Aa
No research on the permanent conditions from treatment??
am stage 2 and Dr. wants to treat- I am older so am getting a bad feeling about the permanent side affects I know would be certain.. so quality of life issues come forward... do I want to live sick and miserable..probably not, do I want to chance 1 1/2 years of waiting for the new treatment that does not have the side affects.. I'm a gambling women, but ...Any input??
i'm feeling really good 4 months post triple/incivek..still some sx but i think even after tough sx while on tx i'll end up way better then before tx....stage 2 can move on into 3...the good thing is with all the folks doing triple everyone is learning more and more about how to deal with symptoms...i would really consider triple tx...first learn everything you can..good luck...billy
I agree w/ the post made by advocate, but would add......
Both Telaprevir and Boceprevir moved from starting Phase 3 trials through review and to new drug approval in well under 3 years.
That was with 48 week placebo arms and "official" EOT 24 week PCR's.
The FDA has implemented fast tracking tools which will further streamline approval process. Some of these new treatments seem to have 12 and 24 week arms (not 48 week) and the FDA now recognizes that a SVR12 is sufficient measurement tool. The trials will even proceed faster now due to these improvements.
If both of these PI's were able to hit market in well under 3 years with the old constraints (from start phase 3 to market) the new therapies should also be able to in even less time.
If one wants to further track one's progression I would recommend annual fibrosure tests (a blood test; a simple blood draw) and if one can a fibroscan. By the way....... I don't often hear about people getting annual biopsies. This is also often a particularly problematic if one is cirrhotic.
willy
Both Telaprevir and Boceprevir moved from starting Phase 3 trials through review and to new drug approval in well under 3 years.
That was with 48 week placebo arms and "official" EOT 24 week PCR's.
The FDA has implemented fast tracking tools which will further streamline approval process. Some of these new treatments seem to have 12 and 24 week arms (not 48 week) and the FDA now recognizes that a SVR12 is sufficient measurement tool. The trials will even proceed faster now due to these improvements.
If both of these PI's were able to hit market in well under 3 years with the old constraints (from start phase 3 to market) the new therapies should also be able to in even less time.
If one wants to further track one's progression I would recommend annual fibrosure tests (a blood test; a simple blood draw) and if one can a fibroscan. By the way....... I don't often hear about people getting annual biopsies. This is also often a particularly problematic if one is cirrhotic.
willy
What is your age? Have you ever treated before? Do you know how long you've had Hep C? What genotype do you have?
Generally speaking, progression of liver damage is believed to be slow, over decades. However, there is no way to predict how slowly or quickly an individual will progress. My husband (age 59, has probably had Hep C for 35+ years, diagnosed in 2007) progressed from f1-2 to f4 between 2007 - 2010, as described on two liver biopsies each of those years. That quick progression happened with close monitoring by a hepatologist and treating with every available option.
When to treat is a decision that you will need to make with your doctor, but based on my husband's personal rate of progression, we have been advised by his hepatologist to treat when treatment options are available, so he did SOC in 2007 (failed), daily infergen injections/1400 mg Riba in 2010 (failed), and is doing triple tx with Incivek now (now in week 27, completed Incivek in late Dec.). My husband has not suffered any long term damage from either of his previous two treatments.
The best advice that I can give is DO NOT COUNT ON SLOW PROGRESSION as it is not always the case. By the way, if I recall correctly Telaprevir was supposed to be available in 2009 but didn't actually become available until 2011, so I agree with can-do-man that at least 3 years is a more realistic time frame for new meds to complete trials and receive FDA approval.
Advocate1955
Generally speaking, progression of liver damage is believed to be slow, over decades. However, there is no way to predict how slowly or quickly an individual will progress. My husband (age 59, has probably had Hep C for 35+ years, diagnosed in 2007) progressed from f1-2 to f4 between 2007 - 2010, as described on two liver biopsies each of those years. That quick progression happened with close monitoring by a hepatologist and treating with every available option.
When to treat is a decision that you will need to make with your doctor, but based on my husband's personal rate of progression, we have been advised by his hepatologist to treat when treatment options are available, so he did SOC in 2007 (failed), daily infergen injections/1400 mg Riba in 2010 (failed), and is doing triple tx with Incivek now (now in week 27, completed Incivek in late Dec.). My husband has not suffered any long term damage from either of his previous two treatments.
