Aa
Fibrosis
I was able to test my current fibrosis state and I am still stage 3-4 transitional. I had hoped that I would see some improvement by now (15 months SVR), but nothing so far. There are some studies in the works for anti fibrotic treatments. I am going to try and get into one. Anyone have any information on particular studies? I only have general rumors and didn't see anything with a Google search.
Hi Lala,
Don't worry, I will be careful about any further trials. First, I will diet, exercise and just lead a healthy life.
Good to hear from you.
Eric
Don't worry, I will be careful about any further trials. First, I will diet, exercise and just lead a healthy life.
Good to hear from you.
Eric
hi Eric! i would be very careful withe the anti fibrotic studies, esp with the new drugs, remember it is your body. it is disappointing that you said people with 3-4 could have a slightly higher risk for cancer, this is scary. but the good news is that there's no further progression. you are wise, i will trust whatever you choose to do.
The comments about the link between HCV and low cholesterol concern me but make sense. My cholesterol has always been low despite not having a "low cholesterol" diet. I chalked this up to genetice, but maybe it is the virus that is keeping it low.
Thanks for the good info here.
Regards,
TryingToBeNotTheWalrus
Thanks for the good info here.
Regards,
TryingToBeNotTheWalrus
There was a study somewhere that said that Statins not only lowered Cholesterol but the other benefit is it "Lowers Inflamation". Inflamation causes a host of problems by itself and Interferon treatment also causes inflamation post treatment in a lot of us.
So some Dr's are recommending statins for Cholesterol even if you are borderline.
Bobby
So some Dr's are recommending statins for Cholesterol even if you are borderline.
Bobby
This is what I was told - got it from MikeSimon so you know it's correct.
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I think this sort of sums it up - from the excerpt.
"Based on the result of this large scale community study, HCV viremia
appears to be associated with lower serum cholesterol and triglyceride
levels which implies that HCV itself might play a significant role on
serum lipid profile of patients with chronic HCV infection."
I think that when you have HCV your cholesterol and triglycerides are
reduced and once the virus is eradicated those markers return to your
normal values. This stuff is so genetic that it's crazy. My diet would
not suggest a cholesterol of 150 - more like 250.
On the bright side I really think that statins are one of those magic
drugs. If I weren't a transplant recipient I think I'd request a
script. Some of the studies are amazing. One study showed that statin
users who smoked had a slower lung function decline than non-smokers
who were not on statins. I think the age span was 60 to 65 or
something close to that. There have been a bunch of other positives
associated with statin use and I probably have some article somewhere.
I just think that, aside form some potential liver issues, statins may
be great drugs for anyone.
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I think this sort of sums it up - from the excerpt.
"Based on the result of this large scale community study, HCV viremia
appears to be associated with lower serum cholesterol and triglyceride
levels which implies that HCV itself might play a significant role on
serum lipid profile of patients with chronic HCV infection."
I think that when you have HCV your cholesterol and triglycerides are
reduced and once the virus is eradicated those markers return to your
normal values. This stuff is so genetic that it's crazy. My diet would
not suggest a cholesterol of 150 - more like 250.
On the bright side I really think that statins are one of those magic
drugs. If I weren't a transplant recipient I think I'd request a
script. Some of the studies are amazing. One study showed that statin
users who smoked had a slower lung function decline than non-smokers
who were not on statins. I think the age span was 60 to 65 or
something close to that. There have been a bunch of other positives
associated with statin use and I probably have some article somewhere.
I just think that, aside form some potential liver issues, statins may
be great drugs for anyone.
Does that mean that my liver is functioning normal since my cholesterol is "high"?
There are a whole bunch of us who went from great cholesterol levels to having high cholesterol post treatment. Someone was explaining it elsewhere to me the other day and what I gathered was that this probably is what our real cholesterol would have been had our livers been working correctly in the first place. I'll see if I can find the 'real' scientific description but in the end that's what I thought it meant.
Grrrr grrrr more reasons to try and lose weight / exercise / get really thin again. I just wanted to enjoy old age and a bowl of ice cream but that seems to have gone out the window in one fell swoop in the past few weeks.
There are a whole bunch of us who went from great cholesterol levels to having high cholesterol post treatment. Someone was explaining it elsewhere to me the other day and what I gathered was that this probably is what our real cholesterol would have been had our livers been working correctly in the first place. I'll see if I can find the 'real' scientific description but in the end that's what I thought it meant.
Grrrr grrrr more reasons to try and lose weight / exercise / get really thin again. I just wanted to enjoy old age and a bowl of ice cream but that seems to have gone out the window in one fell swoop in the past few weeks.
