I have fibrosis

[aberdeen577]

Dear All,
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??

[enolia]

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...

[Rome70]

Dear stef
Thank you so much for your comments!

[stef2011]

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

[StephenCastlecrag]

" 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?

[veteranB]

the more i read all this. The more I understand we need to  organize and demand Replicor to be released to defeat this terrible virus. Look what it does to us.

[stef2011]

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

[Rome70]

Thanks for sharing your thoughts!

[4est]

" 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.  

[4est]

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)

[Rome70]

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...

[pugdaddy]

Hi -

I have iron level of about 160...and want to get it down to less than 100.  

I notice that you have reduced your iron level from 176 downward to 115 (during the year from July 2011 to July 2012) - Congratulations!!...and how did you accomplish this??

Please advise - thanks!

[4est]

Thank you for your comments. I have to read this and also some other stuff in order to understanding correctly and to see the corelations.

I had look on my test results and indeed, once in Nov 2011, beside Iron Serum test I made the Feritin test and was 184 and also Transferrin saturation that was 0.49 (normal range 0.25 - 0.35).

[4est]

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"

[studyforhope]

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.

[4est]

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 ....

[4est]

"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))

[4est]

you mention:
"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.

[stef2011]

So if our immune system not detecting the virus, then can we and the virus co-exist for long time?

of course we can coesist, it doesn t matter how much hbvdna or hbsag if there is no immune response.the virus doesnt kill cells when replicating

[studyforhope]

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.

[ono8ono]

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.

So if our immune system not detecting the virus, then can we and the virus co-exist for long time?

Or will the virus keep multipying to take over the whole liver and cause death. Thank you.

[ono8ono]

why need to pay attention to the dimensions of the spleen ? Thank you.

[studyforhope]

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.

[aberdeen577]

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.

[4est]

as for ALT , this is part of Liver function tests,s o in case that this was declared normal, we can say that you ALT was in the acceptable range.

how old are you (if this is not to personal) ?