The best advice that I can give is DO NOT COUNT ON SLOW PROGRESSION as it is not always the case. By the way, if I recall correctly Telaprevir was supposed to be available in 2009 but didn't actually become available until 2011, so I agree with can-do-man that at least 3 years is a more realistic time frame for new meds to complete trials and receive FDA approval.
Advocate1955
Here is one study;
http://www.natap.org/2008/HCV/022008_02.htm
In this case it is about bone loss possibly caused by SOC, which one may also infer damage to teeth. Using the board search engine you can access numerous threads on damage which seems to be caused by SOC. You are correct that there has not been much inquiry into this. Only recently has it been given a name PIS (post interferon syndrome), although that seems to refer to the worst of the symptoms. Oddly enough, after in excess of a decade of using IFN to treat patients w/ HCV many doctors seem generally unaware of this potential issue.
The board search engine shows that it is hardly a rare phenomena. It also seems to indicate that in addition to being ignorant of the potential issue, many doctors are at a loss of how to diagnose/differentiate the issue and I don't believe that I have ever read of any meaningful treatments for it. To some extent, the medical community has been silent about it to the point of denial.
I'm not sure that I agree with the idea you can wait 18 months and have a treatment which will have no side effects. Probably the soonest there will be an interferon free FDA approved treatment will be about 3 years. Both Gilead and Vertex are estimating filing for approval in late 2014, but I hardly think it a stretch to just round it up to exactly 3 years from now. That would be for 2 drug companies, but I believe that Bristol Myers Squibb could have one soon thereafter and Abbott also has a good treatment in trials; 3 drugs w/ riba for 12 weeks and a high efficacy rate. There will be others coming, just not as soon.
If you were to wait the 5 years that some here have predicted I believe you will be seeing interferon AND ribaviren free treatments.
When you talk about permanent side effects, only a smaller percentage have the PIS type post TX issues 1-5%, perhaps. There is a larger group with general issues that don't seriously impact on daily life; they may be noticeable but for many are well worth it.
My advice is to read up on the potential issues of TX and factor in your staging. You may not be wise in waiting if your staging has been advancing rapidly. That is between you and your doctor.
I agree that there is no certainty of long term side effects. Actually, most people recover with no serious issues. The flip side is that I also know people who treated for shorter periods...... and lower doses of either or both IFN or ribaviren that did end up with long term sides. I also know people who treated several times who had no issues the first 2 times but who had issues on their third treatment. I know people who have treated 6, 7, 8 times who were not seriously impaired and would do it yet another time if it were to give them an opportunity to be cured.
I'm just describing the terrain. I would just read up on new treatments. there will be much to read about in the upcoming weeks following EASL. You need to have a firm grasp of your condition and staging and a good doctor who is up to speed on current and future (potential) forms of TX. There is seldom a lot of certainty with this disease and treatment. There is risk in treating and there is also certainly risk in waiting to treat.
best,
willy
http://www.natap.org/2008/HCV/022008_02.htm
In this case it is about bone loss possibly caused by SOC, which one may also infer damage to teeth. Using the board search engine you can access numerous threads on damage which seems to be caused by SOC. You are correct that there has not been much inquiry into this. Only recently has it been given a name PIS (post interferon syndrome), although that seems to refer to the worst of the symptoms. Oddly enough, after in excess of a decade of using IFN to treat patients w/ HCV many doctors seem generally unaware of this potential issue.
The board search engine shows that it is hardly a rare phenomena. It also seems to indicate that in addition to being ignorant of the potential issue, many doctors are at a loss of how to diagnose/differentiate the issue and I don't believe that I have ever read of any meaningful treatments for it. To some extent, the medical community has been silent about it to the point of denial.
I'm not sure that I agree with the idea you can wait 18 months and have a treatment which will have no side effects. Probably the soonest there will be an interferon free FDA approved treatment will be about 3 years. Both Gilead and Vertex are estimating filing for approval in late 2014, but I hardly think it a stretch to just round it up to exactly 3 years from now. That would be for 2 drug companies, but I believe that Bristol Myers Squibb could have one soon thereafter and Abbott also has a good treatment in trials; 3 drugs w/ riba for 12 weeks and a high efficacy rate. There will be others coming, just not as soon.
