I have just joined the forum today and I have read many threads already over the last few months. I want to now start taking more care AND control.
My history is that I have had hep b since 1991. I had biopsy then and my liver was fine. The consultant put me on alpha interferon for 6 months but it did no good or so I was told. Over the next few years I was put on lamivudine and then combo with adefovir. In 2007 I was taken off combo and my hbvdna fluctuated between und and 2000/3000. Recently I had a fibroscan which was inconclusive (But showed around 11.7 kpa). I then had a second biopsy whic showed that I have fibrosis between stage 3 and 4. I was immediately put on tdf and have been on it now for a year.Having said all that I feel great and do lots of exercise in the gym 3/ 4 times a week. I can run 10k on treadmill in 55 minutes.
I take a 1500mg krill oil tablet each day; 3x 60mg blueberry extract ;1000mg garlic and 1 selenium ACE.
I have seen what tests needs to be done in other threads here and I intend to get them done soon . I know that I am anti HBE positive but i do not know the (critically important) IU/ML for the surface antigen yet.
Thank you all for the support given to others here and I am now joining those ranks. I just hope my condition is not too bad??
Thank you for sharing your medical history here - we can always learn from others' experiences. Even though you were diagnosed in 1991, we don't know when exactly you were infected. It is now known that if you can maintain very low or undetectable viral load and normal ALT with your medication, your fibrosis can be reversed. How is your viral load with tdf?
Overall, I think you are doing all the right things: monitoring by a specialist and a healthy life style to avoid fatty liver.
As for knowing your HbsAg level, it is only important if you are considering stopping medication or opting to try for a cure with Interferon combo treatment. Otherwise, keep an eye on your viral load and ALT.
All the best.
I read somewhere that Entecavir or Tenofovir can reduce the fibrosis after years of treatment, so in you care I think that this will be the case if you ALT if in the range and HVB DNA undetectable during Tenofovir.
Intresting will be if you have some historical date, back when you made the interferon and Lamivudine tratament. How was yourHVB DNA nad ALT during Lamivudine/Adefovir perioad. Why you chose to stop Lamivudine /Adefovir ?
How was you ALT after 2007 (when HVB DNA was 2000/3000 UI)
I am just not sure when I got the virus but I remember the consultatnt telling me in 1991 that I had it for some time. But at least at that time my fibrosis was 0. Since I went on TDF my VL is und but, for one month, it went to 400 and then back to und. My ALT is normal. I go to liver clinic each month now for creatine testing and all is normal.
I am going to the clinic again shortly and I was going to request HBsAG quantitative but I guess there is no real need. I am wondering about cancer risk with fibrosis and should I have an ultrasound with this degree of fibrosis?
Thank you so much for your reply, it has put my mind at rest already.
The problem is that I never thought I would need to keep a check on these issues. I do know that I went on alpha interferon almost immediately after beign diagnosed. I took an injection 3 times a week and the sides were just aweful. At that time HBVDNA was not available as a test until later. I think agter about a year from stopping Inf I started on lam and it did bring down my DNA to a low level but unsure of what it was but I do know it was not und. I was on this for a few years I think and then adefovir came along. So,, I was started on it and taken off lam. Then a few years later again they combo'ed the two for a few years. That brought me up to 2007 when my DNA was und and had been for a number of years before that. I was taken off all treatment to see what would happen and I remained between und and a VL of 2000-3000 over the period laste 2007 until 2011 when I had my first fibroscan. My consultant told me at the time that they go by the number of digits in VL and went on to say that they were not particularly worried when it was in the range of 2,3 or 4 digits (that is 1000 up to 9999). So I guess th eliver damage has happened to me during ht eperiod 2007 to 2011 and maybe it is just the result of the number of years I have the virus.During all of this time my ALT was never brought up to me.
Thank you, I will ask next time at clinic about the possibility of having this done. I have also read that Stef2011 has recommended taking fish oil tablets along with blueberry and vitD supplement (melatonin) for fibrosis regression .As you see I am already taking the blueberry and the krill oil tablet; should I look at getting the melatonin or some other vitD to supplement this? Also I drink lost of white tea and green tea each day, maybe up to 5 mugs.
yes, I did ask for a fibroscan after the first 6 months of tdf but they said it was too early. It is now a year; do you think I should ask again?? There was several readings coming from the machine. I know its the average of 5 sound waves (I think) but mine ranged from 6kpa to 15kpa so they thought the best thing was the biopsy. It is th esecond biopsy that I have had , the first being in 1991 where the reading was F0, now F3/4 :-(
Thanks for sharing your experience.
