Listen to what stef2011 has to say. He has the best knowledge and understanding of HBV I have seen.
If your ALT is high and you have now liver damage then you can try to ride it out with Pegasys injections. And see maybe your immune system will clear HBV..
Or option number 2 is TDF + Alinia like stef said to lower HBV DNA and surface antigen..
I had 500,000,000 HBV DNA copies in 2007 with e negative Hepatitis B and my alt was only twice the normal values. But Entecavir salesman has put me on ETV rather then interferon. But back then I didn't know that some doctors are so corrupt or plain stupid.
based on your results: I would not worry. ALT flare means your immune system fights the virus so. I would go on interferon for six months and see what happens.. And I would add alinia too.. Bottom line listen to what stef2011 here has to say, his advices are great and spot on..
S.G.O.T. (AST) 39.3 U/L
S.G.P.T. (ALT) 85.3 U/L
HBsAg - QUANTITATIVE : 925.00 IU/mL
My ALT is above 80 for past one year ? I fear my liver is getting damaged . How to bring my ALT to normal. Could you please please reply to this post
It would be very important to know the state of fibrosis in yor case, since you seem to experience a series of miniflares, which over time can lead to substantial liver damage. While it holds promise to wait for surface antigen clearance by immune attack and inflammation, this can only be tolerated for a limited time without a strong activation of fibrogenesis. Mind you each case is different in their propensity for fibrosis progression, so the best option would be to monitor it with fibroscans.
The best explanation for the ups and downs in your alt and quant surface antigen results is that individual members of the quasispecies residing as cccDna in yor liver grow preferentially until they trigger a new mutant epitope specific cd8 and cd4 response that attacks the liver, causes high collateral hepatocyte necrosis and an elimination of that mutant, combined with a general decrease of surface antigen production even in non specific mutant infected cells, due to the intense cytokines milieu, that will restrict transcription even in non epitope carrying cells, but not a complete removal of their cccDna.
Nevertheless, this partial collateral removal of cccDna might eventually be sufficient to clear enough cells for surface antigen conversion. The question is, can your liver afford the risk of this prolonged attack with an uncertain outcome.
Each time you clear one mutant, another one, if not completely removed by the collateral effect, will grow and spread until it has sufficiently stimulated, by it's virion output, a new generation of specific lymphocytes that start to attack this new clone.
If you start tenofovir, then the virion output of the spared population will be small and further flares will likely not occur, your alt and fibrosis risk will go down.But your chances of clearance will also reduce.
Based on the picture from your last year, chances for such clearance however are not too good IMO.
Thus in summary, if you can determine your fibrosis stage by Fibroscan or biopsy, you have a better base to decide if you want to risk the ongoing battle a little longer or retreat to a safer alternative that is unpleasant in other ways, ie the long term use of tenofovir.
If your fibrosis score is low enough you could try to further activate the described process, by using interferon as stef suggested. Tight monitoring under physician supervision is advised, since this means putting oil into the fire.But yes, your chances of clearance will go up.
You are obviously in an 'immune cleaance' phase. But than wording does not necessarily mean clearance towords a stable elimination of surface antigen and cccDNA. The variations in how this battle between the virus and the immune system evolves are numerous and only rough rules or predictions can be made.
There is not one mutant or a dozen mutants but there are hundreds of deviations in the HBV genome which serve the virus to adapt towards the immune pressure, more the longer the disease lasts in one patient. It is a Darwinian evolution of HBV against the forces that try to eliminate the swarm of viruses in a body by removing the signals which activate the Tcell system and other mechanisms. Whats left is what is hard to detect or hard to fight in an efficient way, like by cd8 mediated cell lysis. Often a mutation in a critical epitope leads first to "invisibility" by massive destruction of the majority, leaving only a small amount of mutated HBv genomes behind, but this leads later to the evolution of a new set of Tcell clones against the new target, with delay, that explains the new flareup and ALT rise, after the mutant was allowed to rise and spread and then the new Tcell clones start responding and hit again.
At a low surface antigen level, often a new set of previous tolerized HbS specific Tcells start to develop and holding the virus in check with a new set of epitopes to be used for the first time. This is also the power of the artificial removal of the surface antigen with the Replicor drug. The strength and duration of this new force is however also unpredictable, It will work in most cases, but might diminish with decreasing viral load.
The fluctuations that you experienced are most likely due to alterations in core and e antigen epitopes, regardless if you are e-antigen negative. E-Ag neg patients have a more burnt out core epitope repertoire, because they have had their core repertoire eliminated too often, but sometimes a new immunogenic core mutant grows back, leading to a new flare. Here I am not taking about the precore mutants or the standard core promotor mutants, but epitope mutants.
Altogether, if your fibrosis is not advanced and you can afford the cost and side effects, the use of interferon to push the system into victory might be advisable.