If you were to wait the 5 years that some here have predicted I believe you will be seeing interferon AND ribaviren free treatments.
When you talk about permanent side effects, only a smaller percentage have the PIS type post TX issues 1-5%, perhaps. There is a larger group with general issues that don't seriously impact on daily life; they may be noticeable but for many are well worth it.
My advice is to read up on the potential issues of TX and factor in your staging. You may not be wise in waiting if your staging has been advancing rapidly. That is between you and your doctor.
I agree that there is no certainty of long term side effects. Actually, most people recover with no serious issues. The flip side is that I also know people who treated for shorter periods...... and lower doses of either or both IFN or ribaviren that did end up with long term sides. I also know people who treated several times who had no issues the first 2 times but who had issues on their third treatment. I know people who have treated 6, 7, 8 times who were not seriously impaired and would do it yet another time if it were to give them an opportunity to be cured.
I'm just describing the terrain. I would just read up on new treatments. there will be much to read about in the upcoming weeks following EASL. You need to have a firm grasp of your condition and staging and a good doctor who is up to speed on current and future (potential) forms of TX. There is seldom a lot of certainty with this disease and treatment. There is risk in treating and there is also certainly risk in waiting to treat.
best,
willy
My doctor told me when my plateletes were 96 that they were low but not dangerously so.
When I was diagnosed with decompensated cirrhosis, my alt and ast were both under 200.
I had few symptoms.
Hep C does not act the same with everyone.
It's extremely variable making it difficult to put it in a box.
Although Bo had higher alt and ast than me, I was much, much sicker.
When I was diagnosed with decompensated cirrhosis, my alt and ast were both under 200.
I had few symptoms.
Hep C does not act the same with everyone.
It's extremely variable making it difficult to put it in a box.
Although Bo had higher alt and ast than me, I was much, much sicker.
Not sure why you have said your platelet count is abnormally low as 120 is really close to the normal range.... Mine stay at 80 and have been below 30.
In adults, a platelet count of less than 100,000/microliter is considered low, but might occur without symptoms. Abnormal bleeding often occurs when the platelet count is below 30,000/microliter
http://www.answers.com/topic/thrombocytopenia
In adults, a platelet count of less than 100,000/microliter is considered low, but might occur without symptoms. Abnormal bleeding often occurs when the platelet count is below 30,000/microliter
http://www.answers.com/topic/thrombocytopenia
A biopsy is the best way, but they are usually only done once a year.
My Hep C began to progress at a pretty rapid rate, from last July, when ALT/AST was around 160/200 andmy platelets were 150, to last October, when my blood work showed ALT/AST at 400/500, and platelets were abnormally low, at 120. I think platelet count with ALT/AST, plus HGB RBC count, are just something to watch (my HGB and RBC also dropped), but everybody is different. I also was getting lots of physical symptoms at that point,as well
My Hep C began to progress at a pretty rapid rate, from last July, when ALT/AST was around 160/200 andmy platelets were 150, to last October, when my blood work showed ALT/AST at 400/500, and platelets were abnormally low, at 120. I think platelet count with ALT/AST, plus HGB RBC count, are just something to watch (my HGB and RBC also dropped), but everybody is different. I also was getting lots of physical symptoms at that point,as well
Fibrogenesis
Chronic infection with hepatitis C virus (HCV) typically
induces injury and inflammation of the liver, which
appear to be responsible for the associated fibrogenesis.
Fibrogenesis is a dynamic process characterized by the
synthesis of constituents of the extracellular matrix, which
is a complex mixture of glycoproteins (collagen, elastin,
fibronectin, laminin) and proteoglycans organized in a
tridimensional network.1 Fibrogenesis is a non-specific
mechanism, which lasts as long as injury persists in the
liver and is believed to help limit the extension of theinflammatory reaction. Fibrosis, therefore, is a physiologic
mechanism, which is at first beneficial, but which
can become pathological if the viral infection and chronic
hepatocellular injury persist.
