers before tx those who could benefit from a longer course it would eliminate the risk and suffering which is inherent in any re-treatment scenario. -- ML
Science News Share Blog Cite Print Email BookmarkHepatitis C Patients Who Are At High Risk Of Developing Cirrhosis Can Now Be Reliably Identified
ScienceDaily (Apr. 30, 2007) — A researcher at the Stanford University School of Medicine has helped confirm the reliability of a new test for liver disease that is ushering in the long-promised era of personalized medicine based on each individual's genetic makeup.
The Stanford group was one of the five sites that helped determine that the genetic test can identify patients who are at high risk of developing cirrhosis from chronic hepatitis C infection. That means high-risk patients could be directed toward a long course of expensive, debilitating drug therapy, while low-risk patients might be better off delaying treatment.
"Management of cirrhosis patients is challenging," said Ramsey Cheung, MD, associate professor of medicine at the school and chief of hepatology at the Palo Alto Veterans Affairs Health Care System, who led the Stanford arm of the study. "This test is the first of its kind to use the genetic makeup of each patient to determine who is likely to develop cirrhosis. High-risk patients should be targeted for early treatment."
The test looks at variations of seven genes, and was developed by Celera, headquartered in Rockville, Md. Cheung is the senior author of the study, which will be published in the journal Hepatology. Cheung is a paid consultant for Celera, which also funded the study.
"Current therapy for hepatitis C unfortunately is very expensive, has multiple side effects and a suboptimal response rate for most patients," said Cheung. Treatment includes weekly injections of alpha interferon along with the drug ribavirin, which can cost more than $30,000 per year and can cause flu-like symptoms, nausea, depression and other side effects. And only half of patients undergoing this therapy will be cured of the infection.
Nearly 4 million Americans are infected with the hepatitis C virus, of which nearly 80 percent have a chronic infection, according to the American Liver Foundation. Chronic infection can lead to the severe scarring known as cirrhosis, which in turn may result in liver cancer or liver failure. Hepatitis C infection is the most common reason people need a liver transplant in the United States and is responsible for between 8,000 and 10,000 U.S. deaths annually.
But in the majority of people chronically infected with hepatitis C, the virus causes either no symptoms or vague, nonspecific ones. In around one-third of people chronically infected with the virus, the disease progression is slow and they may never develop cirrhosis, even after decades of infection.
The dilemma physicians face, explained Cheung, is deciding who to treat and who can wait for better therapies to come along. The key is being able to determine which patients are likely to see the infection progress to cirrhosis. Doctors consider such factors as age, gender and alcohol consumption to predict such risk, but because of individual variability, these factors don't yield a very accurate prediction. A liver biopsy can indicate the amount of damage to the liver up until the time of the biopsy, but can't reveal how much future damage will occur. The new test assessed by Cheung and his colleagues is a way to hedge the bets.
The lead author of the paper is Hongjin Huang, PhD, associate director of liver diseases at Celera in Alameda, Calif. Huang and her Celera colleagues developed the test by initially scanning the DNA of more than 1,000 people who had hepatitis C. Out of 25,000 genetic variations tested, the researchers discovered seven that could be used together as a "signature" for predicting progression to cirrhosis in Caucasians.
The resulting gene signature - the Cirrhosis Risk Score - was then independently validated on 154 hepatitis C patients at Stanford, the University of Illinois-Chicago and California Pacific Medical Center. Among patients with early-stage liver disease, the researchers were able to divide them into a high-risk category based on their gene pattern, compared with those who had low-risk gene patterns. "The Cirrhosis Risk Score was superior to the known clinical factors, such as alcohol consumption, in predicting the risk of developing cirrhosis," said Cheung.
"This test allows both physicians and patients to make an intelligent decision about the urgency of beginning antiviral therapy," he said. "If a patient turns out to be low-risk, we might advise the patient to consider deferring treatment, avoiding unnecessary side effects and expense of current therapy."
Last June, Celera licensed Specialty Laboratories of Valencia, Calif., to perform the genetic test. The test currently costs about $500.
