Hbv dna is more important than hbsag quuantative i guess… but my dr suggested to do hbsag test after every 3-6 months … just to c how antiviral is performing … coz in the end loss of hbsag is more important… and it also helps in knowing feom where u have started your treatment… but hbv dna test is the one that indicates dange…! I prefer both on my routine checkup…
I was reading on google it say if u hbsag quantative level is above 1000 iu/ml… then it is not considered to be inactive carries … is it true??
My hbsag quantative was 2800iu/ml but hbv dna was 890iu/ml hbeag negative , hbeab reaactive…
Dear @Guru777,
An inactive carrier is someone who has HBV DNA < 2000 IU/mL and normal ALT in the absence of therapy. HBsAg can be < 1000 IU/mL but not always.
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A post was merged into an existing topic: Deciding when to start treatment
Hi, jus want to know what are the chance of autoimmune hepatitis (AIH) in chronic hepatitis b patients….! If chances are more can we avoid this…??
Hi @Guru777,
I am not aware of any linkage between the incidence of autoimmune hepatitis and having Hepatitis B. My understanding is that the two are not linked at all, though happy to have the input of those more immunologically-inclined (@mat, @nina.le.bert, @ateekhakpoor, @Greg, @S.N) or any @HealthExperts.
Thomas
I think there is a real, albeit rare, association
I have seen a case where nucs controlled HBV and AIH resolved with no steroids
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Agree that there is no known clinical linkage with HBV and Autoimmune Hepatitis
However Hepatitis Delta has been associated with development of auto-antibodies but no clear link to overt autoimmune disease.
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Hi is it true that people with hbsag around 2800-3000 and low viral load around 860 -1000 iu/ml with hbeag negative and anti hbeag positive has a high risk of liver disease than people with hbeag positive???
Dear @Guru777 ,
HBeAg- persons with low HBV DNA < 2000 IU/mL (regardless of HBsAg) are at low risk of developing liver disease. In untreated HBeAg+ disease, HBV DNA and HBsAg titers are generally greater than in HBeAg- disease and liver disease progression is much more likely.
Thanks for your answer @availlant
Just wanna ask 1 Thing.. i have read in this forum that many people have started with antiviral when their hbsag was 30k some started with 70k also .. and after the medication of 3,4,5 years their hbsag level resuces to 10k, 7k etc etc..
So why people starting their medication from eg 3000iu/ml or 2000iu/ml or 4000iu/ml remains same or their hbsag level is not reducing to much???
Hi @Guru777,
That is true. My case is an example; I have been on treatment for about 11 years now, and surface antigen quantification has remained above 25,000. For the first time this year, it has dropped to about 21,000. The current antivirals don’t work so well on this, which is the reason why the cure rate for patients on antivirals is very low. My observation is that it takes over 10 years of treatment in some patients to see their surface antigen quantification figures decline.
That is my opinion on this. I hope it is helpful. Bansah1
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Any health complications for the 10 years you have been taking medication???
Nothing related to the medication or hepatitis B. I have other conditions but they don’t interfere with each other and they are managed just as the HBV if it makes sense. Thanks, Bansah1
Thank u so much @Bansah1
so my question is that you are on antivirals for almost 10 years so now u must be in hbeag negative phase.. in that case hbsag is getting protein from iDNA ( intigrated DNA).. what is actually happening to liver in this case.. is this iDNA DAMAGING LIVER .. how do we find out that how much liver cells are actually damaged by this..! And what is antiviral actually doing on this…!
Well, 50 percent of my liver cells are infected and it’s remained at this level throughout. I had multiple cysts on my liver which has remained stable and unchanged, and no new cysts has developed. My overall liver health is just as good as someone without HBV. The antiviral slows down the disease progression to a level that has minimal changes over a number of years. As you can see I have not gotten worse, rather my liver condition is stable. That might not be the case without being on treatment over the last 10 years or so. I believe things would have slowly gotten worse for the same time period. But the antiviral has slowed that down to the point nothing new is happening and what existed before has remained unchanged.
While surface antigen quantification might not change that much, the antiviral do other important work such as slowing down the disease progression, reducing viral load, help normalize liver function, reversing some liver damage, and providing stability. I am not mad at being on treatment at all. Bansah1
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Dear @Guru777 ,
This is a great question.
The answer lies in the source of HBsAg:
- Subviral production from cccDNA.
- Subviral production from integrated HBV DNA.
Source (1) will disappear if cccDNA is silenced but this will have no impact on source (2). The only way for source (2) to disappear is if those cells containing integrated HBV DNA are removed from the liver.
Generally (there are always exception), HBsAg levels are higher earlier on in infection because of active cccDNA. Later on in infection, cccDNA can become largely inactivated but the pool of remaining HBsAg is almost entirely coming from integrated HBV DNA.
Later generation NUCs like ETV and TDF/TAF have two activites. In addition to stopping the maturation of HBV into its infectious form (containing HBV DNA), they also stimulate the innate immune response, leaving to inactivation of cccDNA. NUCs can never have any effect on SVP produced from integrated HBV DNA.
This is why NUC therapy can moderately lower higher levels of HBsAg (inactivation of cccDNA) but cannot have any impact on lower levels of HBsAg (becuase it is mostly derived from integrated HBV DNA).
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Dear @Guru777,
Integrated HBV DNA (and the SVP it produces) has no real impact on liver function. However, the progressive increase of integrated HBV DNA in cells over time is the primary cause for liver cancer in patients with chronic HBV infection.
If NUC therapy is started early enough in the infection, it can lower the risk of HCC (but not eliminate it). If started later on in the infection, is is less effective in lowering the risk of HCC.
The issue is that current treatment guidelines (except in China) advise against the introduction of NUCs until liver disease actually manifests. Sometimes this can lead to persons only starting NUC therapy after that have had chronic infection for more than 10 years.
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Dear @availlant,
Some biotech companies claim that their goal is to offer complete cure bcoz their HBV drugs can eliminate cccDNA and Inactivate iDNA. I have some questions:
1. What is the meaning of “ inactivate iDNA?
2. Does it mean that it can activate itself at some point later in life?
3. How can iDNA be destroyed? Are there any drugs currently under development that can eliminate iDNA?
Thank u so much @availlant for your response..
i would also like to know what is inactive iDNA as nawab said..Can we diagnose this weather our iDNA is active or inactive..!!