Fibrosis is characterized by the deposition of collagen
and other extracellular matrix proteins and their organization
in complex polymers, which are insoluble and induce
loss of the liver architecture.2 In all forms of chronic
hepatitis, including chronic hepatitis C, active fibrosis begins
around the portal areas (periportal or zone 1 fibrosis)
and gradually extends out into the lobules towards the
central veins (zone 3) with septa formation and then
bridging fibrosis3-5 (Fig. 1). The final stage of fibrosis
constitutes cirrhosis with extensive fibrosis linking portal
and central areas and nodular regeneration of the liver
parenchymal.
Collagen and matrix proteins that constitute fibrosis
are largely produced by activated hepatic stellate cells.6,7
The stellate cells are activated from a quiescent lipocyte
phenotype to a fibroblastic phenotype. The activation occurs
in 2 phases: initially activation of stellate cells by
cytokines, chemokines, and other signalling molecules induced
by the inflammatory process, followed by transformation
of the stellate cells into a myofibroblastic
phenotype, in which the cell can proliferate, attract leukocytes,
and produce extracellular collagen and matrix
proteins.
The steps in stellate cell activation and transformation
have been demonstrated to occur in chronic hepatitis C.8
The major fibrogenic cytokine, transforming growth factor
(TGF)-, is increased in expression in the liver in
patients with chronic hepatitis C, and mRNA levels forthis cytokine are also increased.9,10 Serum levels of TGF-
are present in increased amounts in patients with chronic
hepatitis C,9,10 and levels of connective tissue growth factor,
which are associated with the expression of TGF-,
are also markedly increased, serum levels correlating with
the degree of liver fibrosis.11
During the fibrogenesis process, a basal membrane appears
separating the hepatocytes from sinusoidal blood
and perturbing the exchange of nutrients between blood
and hepatocytes, a process known as capillarization of the
sinusoids. Also, the accumulation of the fibrosis components
in the extracellular matrix is responsible for the
storage of very reactive molecules (growth factors and cytokines)
in an inactive form, which may be activated in
certain circumstances.11 In addition, during the progression
of fibrosis, there is a quantitative increase of the
extracellular matrix, but also qualitative changes in repartition
of each different component. Indeed, liver fibrosis
is characterized by the transformation from normal extracellular
matrix (basal membrane) into a reticulated and
dense matrix (fibrillar type), which is much more resistant
to enzymatic degradation.
http://www.hawaii.edu/hivandaids/Fibrosis%20And%20Disease%20Progression%20In%20Hepatitis%20C.pdf
Chronic infection with hepatitis C virus (HCV) typically
induces injury and inflammation of the liver, which
appear to be responsible for the associated fibrogenesis.
Fibrogenesis is a dynamic process characterized by the
synthesis of constituents of the extracellular matrix, which
is a complex mixture of glycoproteins (collagen, elastin,
fibronectin, laminin) and proteoglycans organized in a
tridimensional network.1 Fibrogenesis is a non-specific
mechanism, which lasts as long as injury persists in the
liver and is believed to help limit the extension of theinflammatory reaction. Fibrosis, therefore, is a physiologic
mechanism, which is at first beneficial, but which
can become pathological if the viral infection and chronic
hepatocellular injury persist.
Fibrosis is characterized by the deposition of collagen
and other extracellular matrix proteins and their organization
in complex polymers, which are insoluble and induce
loss of the liver architecture.2 In all forms of chronic
hepatitis, including chronic hepatitis C, active fibrosis begins
around the portal areas (periportal or zone 1 fibrosis)
and gradually extends out into the lobules towards the
central veins (zone 3) with septa formation and then
bridging fibrosis3-5 (Fig. 1). The final stage of fibrosis
constitutes cirrhosis with extensive fibrosis linking portal
and central areas and nodular regeneration of the liver
parenchymal.
Collagen and matrix proteins that constitute fibrosis
are largely produced by activated hepatic stellate cells.6,7
The stellate cells are activated from a quiescent lipocyte
phenotype to a fibroblastic phenotype. The activation occurs
in 2 phases: initially activation of stellate cells by
cytokines, chemokines, and other signalling molecules induced
by the inflammatory process, followed by transformation
of the stellate cells into a myofibroblastic
phenotype, in which the cell can proliferate, attract leukocytes,
and produce extracellular collagen and matrix
proteins.