"GoofyDad's comment about digestion of food damaging the liver."
I may be over-simplifying - but that's how I think of it. There are two processes going on here - one being the liver storing what we eat in the form of useable calories (glucose?), and the other the liver acting as the buffering/detoxifying interface between our tender innards and what we shove down our gullets. Both these processes stress the liver - and in the case of the second I think it's actually designed to sacrifice cells in the process. Then the short-term internal repair processes built into the liver funtion involve collogen and scarring. Slowing food intake to a trickle minimizes the damage.
"promoting the "digestion" of scar tissue" "How does one go about this?"
I think some of the supplements HR recommended went after this. Food group-wise I'm not aware of anything in particular. I mentioned this more in the context of the problems with drugs - something designed to digest our collagen-based tissues could have unwelcome consequences.
I may be over-simplifying - but that's how I think of it. There are two processes going on here - one being the liver storing what we eat in the form of useable calories (glucose?), and the other the liver acting as the buffering/detoxifying interface between our tender innards and what we shove down our gullets. Both these processes stress the liver - and in the case of the second I think it's actually designed to sacrifice cells in the process. Then the short-term internal repair processes built into the liver funtion involve collogen and scarring. Slowing food intake to a trickle minimizes the damage.
"promoting the "digestion" of scar tissue" "How does one go about this?"
I think some of the supplements HR recommended went after this. Food group-wise I'm not aware of anything in particular. I mentioned this more in the context of the problems with drugs - something designed to digest our collagen-based tissues could have unwelcome consequences.
Interesting thread. My transplant docs advised eating smaller, more frequent meals rather than large meals. This makes sense in light of GoofyDad's comment about digestion of food damaging the liver.
My doctor wants me to lose weight as I have gained about 20 lbs since ending TX. I'm working on it. One of the TP docs is a liver transplant recipient himself and I note that he is really "rail thin".
My doctor wants me to lose weight as I have gained about 20 lbs since ending TX. I'm working on it. One of the TP docs is a liver transplant recipient himself and I note that he is really "rail thin".
The folks at Mt Sinai think that people with HCV and fibrosis have a tendency to get fatty liver. In the past, they suggested the South Beach Diet as the best diet to treat fatty liver. Not that I can't sand to lose some weight :).
As far as the number of days treating... that would be difficult. The first few treatments were 6 months, but with interferon doses much lower than today and not pegylated and especially -- no Riba.
As far as the number of days treating... that would be difficult. The first few treatments were 6 months, but with interferon doses much lower than today and not pegylated and especially -- no Riba.
...rail-thin...
Oh boy, finally I get to the normal range of BMI and now have to hear this ;-/ I was starting to really enjoy eating for the first time in my life. I WAS rail thin...couldn't be thinner just about all of my life - wonder if that helped to hold down the fibrosis from 3 to 4?
Andiamo altogether with all the courses of treatment - how many years do you figure you were on treatment? It interests me because we've always been lead to believe that our livers were "getting a break" during this time but it just does not seem to be true. I was hoping that after 72 weeks and 2 1/2 years SVR I'd be down past a 2 now but I have the feeling that it might not be so.
If I wasn't so afraid to find out the answer I'd go get another biopsy myself.
Remember when VeggieDip insisted that in order to get SVR you HAD to be thin (or was it that all thin people automatically got SVR - same difference)? I remember arguing that that had to be wrong but now it's making me wonder.......it seems lately there is so much proof that we really DO have to get quite svelt in order to have any pro-dynamics going on in our livers that it's kind of scary.
Oh boy, finally I get to the normal range of BMI and now have to hear this ;-/ I was starting to really enjoy eating for the first time in my life. I WAS rail thin...couldn't be thinner just about all of my life - wonder if that helped to hold down the fibrosis from 3 to 4?
Andiamo altogether with all the courses of treatment - how many years do you figure you were on treatment? It interests me because we've always been lead to believe that our livers were "getting a break" during this time but it just does not seem to be true. I was hoping that after 72 weeks and 2 1/2 years SVR I'd be down past a 2 now but I have the feeling that it might not be so.
If I wasn't so afraid to find out the answer I'd go get another biopsy myself.
Remember when VeggieDip insisted that in order to get SVR you HAD to be thin (or was it that all thin people automatically got SVR - same difference)? I remember arguing that that had to be wrong but now it's making me wonder.......it seems lately there is so much proof that we really DO have to get quite svelt in order to have any pro-dynamics going on in our livers that it's kind of scary.
"promoting the "digestion" of scar tissue"
How does one go about this?