I'm Asian age 55 and I got HBV in 1986 but I believe I caught the virus from reused needles from the hospital in the '70. Since then I've been a carrier: normal alt, HBV DNA around 500 to 2000 iu/ml all these years. I still have not had any liver biopsy and there is no fibroscan in the US. I have Genotype B and lately I feel kind of tired after lunch. I wonder it has anything to do with the liver? Do you feel tired during the day?
My last ultrasound in 7/2012 was normal.
I dont think so. Sometimes I do get tired in the afternoon but after eating a large lunch!! I am told this is normal but I am not quite sure. I just do not know is a VL of 500 to 2000 iu/ml can cause liver damage. My consultant told me one time that they were not overly worried if the reading was between 1 and 9999 (4 digits) but if went into 5 digits 10,000 upwards they would be concerned. That is one of my issues; is it normal to expect that my liver is on fibrosis stage 3/4 after this many years of having the active virus even with the various treatments that I have been on? Hope someone here can give me a help in understanding why this could have happened. When I had the fibroscan I fully expected my liver to still be f0. How wrong I was.
Your situation is indeed unusual and worrisome. You stated that you do not know any ALT information over the years. I assume that the viral load numbers that you gave are in international units.
The driving force for fibrosis progression is the intensity of the immune response in the liver and more specifically the degree of activation of the stellate cell system.
Normally a low viral load lowers the immune attack on the liver.Thats why antivirals protect the liver health.
Do you have any other risk factors for liver disease like obesity or diabetes or alcohol use or hemochromatosis that could have accelerated the damage?
How frequently was the viral load tested after you came of the antivirals?
As far as I know fibroscan is the average from the 10 measures (at least this was in my case and I have it twice until now (one year apart)).
I think that they say to you that is to early, because they expect some revers of the fibrosis in one year and not in couple of months, so you can ask for a fibroscan now.
you say "During all of this time my ALT was never brought up to me", so that means you don't now your ALT from 1991 until now ?
(maybe you have it under ALAT or GPT or SGPT or Alanine Aminotransferase names)
Anyway I was put in a another form (easy for reading) all your information, please add more information (or correct this ones) is is necessary
- discover the Hbv infection
- First biopsy => F0 (liver was fine)
- Start interferon
- Stop interferon
- ALT - unknown
- Start Lamivudine
- HVB DNA - low level but not undetectable
- ALT - unknown
- Stop Lamivudine and Start Adefovir
- ALT - unknown
- Add Lamivudine (combo with Adefovir)
- ALT - unknown
- HVB DNA - undetecatble
- Stop the antiviral combo
- ALT - unknown
2007 - 2011
- HVB fluctuate around 2000 - 3000 UI/ml
- ALT - unknown
- fibroscan inconclusive ( 11.7 kpa)
- second biopsy => F3/4
- Start Tenofovir
- ALT - unknown
2011 - 2012
- HVB DNA - undetectable (except one month that was 400 UI)
- ALT - unknown
Still have some questions, that can help to figure out what was going on.:
How you discoverd the hbv infection, back to 1991 ? (why you made this tests)
I suspect that you (and you doctor) stop tha Lamivudine and start the Adefovir becuse the HBV DNA was not undetectable.
How was your HVB DNA over the Adefovir period ? And why you decided to add Lamivudine ?
How you where monitorised after stooping the antiviral combo (after 2007) ? (test was only HBV DNA?)
Do you remember when after starting the Tenofovir treatment was the month that you notice HBV DNA to 400 UI ? (was first test ?, or was something like start Tenofovir - HBV DNA - undetectable .... HBV DNA - 400 UI...... HBV DNA - undetectable .... ?)
This is pretty much the history. I am sure that I was not always DANA und over these years. My doctor never mentioned ALT to me on any occasion except to say my liver functions were always normal. He put me on adefovir to give lamivudine a "holiday". And later he tried both in combo. My DNA def became und during this time becasue I remember him saying. And in 2007 they decided to stop treatment because I guess that I was und for quite some time. Whilst I remained und sometimes it would flare up to the IU levels that I have indicated. But they did not seem to worry about this . It wasnt until I had the fibroscan that further action was taken. I guess I could have gone to tdf in 2007 but it was not offered and I didnt even know that it existed. I go to clinic each month to check creatine levels and next time I go I will ask for ALT at baseline one year ago when I started tdf and will also ask to see what it is now.
Thank you so much for detailing my history and making this effore for me. I tryuly appreciate it.
HAve been doing this for years now , just for general health reasons. But I idid read somewhere here where Stef was suggesting fish oil/blueberry/melatonin (I think) as a means to help reduce fibrosis. I am wondering is he still on this regimen as well as the heptech meds.