In addition to Cheung and Huang, the other 12 authors of the study are from Celera, Virginia Commonwealth University, Mount Sinai School of Medicine, California Pacific Medical Center, the University of Illinois-Chicago and the University of California-San Francisco.
Science News Share Blog Cite Print Email BookmarkHepatitis C Patients Who Are At High Risk Of Developing Cirrhosis Can Now Be Reliably Identified
ScienceDaily (Apr. 30, 2007) — A researcher at the Stanford University School of Medicine has helped confirm the reliability of a new test for liver disease that is ushering in the long-promised era of personalized medicine based on each individual's genetic makeup.
The Stanford group was one of the five sites that helped determine that the genetic test can identify patients who are at high risk of developing cirrhosis from chronic hepatitis C infection. That means high-risk patients could be directed toward a long course of expensive, debilitating drug therapy, while low-risk patients might be better off delaying treatment.
"Management of cirrhosis patients is challenging," said Ramsey Cheung, MD, associate professor of medicine at the school and chief of hepatology at the Palo Alto Veterans Affairs Health Care System, who led the Stanford arm of the study. "This test is the first of its kind to use the genetic makeup of each patient to determine who is likely to develop cirrhosis. High-risk patients should be targeted for early treatment."
The test looks at variations of seven genes, and was developed by Celera, headquartered in Rockville, Md. Cheung is the senior author of the study, which will be published in the journal Hepatology. Cheung is a paid consultant for Celera, which also funded the study.
"Current therapy for hepatitis C unfortunately is very expensive, has multiple side effects and a suboptimal response rate for most patients," said Cheung. Treatment includes weekly injections of alpha interferon along with the drug ribavirin, which can cost more than $30,000 per year and can cause flu-like symptoms, nausea, depression and other side effects. And only half of patients undergoing this therapy will be cured of the infection.
Nearly 4 million Americans are infected with the hepatitis C virus, of which nearly 80 percent have a chronic infection, according to the American Liver Foundation. Chronic infection can lead to the severe scarring known as cirrhosis, which in turn may result in liver cancer or liver failure. Hepatitis C infection is the most common reason people need a liver transplant in the United States and is responsible for between 8,000 and 10,000 U.S. deaths annually.
But in the majority of people chronically infected with hepatitis C, the virus causes either no symptoms or vague, nonspecific ones. In around one-third of people chronically infected with the virus, the disease progression is slow and they may never develop cirrhosis, even after decades of infection.
The dilemma physicians face, explained Cheung, is deciding who to treat and who can wait for better therapies to come along. The key is being able to determine which patients are likely to see the infection progress to cirrhosis. Doctors consider such factors as age, gender and alcohol consumption to predict such risk, but because of individual variability, these factors don't yield a very accurate prediction. A liver biopsy can indicate the amount of damage to the liver up until the time of the biopsy, but can't reveal how much future damage will occur. The new test assessed by Cheung and his colleagues is a way to hedge the bets.
The lead author of the paper is Hongjin Huang, PhD, associate director of liver diseases at Celera in Alameda, Calif. Huang and her Celera colleagues developed the test by initially scanning the DNA of more than 1,000 people who had hepatitis C. Out of 25,000 genetic variations tested, the researchers discovered seven that could be used together as a "signature" for predicting progression to cirrhosis in Caucasians.
The resulting gene signature - the Cirrhosis Risk Score - was then independently validated on 154 hepatitis C patients at Stanford, the University of Illinois-Chicago and California Pacific Medical Center. Among patients with early-stage liver disease, the researchers were able to divide them into a high-risk category based on their gene pattern, compared with those who had low-risk gene patterns. "The Cirrhosis Risk Score was superior to the known clinical factors, such as alcohol consumption, in predicting the risk of developing cirrhosis," said Cheung.
"This test allows both physicians and patients to make an intelligent decision about the urgency of beginning antiviral therapy," he said. "If a patient turns out to be low-risk, we might advise the patient to consider deferring treatment, avoiding unnecessary side effects and expense of current therapy."
Last June, Celera licensed Specialty Laboratories of Valencia, Calif., to perform the genetic test. The test currently costs about $500.