I am going to take the diet advice you pass on.
How does one go about this?
I am going to take the diet advice you pass on.
I wnet on the diet when I first stopped treatment that was March of 07. I stayed on the diet for three months.
Low cholesterol is a sign of possible liver malfunction; I don't know what high cholesterol means.
Eric
Low cholesterol is a sign of possible liver malfunction; I don't know what high cholesterol means.
Eric
I haven't spoken to HR in a long while. Back toregressing - there are two approaches, reduce the ongoing laying-down of collegen via liver frienly lifestyles (limiting cellular damage) - and promoting the "digestion" of scar tissue. The former is a best first line of attack strategy. HR wanted us to precede meals with fiberous veggies and eat in many small meals - thus keeping the entry of calories to a trickle.
Keep weight off and exercise.
He cited the American breakfast as about the worst thing you could do: slamming the liver with immediate calories from fruit juice, bagels, donuts, plus the fatty bacon, etc. Eat the fruit - don't drink the juice he says. One of his suggestions is eat raw spinach before the rest of your breakfast. I find that one suprisingly easy - but often it's cooked spinach for me. I have it with eggs and salsa picante. Mmmmmmm.
Keep weight off and exercise.
He cited the American breakfast as about the worst thing you could do: slamming the liver with immediate calories from fruit juice, bagels, donuts, plus the fatty bacon, etc. Eat the fruit - don't drink the juice he says. One of his suggestions is eat raw spinach before the rest of your breakfast. I find that one suprisingly easy - but often it's cooked spinach for me. I have it with eggs and salsa picante. Mmmmmmm.
"I went on the South Beach diet and they dropped to normal within a few weeks."
So you've been on the South Beach diet before? When, and how long?
Does that mean that my liver is functioning normal since my cholesterol is "high"?
Thanks,
Janice
So you've been on the South Beach diet before? When, and how long?
Does that mean that my liver is functioning normal since my cholesterol is "high"?
Thanks,
Janice
Same boat, since I started at stage 4. Would REALLY like to get down to at least 2 so I don't have to spend the rest of my life being screened for liver cancer, and excited about the study figures of 10% of cirrhotics regressing to zero (martinis have crossed my mind too).
Thanks, Goofydad for the concept of problems associated with antifibrotics that target collagen breakdown. Guess I will keep searching along with the rest of you.
Thanks, Goofydad for the concept of problems associated with antifibrotics that target collagen breakdown. Guess I will keep searching along with the rest of you.
I read somewhere that a blood thinner was being looked at for it's anitfibrotic properties. I tried to find that article and had no luck so far but I found the following....
Melatonin May Be Served As Potential Anti-fibrotic Drug
ScienceDaily (Apr. 7, 2009) — In China, the incidence of liver cirrhosis is still high. Liver cirrhosis results from fibrosis. If treated properly at fibrosis stage, cirrhosis can be prevented. However, no effective antifibrosis drugs are available at present. Several lines of evidences suggest that oxidative stress plays an important role in the etiopathogenesis of hepatic fibrosis.
Melatonin can protect cells, tissues, and organs against oxidative damage induced by a variety of free-radical-generating agents and processes.
A research team led by Professor Jian-Ming Xu from the First Affiliated Hospital of Anhui Medical University, China evaluated the possible fibrosuppressant effect of melatonin in rat.
In this study, hepatic fibrosis in rats was successfully induced by subcutaneous injection of sterile CCl4 twice weekly for a total of 12 wk. At the beginning of injection of CCl4, melatonin (2.5, 5, 10 mg/kg body weight) was intraperitoneally administered to the rats daily for 12 wk. Hepatic fibrotic changes were evaluated biochemically by measuring tissue hydroxyproline levels and histopathogical examination. The serum activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) were used to evaluate the hepatic injury. Hepatic oxidative stress markers were evaluated by changes in the amount of lipid peroxides, measured as malondialdehyde (MDA) and glutathione peroxidase (GPx) in liver homogenates. Serum hyaluronic acid (HA), laminin (LN), and procollagen 3 N-terminal peptide (P3NP) were determined as serum markers of hepatic fibrogenesis.
Their results suggested that treatment with melatonin (10 mg/kg) could decrease the scores of hepatic fibrosis grading, reduced the contents of HA, LN in serum and Hydroxyproline (HYP) in liver, treatment with melatonin (5,10 mg/kg ) could decrease serum levels of ALT, AST and blocked the increase in MDA in rats with hepatic injury caused by CCl4.