Why do you say unusual and worrisome? I have no other sides that I know of. I have been taking a fish oil/garlic/seleniumACE/blueberry extract tablets for quite afew years now unless some of them are having a bad effect on my liver. I also do quite a bit of exercise. And the thing is my doctor never talked to me in any detail about my results; it was always just my lfts are normal and dna is at whatever level. My VL was checked at 6 monthly intervals. But I would never know what the real results were at any time. And, more importantly, until I found this great firum I would not have thought to ask. Do you think that I should not have any fibrosis given the history above and with no other issues to cause damage?
Routine blood test for company pension brought this up, I didnt realise I had it and I do not know when I was infected. I wish I did.
I think they put me on combo because I was not achieveing und and I am wondering during all of this time taht, even my VL might have been low, that it was causing this damage.
When I went on tdf in september last year my VL was und bit I dont know about ALT. It remained und each month until Feb this year when it went to 400iu/ml but then went back to und and remains there so far. I am goijg to ask what my ALT was when I started tdf and what it is presently next time I go to clinic.
hello, I am worried about my husbands health, he was diagnosed with hep b since 3 months. His dna test has 8,6x10 (4) ( 10 in power 4). alt level a bit higher than normal. Is the dna high ? we havent gone to the doctor yet..I would appreciate any answer from you all..thanks. Linda
the tests on virus are not correlated to liver damage and most carriers have no damage but only fibroscan can tell, not blood tests
also be aware that it is our immune system to make liver damage and not the virus
My understanding of what @studyforhope try to say for you case:
Hepatitis B virus is not destroy the liver cell, liver cell are destroy by our immune system when he try to get out the virus. (ALT is release from the liver during this action)
This destroy of cells causes the fibrosis.
Immune system is believe that is activated by the high viral load numbers
You have been under the treatment and you say that your viral load was low (close to undetectable or 3000 UI max), so for this reason your immune system should not atac the virus and destroy the liver, so no fibrosis (or small fibrosis ) should be detected
this is why @studyforhope considered you case (on the data that you provide) "unusual and worrisome".
So maybe some other factors was the causes for this fibrosis and this is why he as
"Do you have any other risk factors for liver disease like obesity or diabetes or alcohol use or hemochromatosis that could have accelerated the damage? "
I am a very fit 55 yr old. approc 185 cm in height with 88 kg.
I am wondering now if it is the selenium or fish oil or garlic tablets that is causing this amount of damage because I am still taking all of them.
It is possible that you had silent flares in between the test times after you were taken off the antivirals, that your ALT - indicating liver inflammation, infiltration and activation of fibrosis forming stellate cells ( myofibroblasts) was close to the upper border of so called "normal" and that you are what has been characterized a "fast fibroser".
That term was coined to describe the fact that in some patients, due to a high responsiveness of the fibrosis/scar forming stellate system , a much more rapid progression of fibrosis was found under relatively mild stimulating conditions.
You are now on TDf and that should keep your VL permanently very low. This is often referred to as "UND" because most labs do not have an ultrasensitive detection test.
Using the heptech supplements should give you a very good chance to suppress further fibrosis progression.Their formula BTW contains among many other substances a blueberry extract, which is probably however not one of the key antifibrotic components.
If you have an abdominal ultrasound, which should be done anyway and regularly as an early HCC detection measure, you should ask and insist that they tell you the dimensions of your spleen in cm.
Your worries that you current supplement regiment might have caused this are understandable but are most likely unwarranted.
In your lab values, of which you always should obtain a copy, you need to pay attention to the platelet number, the Albumin and the bilirubin results aside from the AST ALT values.
Note that most labs have misleading "normal ranges" for ALT,
like up to 55 or even 60 when 25 should be the top number for a male. This is caused by the widespread use of alcohol and the presence of liver damaging adipositas in the so called normal" population, from which these ranges are derived.
Ask for a ferritin test also, next time, to see how your iron stores are.
Your "inconsistent" fibroscan values are indicative of localized scarring in the liver.
They should do much more than 5 shots until they find enough high quality shots ( as reflected in the individual images) that truly reflect the current stiffness of your average parenchymal liver tissue.I know this is not ging to happen.
If you can get a gastroscopy it would be good to know that there are no signs of esophageal varizes and no signs of high portal pressure in the stomach ( red signs) present.
Advanced fibrosis makes it harder for the blood coming from the portal vein to pass though the liver capillary system, causing an increase in portal blood presssure, also called portal hypertension.
the spleen is part of the portal system, increased pressure will tend to increase/expand the spleen to a larger sice. It often increases up to 15cm or higher.