The steps in stellate cell activation and transformation
have been demonstrated to occur in chronic hepatitis C.8
The major fibrogenic cytokine, transforming growth factor
(TGF)-, is increased in expression in the liver in
patients with chronic hepatitis C, and mRNA levels forthis cytokine are also increased.9,10 Serum levels of TGF-
are present in increased amounts in patients with chronic
hepatitis C,9,10 and levels of connective tissue growth factor,
which are associated with the expression of TGF-,
are also markedly increased, serum levels correlating with
the degree of liver fibrosis.11
During the fibrogenesis process, a basal membrane appears
separating the hepatocytes from sinusoidal blood
and perturbing the exchange of nutrients between blood
and hepatocytes, a process known as capillarization of the
sinusoids. Also, the accumulation of the fibrosis components
in the extracellular matrix is responsible for the
storage of very reactive molecules (growth factors and cytokines)
in an inactive form, which may be activated in
certain circumstances.11 In addition, during the progression
of fibrosis, there is a quantitative increase of the
extracellular matrix, but also qualitative changes in repartition
of each different component. Indeed, liver fibrosis
is characterized by the transformation from normal extracellular
matrix (basal membrane) into a reticulated and
dense matrix (fibrillar type), which is much more resistant
to enzymatic degradation.
http://www.hawaii.edu/hivandaids/Fibrosis%20And%20Disease%20Progression%20In%20Hepatitis%20C.pdf
Will’s point being (I’m pretty sure :o)), that while elevated liver enzymes usually suggest something is going on with the liver, the opposite isn’t always true. It‘s quite possible to advance through and into cirrhosis with liver enzymes within reference range:
“...Abnormal LFTs often, but not always, indicate that something is wrong with the liver, and they can provide clues to the nature of the problem. However, normal LFTs do not always mean that the liver is normal. Patients with cirrhosis and bleeding esophageal varices can have normal LFTs...”
http://www.aafp.org/afp/1999/0415/p2223.html
We’d hate to rely on ALT/AST for decision power to undergo antiviral therapy, only to have patients fall between the metaphorical cracks.
--Bill
“...Abnormal LFTs often, but not always, indicate that something is wrong with the liver, and they can provide clues to the nature of the problem. However, normal LFTs do not always mean that the liver is normal. Patients with cirrhosis and bleeding esophageal varices can have normal LFTs...”
http://www.aafp.org/afp/1999/0415/p2223.html
We’d hate to rely on ALT/AST for decision power to undergo antiviral therapy, only to have patients fall between the metaphorical cracks.
--Bill
If the liver enzymes are consistantly elevated, it in indicative of inflamation. It is showing that the immune system is attempting to fight of the virus, which causes the scarring (fibrosis)
The Hep C virus isn't what harms the liver, it's our own immune systems, attempting to fight off the virus, that causes the damage.
I got this imfo, form my Internal Medicine Doctor, a leading Specialist in Hep C research, who gives us a half houur lecture, once a week, so I dont have 'the link" for this imfo, but believe me, she is reknowned and well respected, in her field, and also a proffesor
The Hep C virus isn't what harms the liver, it's our own immune systems, attempting to fight off the virus, that causes the damage.
I got this imfo, form my Internal Medicine Doctor, a leading Specialist in Hep C research, who gives us a half houur lecture, once a week, so I dont have 'the link" for this imfo, but believe me, she is reknowned and well respected, in her field, and also a proffesor
Watching you liver enzymes is not the best way to decide when to treat, mine never did get very high and i was cirrhotic...
Why if the OP were to consider waiting should she watch her liver enzymes as a means on when to decide to treat??
Everyone is different. I chose to treat at stage 2, because I was experiencing terrible symptoms, and my platelets dropped below normal.
It is easier to be cured, at stage 2, rather then stage 4. If you decide to wait, I would get another Biopsy,in a year, and watch your ALT/AST level, those are liver enzymes, and do you know if yours are elevated?
It is easier to be cured, at stage 2, rather then stage 4. If you decide to wait, I would get another Biopsy,in a year, and watch your ALT/AST level, those are liver enzymes, and do you know if yours are elevated?