In addition to Cheung and Huang, the other 12 authors of the study are from Celera, Virginia Commonwealth University, Mount Sinai School of Medicine, California Pacific Medical Center, the University of Illinois-Chicago and the University of California-San Francisco.
I feel that alot of these studies are just another way for the insurance companies to use this information to get out of paying for the treatment drugs..., especially in light of the newer drugs that will be coming down the road. Just as there will always be people who make a decision to fight cancer with all the chemo and radiation that they can handle and others who chose not to..., the decision should be left up to the patient. Not some study, some insurance company, or some predictors. I've treated 10 times and I honestly feel that it has helped me to keep from progressing even further than I already have, even though, I have not cleared. Despite all of these treatments, I've progressed to bridging fibrosis which I've had for going on 6 yrs. If I had done no treatments, I very well could be cirrhotic by now. IMHO. Susan400
Hi Mr. Liver,
Thanks for this interesting info. As the opening study says, "If a patient turns out to be low-risk, we might advise the patient to consider DEFERRING [my emphasis] treatment, avoiding unnecessary side effects and expense of current therapy."
This would have been very relevant to my case back in 2008. After presumably forty years of HCV (and almost fifteen since diagnosis in 1995), I'd 'progressed' from stage zero to stage zero. At the time, I had what my doc considered positive predictors in terms of gender,weight, lifestyle but thought I should wait to treat, given the landscape was changing fast.
For people like myself with little damage, a cirrhosis risk score would have been a very useful tool for me to weigh what to do. I panicked that my getting older was hurting my prognosis, so I pushed for treatment, despite my doc's opinion to wait, drawn from longtime experience in his field.
"This test allows both physicians and PATIENTS [my emphasis] to make an intelligent decision about the urgency of beginning antiviral therapy." I think it was the doc being intelligent in my case, not me. :)
It will be interesting to see how Vertex's genetic samples further this perhaps critical area of study.
xoxo,
Susan
Thanks for this interesting info. As the opening study says, "If a patient turns out to be low-risk, we might advise the patient to consider DEFERRING [my emphasis] treatment, avoiding unnecessary side effects and expense of current therapy."
This would have been very relevant to my case back in 2008. After presumably forty years of HCV (and almost fifteen since diagnosis in 1995), I'd 'progressed' from stage zero to stage zero. At the time, I had what my doc considered positive predictors in terms of gender,weight, lifestyle but thought I should wait to treat, given the landscape was changing fast.
For people like myself with little damage, a cirrhosis risk score would have been a very useful tool for me to weigh what to do. I panicked that my getting older was hurting my prognosis, so I pushed for treatment, despite my doc's opinion to wait, drawn from longtime experience in his field.
"This test allows both physicians and PATIENTS [my emphasis] to make an intelligent decision about the urgency of beginning antiviral therapy." I think it was the doc being intelligent in my case, not me. :)
It will be interesting to see how Vertex's genetic samples further this perhaps critical area of study.
xoxo,
Susan
People have suggested for some time that a study should be done to see what differences exist between those who spontaneously clear and those who do not. This has been done in several studies and its been found that a difference exists in a gene, IL28B. Until tests become more accepted and refined no one should base decisions on one predictor, but to use all of them to enhance the predictability of tx outcomes. Just like its always been done. -- ML
Funny some who started tx did so based on a variety of tests they had no clue about or how accurate they were. Now, they are experts.
Nature 461, 798-801 (8 October 2009) | doi:10.1038/nature08463; Received 16 August 2009; Accepted 28 August 2009; Published online 16 September 2009; Corrected 8 October 2009
1.Johns Hopkins University, Division of Infectious Diseases, Baltimore, Maryland 21205, USA
2.Cancer and Inflammation Program, Laboratory of Experimental Immunology, SAIC Frederick, Inc., NCI-Frederick, Frederick, Maryland 21702, USA, and Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Boston, Massachusetts 02114, USA
3.Institute for Genome Sciences & Policy, Center for Human Genome Variation, Duke University, Durham, North Carolina 27708, USA
4.Department of Genetics, Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06520, USA
5.Division of Medicine, Imperial College, London W2 1NY, UK
6.Department of Medicine, University of Cambridge, Cambridge CB2 2QQ, UK
7.Infections & Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland 20852, USA
8.Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland 21205, USA
9.Rho, Inc., Chapel Hill, North Carolina 27517, USA
10.University of Colorado Health Sciences Center, Division of Gastroenterology and Hepatology, Aurora, Colorado 80045, USA
11.Blood Systems Research Institute, San Francisco, California 94118, USA
12.Duke Clinical Research Institute and Division of Gastroenterology, School of Medicine, Duke University, Durham, North Carolina 27705, USA
13.Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Boston, Massachusetts 02114, USA
14.These authors contributed equally to this work.