Their result indicated melatonin could ameliorate CCl4-induced hepatic fibrosis in rats. The protective effect of melatonin on hepatic fibrosis may be related to its antioxidant activities. This may provide a basis for further studies on the potentially protective effect of melatonin on liver function in cirrhotic patients
link for the article above>>
http://www.sciencedaily.com/releases/2009/03/090330123210.htm
here are some other articles that I found interesting....
http://www.scielo.br/scielo.php?pid=S1413-86702007000700007&script=sci_arttext
http://www.ncbi.nlm.nih.gov/pubmed/12445421
http://www.scielo.br/scielo.php?pid=S1413-86702007000700007&script=sci_arttext
Melatonin May Be Served As Potential Anti-fibrotic Drug
ScienceDaily (Apr. 7, 2009) — In China, the incidence of liver cirrhosis is still high. Liver cirrhosis results from fibrosis. If treated properly at fibrosis stage, cirrhosis can be prevented. However, no effective antifibrosis drugs are available at present. Several lines of evidences suggest that oxidative stress plays an important role in the etiopathogenesis of hepatic fibrosis.
Melatonin can protect cells, tissues, and organs against oxidative damage induced by a variety of free-radical-generating agents and processes.
A research team led by Professor Jian-Ming Xu from the First Affiliated Hospital of Anhui Medical University, China evaluated the possible fibrosuppressant effect of melatonin in rat.
In this study, hepatic fibrosis in rats was successfully induced by subcutaneous injection of sterile CCl4 twice weekly for a total of 12 wk. At the beginning of injection of CCl4, melatonin (2.5, 5, 10 mg/kg body weight) was intraperitoneally administered to the rats daily for 12 wk. Hepatic fibrotic changes were evaluated biochemically by measuring tissue hydroxyproline levels and histopathogical examination. The serum activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) were used to evaluate the hepatic injury. Hepatic oxidative stress markers were evaluated by changes in the amount of lipid peroxides, measured as malondialdehyde (MDA) and glutathione peroxidase (GPx) in liver homogenates. Serum hyaluronic acid (HA), laminin (LN), and procollagen 3 N-terminal peptide (P3NP) were determined as serum markers of hepatic fibrogenesis.
Their results suggested that treatment with melatonin (10 mg/kg) could decrease the scores of hepatic fibrosis grading, reduced the contents of HA, LN in serum and Hydroxyproline (HYP) in liver, treatment with melatonin (5,10 mg/kg ) could decrease serum levels of ALT, AST and blocked the increase in MDA in rats with hepatic injury caused by CCl4.
Their result indicated melatonin could ameliorate CCl4-induced hepatic fibrosis in rats. The protective effect of melatonin on hepatic fibrosis may be related to its antioxidant activities. This may provide a basis for further studies on the potentially protective effect of melatonin on liver function in cirrhotic patients
link for the article above>>
http://www.sciencedaily.com/releases/2009/03/090330123210.htm
here are some other articles that I found interesting....
http://www.scielo.br/scielo.php?pid=S1413-86702007000700007&script=sci_arttext
http://www.ncbi.nlm.nih.gov/pubmed/12445421
http://www.scielo.br/scielo.php?pid=S1413-86702007000700007&script=sci_arttext
Thanks for the info. Are you still in touch with HR? I don't see him posting any longer.
The south beach diet is no carbs, low fat and high veggie for the first two weeks and low cartbs after that. I have been on it for a few days now and I feel better already.
Interesting comment on the anti-fibrotics. It certainly makes sense if it targets collegen and not a specialized process in the liver. I will do my usual reading before I start any trial, but will pay special attention now that you passed on this information.
Thanks again and good luck to you as well,
Eric
The south beach diet is no carbs, low fat and high veggie for the first two weeks and low cartbs after that. I have been on it for a few days now and I feel better already.
Interesting comment on the anti-fibrotics. It certainly makes sense if it targets collegen and not a specialized process in the liver. I will do my usual reading before I start any trial, but will pay special attention now that you passed on this information.
Thanks again and good luck to you as well,
Eric
I'm in about the same boat as you Andiamo - though a bit further fibrosed, I think. I'm hoping for some regression - there's the obvious cancer thing, plus, well the long term prognosis can't be great with a buggered up liver, I wouldn't think.
At my SVR (6 mos post) my Dr (major hepatology center) told me to think in 5 year increments. He said "I think you can expect to be healthier in 5 years from now than you are today." I figured not many people get to say that at 47, so I was cool. I don't know that I've made a great deal of progress in three years, so I'm a little less cool now. But it will take time - and thankfully that seems to be something we both have.