A normal spleen size (up to 11cm)is a good indicator, that the portal pressure is not substantially increased.
Increased portal pressure is a major cause of death from liver disease, because the back pressure in the lower esophageal veins will cause varizes in the lower esophagus, that can rupture abruptly and cause massive deadly bleeding episodes, if not treated immediately.
"In your lab values, of which you always should obtain a copy, you need to pay attention to the platelet number, the Albumin and the bilirubin results aside from the AST ALT values. "
could you, please, teach us more regarding the relations between Platelet number, Albumin, Bilirubin and ALT /AST.
I suspect that somehow the Platelet number (or a fraction of it) is related to the natural production of interferon, so I suppose that a increase number (bigger then the lab threshold) will indicate a immune response and this can be related to ALT/AST value to determine if the immune response is related to the liver (HBV) or not. - this is one interpretation from a engineer, so can be wrong.
"Ask for a ferritin test also, next time, to see how your iron stores are. "
Could you please be mo re specific on this.
What is the normal range for ferritin test result ?
This is a personal question, because I know that I'm high on iron store, but I can establish if is the time to take some actions or not. (my Iron Ser level was 176 in July 2011, 157 in Nov 2011, 118 in March 2012 and 115 in July 2012 (all in μg/100 ml))
So if our immune system not detecting the virus, then can we and the virus co-exist for long time?
I think so and also i think that this explain the first part of the HBV infection named imunotolerant phase where the virus is not trigger a immune response.
What I don't know is if some relation between the VL in imunotolerant phase and immune response in immune clearance phase exist or not. (some how this question is if is a good think to treat people in imunotolerant phase in oreder to reduce the immune response in immune clearance phase and to limit liver damage )
But after the immune clearance phase, usually ended with HBeAg negative and low or und VL, is a good think not to have immune response and to have a low ALT/AST and low VL.( all this some how say that a balance between immune response and virus multiplication was establish)
this is my understanding, but like I mentioned I'm not a doctor, os my interpretation can be wrong or incomplete ....
When the degree of cirrhosis advances ( there is a wide range of cirrhosis progression) liver synthetic functions are increasingly impaired and a platelet growth factor is produced in insufficient quantities.
Thats why platelet numbers are typically decreasing below the range ( normal 140000 to 350000) when cirrhosis progresses, first below for example 100000 then as low as 20000.
It is considered a good indicator of overall liver function and should be part of any liver evaluation.
In advancing cirrhosis Albumin will eventually starting to fall below the lower limit of norm eg 3.5 gram/100ml of plasma.
Similarly the bilirubin processing function of the liver will be impaired eventually, leading to an increased bilirubin level.
At the same time, paradoxically, ALT/AST values are often getting lower in the advanced stages of cirrhosis since there are less hepatocytes available to kill or damage.
The normal ferritin levels are from 30 to 400ng/ml.
Ferritin is they key iron storage container with thousands of iron atoms stored in a thick protein shell with elaborate mechanisms to set them free on demand. While Ferritin is mainly stored intracellular , like in the liver, the duodenal enterocytes and the macrophages, its plasma concentration reflects the total ferritin content quite well and it is the preferred test to judge your bodywide iron storage situation.
The serum iron that you measured is the iron almost completely bound to transferrin and it reflects more the activity of the ferroportin system that solely controls the iron efflux from cells containing stored iron.
The ferroportin availibility and from that the available circulating iron level are controlled by the hepcidin peptide, produced by the liver in response to iron stores, but also in response to inflammation and oxygen transport capacity/hypoxia.
These insights into iron metablism have been discovered only very recently.
I just realized that in my previous comment I confuse Leukocyte with Platelet - so I want to say that:
"I suspect that somehow the Leukocyte (not Platelet ) number (or a fraction of it) is related to the natural production of interferon, so I suppose that a increase number (bigger then the lab threshold"
Please comment on the this contradiction. It is common knowledge that it is not the virus but the immune system that make the damage to the liver, but how then a spontaneous virus clearance is explained, It happens without uprising of ALT and liver inflammation? Is it not the immune system who cleans the virus?
And another question. If the immune system causes the damage, then why do we need to take all those vitamins and minerals to stimulate the immune system? interferon treatment actually simulates it too and the damage is suspended while you are on INF.
If we to follow this logic than it would be a good strategy for inactive carriers to keep the immune system down and wait till new drug gets to the market...
Nothing special, just reduce the meat quantity from diet.