Correspondence to: Mary Carrington2,13 Correspondence and requests for materials should be addressed to M.C. (Email: ***@****).
Hepatitis C virus (HCV) infection is the most common blood-borne infection in the United States, with estimates of 4 million HCV-infected individuals in the United States and 170 million worldwide1. Most (70–80%) HCV infections persist and about 30% of individuals with persistent infection develop chronic liver disease, including cirrhosis and hepatocellular carcinoma2. Epidemiological, viral and host factors have been associated with the differences in HCV clearance or persistence, and studies have demonstrated that a strong host immune response against HCV favours viral clearance3, 4. Thus, variation in genes involved in the immune response may contribute to the ability to clear the virus. In a recent genome-wide association study, a single nucleotide polymorphism (rs12979860) 3 kilobases upstream of the IL28B gene, which encodes the type III interferon IFN-3, was shown to associate strongly with more than a twofold difference in response to HCV drug treatment5. To determine the potential effect of rs12979860 variation on outcome to HCV infection in a natural history setting, we genotyped this variant in HCV cohorts comprised of individuals who spontaneously cleared the virus (n = 388) or had persistent infection (n = 620). We show that the C/C genotype strongly enhances resolution of HCV infection among individuals of both European and African ancestry. To our knowledge, this is the strongest and most significant genetic effect associated with natural clearance of HCV, and these results implicate a primary role for IL28B in resolution of HCV infection.
Funny some who started tx did so based on a variety of tests they had no clue about or how accurate they were. Now, they are experts.
Nature 461, 798-801 (8 October 2009) | doi:10.1038/nature08463; Received 16 August 2009; Accepted 28 August 2009; Published online 16 September 2009; Corrected 8 October 2009
1.Johns Hopkins University, Division of Infectious Diseases, Baltimore, Maryland 21205, USA
2.Cancer and Inflammation Program, Laboratory of Experimental Immunology, SAIC Frederick, Inc., NCI-Frederick, Frederick, Maryland 21702, USA, and Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Boston, Massachusetts 02114, USA
3.Institute for Genome Sciences & Policy, Center for Human Genome Variation, Duke University, Durham, North Carolina 27708, USA
4.Department of Genetics, Yale University School of Medicine, 333 Cedar Street, New Haven, Connecticut 06520, USA
5.Division of Medicine, Imperial College, London W2 1NY, UK
6.Department of Medicine, University of Cambridge, Cambridge CB2 2QQ, UK
7.Infections & Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland 20852, USA
8.Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland 21205, USA
9.Rho, Inc., Chapel Hill, North Carolina 27517, USA
10.University of Colorado Health Sciences Center, Division of Gastroenterology and Hepatology, Aurora, Colorado 80045, USA
11.Blood Systems Research Institute, San Francisco, California 94118, USA
12.Duke Clinical Research Institute and Division of Gastroenterology, School of Medicine, Duke University, Durham, North Carolina 27705, USA
13.Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology and Harvard University, Boston, Massachusetts 02114, USA
14.These authors contributed equally to this work.
Correspondence to: Mary Carrington2,13 Correspondence and requests for materials should be addressed to M.C. (Email: ***@****).