Thanks a lot for your kind reply. I have one final question. This immune system battle will be associated with any symptoms like mild piercing pain in the right upper abdomen especially in the Liver area and mild fever . I have the above symptoms for past 3 months .
The accumulation of immune cells in the liver, called an infiltrate, together with numerous pro inflammatory cytokines, can lead to swelling and the characteristic right upper quadrant pain that you describe. Fever is more rare, it speaks for substantial interferon and other cytokines being produced by that infiltrate.
No, proinflammatory cytokines like eg tnfalpha or interleukin6 are also inhibitory for hbv replication and transcription, but not efficient in the elimination of cccDNA.
Ifngamma in high local concentrations is efficient to eliminate cccdna.It is produced by activated cd8 cells that have encountered their specific recognized epitope presented on the surface of an infected liver cell.
Anti inflammatory cytokines like Il10 will inhibit tcell activation and help hbv to replicate.
LKALINE PHOSPHATASE PHOTOMETRY 64.8 U/l M:53 to 128 - F:42 to 98
BILIRUBIN - TOTAL PHOTOMETRY 0.84 mg/dl 0.30 - 1.20
BILIRUBIN -DIRECT PHOTOMETRY 0.26 mg/dl 0 - 0.20
BILIRUBIN (INDIRECT) CALCULATED 0.58 mg/dl 0 - 0.9
ASPARTATE AMINOTRANSFERASE (SGOT ) PHOTOMETRY 201.3 U/l M: 0 to 37 - F: 0 to 31
ALANINE TRANSAMINASE (SGPT) PHOTOMETRY 506 U/l M: 13 to 40 - F: 10 to 28
GAMMA GLUTAMYL TRANSFERASE (GGT) PHOTOMETRY 21.8 U/l M: 0 to 55 - F :0 to 38
PROTEIN - TOTAL PHOTOMETRY 7.35 gm/dl 6.6 - 8.3
ALBUMIN - SERUM PHOTOMETRY 4.22 gm/dl 3.5 - 5.2
SERUM ALBUMIN/GLOBULIN RATIO CALCULATED 1.35 Ratio 0.9 - 2.0
My ALT = 506 and AST = 201.3 which is very high for almost past 2 years. Yet to take DNA and QHbsAg. Could you please help me on this. Also BILIRUBIN -DIRECT PHOTOMETRY is 0.26 mg/dl where normal range is 0 - 0.20.
you have to check for hbsag quant and fibroscan at least, also hbvdna should be done
liver damage is now a possibility so you d best check fibroscan and then start tenofovir if there is damage.remember that fibroscan is increased if alt were more than 200, in this case you need to wait few months before fibroscan is very reliable
I do not know how to interpret your LFT results. My concerns, just as studyforhope pointed out previously, are that you have many ALT flares for the last two years. Therefore it is important to know the state of your liver, either from a Fibroscan (mindful of what stef2011said) or a biopsy. You should seriously consider treatment.
It looks like you have a mutated form of surface antigen, that escapes proper quant measurement.
I would use tenofovir to suppress future flares. These flares can accelerate development of fibrosis and cirrhosis.
Fibroscan or liver biopsy are needed to determine your current fibrosis status.
The following information from www.hbvadovcate.org may convince your doctor not to prescribe Lamivudine.
Researchers Suggest Banning or Restricting Lamivudine to Avoid Drug Resistance
A global team of researchers suggest lamivudine (Epivir-HBV) never be used to treat hepatitis B patients because it frequently leads to drug resistance and sets the stage for resistance to other antivirals, such as entecavir (Baraclude).
Lamivudine, the first antiviral approved for hepatitis B treatment, has fallen out of favor in North America and Europe because of its high rate of drug resistance. But because of its low cost, it continues to be commonly used to treat hepatitis B virus (HBV) infection in Asia and Africa, where the majority of the world's hepatitis B patients live.
This report, published in the July 30 issue of PLoS One, examined the molecular make-up of the virus in many patients who had been treated with lamivudine as well as patients who had never been treated. They found the many untreated patients carry a mutation that allows HBV to quickly mutate and develop resistance to lamivudine.
"Our findings strongly suggest that the use of lamivudine will not benefit ...patients," they wrote because of the high risk of lamivudine resistance.
"Finally, since patients can quickly develop drug resistance to entecavir in the presence of lamivudine mutations, the lamivudine mutations can significantly compromise the efficacy of entecavir," they concluded.
They proposed that doctor screen patients for these mutations before ever prescribing lamivudine,"... to most effectively treat chronic hepatitis B patients by selecting only sensitive drugs."