Also I take some vit D supliments, but I don't know if any relation between this and reduce iron level.
as far as i know you can go and "donate" blod in order to decrease your iron level ("donate" = give away because you have to declare that you have hbv in order that your blood not to be pass to other people)
" It is common knowledge that it is not the virus but the immune system that make the damage to the liver, but how then a spontaneous virus clearance is explained" - yes is common understanding that immune system make the damage, but I wish to know to explain spontaneous clerance :)
"It happens without uprising of ALT and liver inflammation? Is it not the immune system who cleans the virus? " - I don't know. I think that immune sistem clear the virus and I assume that some liver inflammation can occurred, but this will be regenerated after that
"f the immune system causes the damage, then why do we need to take all those vitamins and minerals to stimulate the immune system?" - Not necessary to stimulate, maybe to help will be a better word (help can also mean to lower down the inflammation)
"interferon treatment actually simulates it too and the damage is suspended while you are on INF." - I don't think that damage is suspended, contrary I think that damage is some how bigger, but it will be suspended after that and the liver can regenerate beater
"If we to follow this logic than it would be a good strategy for inactive carriers to keep the immune system down and wait till new drug gets to the market..." - can be, I have no idea what is the best, but I think that with normal ALT/AST, Fibroscan F0/1, HVB DNA < 2000 UI we are on the safe part - this has to be monitored. Also I think that qHBSAg has to be monitored and if we found qHBSAg less then 1500 UI we can try to go on interferon and try to lose HBSAg and also for the people that have more then 45 year old I think that is indicated to go on the NUC and stay on the NUC if HVB DNA is not undetectable. But all this is only what I think, I'm not a doctor and my understanding on this subject is limited.
hbv is cleared by immune system mainly by purging cccdna out of cells without killing and then just kill the few remaining infected cells at the end of hbv clearance when hbvdna is und and hbsag and the low levels.this happens in acute hbv and liver has no damage from this just little inflammation, fibrosis develops only after years of damage on chronic carriers
this is how an immune system which is not suppressed and controlled by hbv works, of course chronic carriers have their immune system controlled by hbv mainly and it doesn t work to clear hbv, it just kills cells but dont purge anything out of cells without killing
some clear cccdna without alt rise because the purge effect works very well or by very slow decrease of cccdna in years of hbv suppression by nucs...the cccdna will get slowly to very low levels by diluition when infected liver cells repliactae, ths process is extremely slow and even the damage of fatty liver makes this process a litlle faster
" ths process is extremely slow and even the damage of fatty liver makes this process a litlle faster " - I find this comment very interesting. I read in a recent paper by Chinese researchers:
Impact of liver steatosis on antiviral effects of pegylated interferon-alpha in patients with chronic hepatitis B.
In the abstract, it was stated that: "The HBV DNA titer in the steatosis group was significantly lower than that of the non-steatosis group (6.961.27 vs. 7.541.28 log10 copies/ml; t=2.161, P=0.033).".
Now whether this implies patients with fatty liver will also have lower qHBsAg is a moot point because from the abstract:
"After 48 weeks of PEG-IFNa treatments, there was no significant difference in HBeAg seroconversion or the percentage of undetectable HBV DNA (less than 3 log10 copies/ml) between steatosis and non-steatosis patients. However, the steatosis patients presented with a significantly lower complete response rate (virologic response plus biochemical response) compared to non-steatosis patients (26.5% vs. 48.4%; x² =4.373, P=0.037). Of the 45 CHB patients with undetectable HBV DNA after 48 weeks of treatment, seven did not achieve ALT normalization. The rate of patients with non-biochemical response was significantly higher in the steatosis group than in the non-steatosis group (33.3% vs. 6.67%; P=0.032)."
This would not support the idea that patients with fatty liver have lower level of qHBsAg.
So, Stef2012, do you have a reference to your comment that "damage of fatty liver makes this process a little faster?
its about the study just pubblished on people off drugs with faster decline of hbsag during the years, but not important to coment too much on it since it is such a little difference
fatty liver can make higher alt and this just makes cccdna less stable than in livers with normal alt, so hbsag gets lower a little faster but i agree this is such a slow process that it is best not to have fatty liver and not count on it
Hi all, I didn't get the chance to read all messages but I believe Replicor will not go far in making the drug available to patients because they want and need lots of money to be able to make official big scale trials and go through the process quickly. They are a private company with a few employees and have not enough money to finance big scale trials, that is why they are now basically doing only marketing and hoping to get as much investors as they can, that is too bad for us. I believe that if they invested more in the human capital, they would gain a lot, sooner or later but they want money first. If they give the chance to have people from this forum try the drug and pass the info to everyone around here and all the people they know...I mean, they could take some risk and save the humanity rather than calculating how much more money they are making every month! This is SAD to realize, I am not necessarily thinking about myself here but I am just saying, it is sad to see how much money has become important...
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