Hepatitis C virus (HCV) infection is the most common blood-borne infection in the United States, with estimates of 4 million HCV-infected individuals in the United States and 170 million worldwide1. Most (70–80%) HCV infections persist and about 30% of individuals with persistent infection develop chronic liver disease, including cirrhosis and hepatocellular carcinoma2. Epidemiological, viral and host factors have been associated with the differences in HCV clearance or persistence, and studies have demonstrated that a strong host immune response against HCV favours viral clearance3, 4. Thus, variation in genes involved in the immune response may contribute to the ability to clear the virus. In a recent genome-wide association study, a single nucleotide polymorphism (rs12979860) 3 kilobases upstream of the IL28B gene, which encodes the type III interferon IFN-3, was shown to associate strongly with more than a twofold difference in response to HCV drug treatment5. To determine the potential effect of rs12979860 variation on outcome to HCV infection in a natural history setting, we genotyped this variant in HCV cohorts comprised of individuals who spontaneously cleared the virus (n = 388) or had persistent infection (n = 620). We show that the C/C genotype strongly enhances resolution of HCV infection among individuals of both European and African ancestry. To our knowledge, this is the strongest and most significant genetic effect associated with natural clearance of HCV, and these results implicate a primary role for IL28B in resolution of HCV infection.
NYgirl agrees with the posters before her. I'd hate to put my life in the hands of something that hasn't been proven to be without flaw - not when it's this critical and seems like an awful lot of guessing.
I also totally agree, who wants to watch and wait themself into stage 3/4 and then fail at their attempt and end up cirrhotic? That never made any sense to me at all.
I also totally agree, who wants to watch and wait themself into stage 3/4 and then fail at their attempt and end up cirrhotic? That never made any sense to me at all.
It's quite a leap to take and article about "Hepatitis C Patients Who Are At High Risk Of Developing Cirrhosis Can Now Be Reliably Identified" and title a thread "New tests help pinpoint who will SVR before tx" Very misleading.
I think it is a sound idea. I just wish that they had done it 10 years earlier. Part of my issue with it is that for many people this may be arriving too late. They have already treated when they could have waited. Conversely, I'm of the opinion that this is going to become a very curable disease in 5 years; perhaps not 100% mind you but many people will be cured or curable. The issue may be whether some can wait further for prices to come down more, or whether they could wait even longer for shorter and shorter (or less toxic, problematic) forms of TX. It has been pointed out that the drugs are coming, but it remains unknown what they will cost, who will get them, etc.
What is also unknown is about what will happen with all these various drugs in development when they get approved. My feeling is that the price will come down, even for what seems like a good treatment for us now; triple therapy w/ a PI. When STAT C drugs get approved in 4 -5 years this will virtually become discarded treatment.
My point remains though, that I don't think that many of us will have to decide whether to wait a lifetime to treat.
My question is how accurate will these tests be?
My presumption is that they are to be used at predicting the efficacy of current SOC on patients based on genetics. Isn't that about to be changed, perhaps discarded with the addition of PI's to the mix?
When STAT-C combination PI's are used in the future there may still be a profile of people more/less likely to succeed but in general, the drugs will tend to work on more people, perhaps everyone, since they stop viral replication. Further, since there may be few sides there may not be an issue of broadcasting.....giving the drugs combo to anybody.
There may not be a need for such a test in 5 years if one were to assume that the cost of TX were to be accessible- a big IF perhaps.
Willy
What is also unknown is about what will happen with all these various drugs in development when they get approved. My feeling is that the price will come down, even for what seems like a good treatment for us now; triple therapy w/ a PI. When STAT C drugs get approved in 4 -5 years this will virtually become discarded treatment.
My point remains though, that I don't think that many of us will have to decide whether to wait a lifetime to treat.
My question is how accurate will these tests be?
My presumption is that they are to be used at predicting the efficacy of current SOC on patients based on genetics. Isn't that about to be changed, perhaps discarded with the addition of PI's to the mix?
When STAT-C combination PI's are used in the future there may still be a profile of people more/less likely to succeed but in general, the drugs will tend to work on more people, perhaps everyone, since they stop viral replication. Further, since there may be few sides there may not be an issue of broadcasting.....giving the drugs combo to anybody.
There may not be a need for such a test in 5 years if one were to assume that the cost of TX were to be accessible- a big IF perhaps.
Willy
I don't have enough info to comment on the Celera product, but here's another tack on genetic analysis.