One think Dr Liver admonished: Just don't get fat on me. HR took that a step (actually a leap) further, saying I should be rail thin - "like one of these distance runners you see." Well I'm somewhere in between: Normal BMI - but not at any risk of falling out of normal range to the low side anytime soon, LOL.
As I understand it from HR, normal eating damages the liver, as it "streches" to hold calories. This causes a normal cycle of scarring followed by scar regression. We want to reduce the scarring part to tip the balance point in favor of regressing.
I dunno what the SouthBeach allows - but if it's low-fat, no-sugar, high-vegie it's probably aligned with HR. Some months I do better than others. Time to get cracking again for me.
Another tidbit from HR - the dificulty with anti-fibrotics is we need the normal addition of collegen elsewhere in the body - for one thing the repair and maintenance of joint cartilage. So any drugs will likely have risks and downsides (arthritis?) - there's not likely to be a silver bullet.
Good luck to us and all the others hoping to recover their livers.
At my SVR (6 mos post) my Dr (major hepatology center) told me to think in 5 year increments. He said "I think you can expect to be healthier in 5 years from now than you are today." I figured not many people get to say that at 47, so I was cool. I don't know that I've made a great deal of progress in three years, so I'm a little less cool now. But it will take time - and thankfully that seems to be something we both have.
One think Dr Liver admonished: Just don't get fat on me. HR took that a step (actually a leap) further, saying I should be rail thin - "like one of these distance runners you see." Well I'm somewhere in between: Normal BMI - but not at any risk of falling out of normal range to the low side anytime soon, LOL.
As I understand it from HR, normal eating damages the liver, as it "streches" to hold calories. This causes a normal cycle of scarring followed by scar regression. We want to reduce the scarring part to tip the balance point in favor of regressing.
I dunno what the SouthBeach allows - but if it's low-fat, no-sugar, high-vegie it's probably aligned with HR. Some months I do better than others. Time to get cracking again for me.
Another tidbit from HR - the dificulty with anti-fibrotics is we need the normal addition of collegen elsewhere in the body - for one thing the repair and maintenance of joint cartilage. So any drugs will likely have risks and downsides (arthritis?) - there's not likely to be a silver bullet.
Good luck to us and all the others hoping to recover their livers.
The general opinion of my doc is that the longer you have the disease and the longer it takes for fibrosis to develop, the longer it takes to regress. I don't think I agree with that, but I have no scientific fact to refute it. I would imagine that the younger you are, the faster you will regress. I think that all regression depends on a healthy life style and little to no alcohol.
My liver panel returned all normal results and my cholesterol is low due to liver damage. I did have fatty liver when I stopped treatment and my AST/ALT were both elevated. I went on the South Beach diet and they dropped to normal within a few weeks.
I have been on the diet for one week now and I am feeling more alert. It is a healthy diet and is probably good for most people anyway.
Take care,
Eric
I have been on the diet for one week now and I am feeling more alert. It is a healthy diet and is probably good for most people anyway.
Take care,
Eric
Not lipitor; lovastatin. I haven't filled it yet, but I did drink a bottle of red wine for breakfast to help my cholesterol. It should help, right?
Did the drs tell you when you can expect some regression, or what kind of time line it takes for the liver to regenerate?
What do your liver panel labs look like? Does your ALT remain high? Just curious.
Ok, now about me...:)
I had recent labs and the main thing my dr was concerned about was my thyroid and cholesterol. I'm already on medicine for my hypothyroidism, but she wanted me to take lipitor and my total cholesterol is only 205. I know that's a little high but maybe she's more worried about a fatty liver, ?
Maybe I need the South Beach diet.
I felt like the red wine might be beneficial to my cholesterol, but she didn't say that, and I didn't ask.
Take care Eric.
Janice
What do your liver panel labs look like? Does your ALT remain high? Just curious.
Ok, now about me...:)
I had recent labs and the main thing my dr was concerned about was my thyroid and cholesterol. I'm already on medicine for my hypothyroidism, but she wanted me to take lipitor and my total cholesterol is only 205. I know that's a little high but maybe she's more worried about a fatty liver, ?
Maybe I need the South Beach diet.
I felt like the red wine might be beneficial to my cholesterol, but she didn't say that, and I didn't ask.
Take care Eric.
Janice
Thank you for the elaboration. I now understand your concern. I suspect you would feel better too if there were some regression of fibrosis. Knowing what you know, to be Stage 2 or 3 would simply give you more peace of mind in the absence of other probabilities, regardless of how small. Peace of mind is worth alot so for that alone I hope you find ways and means to regress. If you got to Stage 0, I would *buy* you the martini - in person!
Trish
Trish
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