"When "and with " what" to treat HCV is always a very personal decision ,one that should be discussed in depth with a doctor knowledgeable and experienced treating HCV and that knows your history.
You have not mentioned what Geno type you have. If type 1 then the therapy includes 3 different drugs(Peginterferon/Ribaviran and either Victrelis or Incivek) and very often would last for 24 weeks(depending on early response)
If type 2 or 3 then the combo of just PEG/Riba is used for the same length of time.
Side effects vary quite dramatically for each individual from mild to somewhat more harsh .especially if the triple therapy is needed.
The treatments above are approx. 70 -80% succesful(depending on varying factors)
At St.2 there are options to consider. Do you wait until possibly a number of different modalities are avail.(some possibly without Interferon) ?.
Keeping in mind no -one knows currently when these may be avail. however the speculation is from be wen 3 -5 years.
Will you have developed cirrhosis by then ? Possibly or possibly not,,no one can ascertain that with any certainty.
Where you are at personally in your life is usually a consideration as well..(family life employment,finances etc)
Again ... always best discussed with your doctor when considering what may be best for each individual...
welcome to the group...
Will
You have not mentioned what Geno type you have. If type 1 then the therapy includes 3 different drugs(Peginterferon/Ribaviran and either Victrelis or Incivek) and very often would last for 24 weeks(depending on early response)
If type 2 or 3 then the combo of just PEG/Riba is used for the same length of time.
Side effects vary quite dramatically for each individual from mild to somewhat more harsh .especially if the triple therapy is needed.
The treatments above are approx. 70 -80% succesful(depending on varying factors)
At St.2 there are options to consider. Do you wait until possibly a number of different modalities are avail.(some possibly without Interferon) ?.
Keeping in mind no -one knows currently when these may be avail. however the speculation is from be wen 3 -5 years.
Will you have developed cirrhosis by then ? Possibly or possibly not,,no one can ascertain that with any certainty.
Where you are at personally in your life is usually a consideration as well..(family life employment,finances etc)
Again ... always best discussed with your doctor when considering what may be best for each individual...
welcome to the group...
Will
As can-do said there is no way to know if you will have long term side effects of not.
Nobody really can say when the new meds will become generally available.
If you are interested in doing them, why don't you look into doing a clinical trial?
Nobody really can say when the new meds will become generally available.
If you are interested in doing them, why don't you look into doing a clinical trial?
“I am older so am getting a bad feeling about the permanent side affects I know would be certain...”
What led you arrive at this conclusion? Did a qualified medical professional suggest there was a certainty of developing long term complications from HCV therapy?
I treated for years without any discernable long term issues; and actually very few during the treatment itself. If you’re basing your assumption on material from internet discussion groups, you might not be doing yourself any favors.
Browse peer-reviewed, scholarly articles; talk with medical care providers and make decisions based on factual data, not emotional responses.
There are indeed all-oral drug regimens now in clinical trial. If this interests you have your doctor help you weigh relative benefits vs. risk it sounds as though your doctor has already discussed this with you and prefers that you begin earlier rather than later.
For what it’s worth, I would personally allow those trials develop further before I considered involvement. Interferon is generally required to address viral mutation as it develops as a result of these new drugs.
Good luck-
--Bill
What led you arrive at this conclusion? Did a qualified medical professional suggest there was a certainty of developing long term complications from HCV therapy?
I treated for years without any discernable long term issues; and actually very few during the treatment itself. If you’re basing your assumption on material from internet discussion groups, you might not be doing yourself any favors.
Browse peer-reviewed, scholarly articles; talk with medical care providers and make decisions based on factual data, not emotional responses.
There are indeed all-oral drug regimens now in clinical trial. If this interests you have your doctor help you weigh relative benefits vs. risk it sounds as though your doctor has already discussed this with you and prefers that you begin earlier rather than later.
For what it’s worth, I would personally allow those trials develop further before I considered involvement. Interferon is generally required to address viral mutation as it develops as a result of these new drugs.
Good luck-
--Bill
Not sure where the 1 and 1 1/2 years come from as any drugs that are in the pipline are said to be 3 to 5 years out, besides that does anyone know what permanent sides they will have? Also how can one be certain there will be lasting sides from these current drugs? For the most of us thats just not true........... Good luck
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