Vertex have sequenced the HCV RNA for every subject in each of their Telaprevir trials. Now, several years after the first trials, they know which subjects achieved SVR and which did not and can now attempt to isolate genetic markers that characterize those that failed treatment. I can't comment on their progress with this analysis, but if it turns out that there are unique genetic markers that predict successful tx, surely that would be a major therapeutic advance. The only caveat is that [initially at least] such markers may only be reliable for the tx protocol of the trials - PI + SOC for n weeks.
Its really hard to see how anyone could even approach this problem without an extensive library of genetic samples from a large cohort of subjects both pre and post tx.
Vertex have sequenced the HCV RNA for every subject in each of their Telaprevir trials. Now, several years after the first trials, they know which subjects achieved SVR and which did not and can now attempt to isolate genetic markers that characterize those that failed treatment. I can't comment on their progress with this analysis, but if it turns out that there are unique genetic markers that predict successful tx, surely that would be a major therapeutic advance. The only caveat is that [initially at least] such markers may only be reliable for the tx protocol of the trials - PI + SOC for n weeks.
Its really hard to see how anyone could even approach this problem without an extensive library of genetic samples from a large cohort of subjects both pre and post tx.
I don't get the title of this thread as "New tests help pinpoint who will SVR before tx". It should be "Celera Needs Money, Comes Up With Cirrhosis Guessing Tool".
Based on what I'm reading and to the extent that I understand, I don't see how the test can be validated. It seems that they looks at the 7 genes to arrive at a signature. I don't see where they have completed multi-year follow-up to see if the gene guessing is correct. Even if they did follow speed of progression all the way to cirrrhosis how would they know the point of infection when most patients don't know.
I don't know about this one. I admit that I don't get the whole concept of genes or even planet formation.
Based on what I'm reading and to the extent that I understand, I don't see how the test can be validated. It seems that they looks at the 7 genes to arrive at a signature. I don't see where they have completed multi-year follow-up to see if the gene guessing is correct. Even if they did follow speed of progression all the way to cirrrhosis how would they know the point of infection when most patients don't know.
I don't know about this one. I admit that I don't get the whole concept of genes or even planet formation.
My spell check is wacked so here is proponent and ludicrous spelled correctly.
And just to clarify, I'm not saying those with stage 2 should not wait for the PI's if indeed they arrive in 2011. I'm saying once the best available treatment is on the market and the odds for SVR have increased significantly, watchful waiting at stage 2 or even stage 1 with a genetic marker for cirrhosis does not make any sense to me.
And just to clarify, I'm not saying those with stage 2 should not wait for the PI's if indeed they arrive in 2011. I'm saying once the best available treatment is on the market and the odds for SVR have increased significantly, watchful waiting at stage 2 or even stage 1 with a genetic marker for cirrhosis does not make any sense to me.
Among patients with early-stage liver disease, the researchers were able to divide them into a high-risk category based on their gene pattern, compared with those who had low-risk gene patterns. "The Cirrhosis Risk Score was superior to the known clinical factors, such as alcohol consumption, in predicting the risk of developing cirrhosis," said Cheung.
"This test allows both physicians and patients to make an intelligent decision about the urgency of beginning antiviral therapy," he said. "If a patient turns out to be low-risk, we might advise the patient to consider deferring treatment, avoiding unnecessary side effects and expense of current therapy."
______________________________________________________________________
On the other hand what about those that are high risk even with early stage liver disease? What does that say about the "watch and wait" approach? I'm not a proponet of watch and wait even if the damage is staged at 2. To tell someone to wait until their damage advances past stage 2 is ludicuious to me with or without and cirrhosis marker test.
"This test allows both physicians and patients to make an intelligent decision about the urgency of beginning antiviral therapy," he said. "If a patient turns out to be low-risk, we might advise the patient to consider deferring treatment, avoiding unnecessary side effects and expense of current therapy."
______________________________________________________________________
On the other hand what about those that are high risk even with early stage liver disease? What does that say about the "watch and wait" approach? I'm not a proponet of watch and wait even if the damage is staged at 2. To tell someone to wait until their damage advances past stage 2 is ludicuious to me with or without and cirrhosis marker test.
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