An unrelated article published in the Annals of Medical and Health Sciences Research, also criticized the over-use of lamivudine in hepatitis B patients in Sub-Saharan Africa. Lamivudine was originally developed to treat HIV, but today African providers use it frequently to treat anyone with hepatitis B (when HIV is not present) because it is inexpensive and more effective hepatitis B antivirals, such as tenofovir (Viread) or entecavir, are more costly or unavailable.
But over-prescription of lamivudine for hepatitis B in this region has:
Increased drug resistance in African hepatitis B patients
Reduced availability of the antiviral to both HIV and HBV patients
And driven up the drug’s cost, which reduces its availability for more appropriate HIV treatment.
Critics say a bioethical dilemma has evolved, where doctors prescribe lamivudine to hepatitis B patients without explaining alternative treatment because they assume the patients don’t understand or are too poor to pay for more effective antivirals.
“Implied consent is no justification to embark on a particular treatment course,” researchers from Njala University in Sierra Leone wrote. “To tackle the growing problems of drug resistance and shortages with respect to lamivudine and other antivirals in HIV/AIDS treatment, health care resources should be prescribed with caution, irrespective of whether implied or explicit informed consent has been sought.”
Association of Preexisting Drug-Resistance Mutations and Treatment Failure in Hepatitis B Patients
Lurking Dangers Behind Overuse of Lamivudine to Treat Non-HIV Hepatitis B Patients in Africa
Chronic inflammation reduces the synthetic activity in the hepatocytes. Intense fibrosis is an independent reason for decreased functional capacity of the liver.
Therefore patients with hepatitis tend to have lower cholesterol levels.
This has to be seen however in consideration of the genetic background and other functional impairments like fatty liver and insulin resistance, which typically reduces HDL more than LDL cholesterol.
One last question . Kindly reply
I met a doctor today He prescribed me Tenofovir 300mg . Already I'm taking Olmesartan 40 mg for Hypertension. Whether Olmesartan drug will have any interactions with antivirals.
He also asked me to consider IFN treatment too. Before that he wants to take Fibroscan before that.
I am not aware of any interactions of olmesartan and tenofovir.That does not mean that they do not exist. Check all drug interactions of tenofovir, also in case you might receive additional medications in the future.
hi studyfor hope..i need your inside..hep b hbeag positive, high viral load 8 log sgpt around 60 three years before so started baraclude and after 3 month combo with interferon.. only little hbsag decrease so stopped peg intf b..then onwards on baraclude..from 2.5 years dna undo alt normal ..but hbsag continuously around 5 log too high..added pegint b recently no stable hbsag decrease ..many times seen hbsag fluctuations between 60000 iu to 100000 iu in between weeks..does it show any immune response..whenever this fluctuation takes place lympho count increases and platelate decreases..but never found sustained value of hbsag and alt is always normal..what do you think if i stopped baraclude and continue pegintf ..do you think it will be useful to trigger immune system as dna will increase after baraclude discontinuation..i m currently undo dna so do you think stopping baraclude will develope any resistance if again used in future..please give your deep precious views about the condition and future management. waiting for ur kind response..thank u.
At this time, considering your lab results, the available treatments or combos are unlikely to bring you to a state of surface antigen seroconversion or loss.
The effect of the antiviral that you take is to reduce the amount of circulating virions dramatically. This in turn reduces the activation of the immune system and threby prevents damaging attacks that cause liver damage and fibrosis. this means your liver disease will not progress and an existing fibrosis might even improve.
The idea that you want to induce an immune attack is only useful when it can lead to final clearance. If it is unsuccessful, more damage is done and the flares will continue, with no eradication.
You should be grateful that with entecavir and tenofovir two antivirals with little and no resistance development are available. They work by reducing the immune attack on your liver, almost completely eliminating liver disease and that is what mainly matters. It is not clear if they have long term side effects that truly matter, this issue will take a long time to resolve.
While interferon has some chance to achieve a hbsag seroconversion, it is typically only achieved in patients that are already primed in that direction, by showing a low surface antigen before treatment starts.
The arrowhead treatment if it becomes available is not likely to achieve such a seroconversion for you. Only the Replicor treatment combined with immunotherapy has, IMO, a resonable chance to clear someone in your position.
if i stop baraclude for now after 2.5 undo dna..and see response on intrf without baraclude for few months..and if necessary after few month i can restart baraclude again..do you think this will create baraclude resistance after restart..very high hbsag seems that i started the treatment when i was in immune tolerant phase, 28 years old, e+, high dna, usg normal..just a possibility..please provide your views.
Could you please tell me whether there is any relationship between Hypertension & Hep -B
I'm taking olmesartan for Hypertension . But last week my BP went to 150/90. My doctor prescribed me amlodipine 5mg & rosuvastatin 10mg and asked me stop olmesartan . Is there any sideeffects on Liver due to above medicines?
Also my HDL is very low which is 27 mg/dL (normal >40)
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