stoppingntz doesn not change your situation but i think liv52 did because hbsag has increased frominactive carrier to cronic hbv
anyway having alt 200 is not bad at all if hbvdna is extremely low or undetactable because it means your immune system see the virus and is fighting, if you find also hbvdna high that would be a big problem
get back to ntz+vitd3 (37 is too low, get it to 80ng/ml)
then check hbvdna too, if hbvdna is low i d go for ntz lead in for 12 weeks and then addon generic interferon+simvastatin+vit d3 to clear hbv
creatinine is a very poor test for kidnesys because big muscles can make creatinine even 1.4 not correlated with kidneys.if you want to be on the safest side take a 24hrs urine test of creatinine clearance that will confirm kidneys function.i stress again this is to be ultra safe side and to prevent in any case.
kidneys function can be improved by making hbvdna und, by fibroguard, by antioxidants like vit d and gluta injection or liposomal
anyway youare still close to hbsag 1500iu/ml which has highest chances to clear hbv, according to the hbvdna level we may think an off label combo like this:
alinia-tenofovir lead in 24 weeks and then recheck hbsag/hbvdna if low
alinia-tenofovir-interferon or peginterferon-simvastatin-vitd3, i am sure you ll clear fast like it happened to otan on such a combo
since we dont know your baseline hbsag and hbvdna there is another way to think about what happened.
your baseline could have been hbsag 1700iu/ml and hbvdna 9000iu/ml, alinia lowered them and when you stop they just got back to baseline values
the difference can be your immune system is now stronger and made a alt flare trying to clear the infected cells, it is better to act while we have the alt flare and i think alinia is the best to retry now and then add interferon
" .. After 2 months of taking Ntz it came to 1000iu/ml and after 4 months it even came to 500 iu/ml. But after that it gradually increased to 730 iu/ml (with Ntz) . So I stopped Ntz and later I started with Liv 52 HB, After that my qHbsAg has increased t0 1789 iu/ml "
so it seams that NTZ is not fully responsible for HBsAg variation (qHBsAg decrease and increase also under NTZ).
Could you please give us the date's when you made the qHBsAg tests (all dates). I was thinking to see that after you stop the NTZ HBsAg increase faster or just increase with the same rate.
could you remember something different during the decrease period vs increase period (what yoe eat, sport or eating or sunbath or .... )
Before taking Ntz (i.e on Dec-2010 my HBV DNA was 9000 copies/ml (i.e around 3000 iu/ml). Had No idea of qHbsAg. ALT/AST was Normal
I didn’t check my qhbsag before taking Ntz. I started taking Ntz around Jan -end -2011
5th,March -2011 – 1088 iu/ml (During this period Ntz was 1.5 g per day)
2nd April -2011 – 567 iu/ml – During this time I played badminton often and took lot of fruits and fresh juices. Also Included Oat Meal (Ntz was 2g).Also in end of April started taking Lypo-SphericTM Vitamin C and Lypo-SphericTM GSH – Glutathione + Omega 3 +Selenieum
21st April – 542 iu/ml –Ntz -2.5 g per day
20th May – 606 iu/ml – Ntz 2.5 g
3rd June -2011 – 652 .33 iu/ml – Stopped playing and less physical work. Also added 20mg Simvastanin and stopped taking Vit C and Glutathione
15th Aug -2011 – 733 iu/ml - So I decided to stop Ntz gradually and started taking Liv 52 HB and added Vit D 5000 iu/ml
5th,Nov -2011 – 1091 iu/ml – only on Liv52HB + Vit D
24th Feb ,2012 – 1789 iu/ml - only on Liv52HB + Vit D
maybe it is best to retry alinia 2,5g daily and no fruits, liposomal vit c and glutathione, no omega 3 and see
we nedd to keep in mind hbsag less than 1500iu/ml respond to interferon wit h clearance and sme thing may apply to alinia
and 500iu/ml or less might respond like otan to interferon+alinia with hbsag clearance before 24weeks
to me the best thing in this case is: alinia 12weeks or 24 weeks until hbsg gets back to around 500iu/ml and then add on interferon, if hbvdna is detactable higher than 100iu/ml i d add tenofovir too right before making interferon add on so that hbvdna is already und when adding interferon.i think you will clear hbv by 24-48weeks on this combo
I don't think that is a real connection between NTZ and qHBsAg, even if the daily increase jump from 1.56 to 4.48 when you stoped the NTZ (but also with the NTZ you experience a increase of 1.4 per day )
retreatment with alinia will tell us if hbsag decrease was due to alinia, please let us know one month results with alinia 2,5g daily, also consider that you may use even 4g daily if you can tollerate because aids patients non responding to lower doses have been treated with 3-4g daily with no severe sides and of course the higer dose the better
not alinia for sure......., this is a very high level for you which has nothing to do with inactive carrier you were, nothing to be scared of but if we dont act now you may lose the low hbsag and the chances to clear hbv easily on interferon combos
if you can afford i d go with tenofovir+alinia and add interferon when hbsag gets lower than 1000iu/ml
with this hbvdna the trends are towards hbsag increase if we dont stop relication, although hbsag and hbvdna are not correlated i think this is wht may happen
if something that henances viral replication is used this may happen in days, since liv52 research is just smoke i tend to make it responsible for this.the minumum result should have been keep alinia results
It is due to sudden stop of Ntz(Alinia)?
no if you stop alinia you can get back to your baseline status not getting it worse.my sister and a german guy stopped it and both had improved status, normal ast/alt and lowering hbvdna.since alinia act like interferon boosting immmune response and interfering with antigens release inside the cells it cannot make status worse than baseline
alinia does not produce mutants even in hcv which is the most mutant virus, even more than hiv.
he sent me lab result by email but anyway hbvdna pcr has no decimals in the results he just wrote it wrong
his hbvdna is now 651.801copies/ml so his stauts is:
increasing hbvdna, increasing hbsag, increasing ast/alt which confirms the virus is spreding and the alt flare is not immune system fighting but just the virus spreading without immune control
on the contrary if you have increase of alt with decrease of hbsag and hbvdna it means immune system is getting control of hbv infection and killing infected cells
the best scenario is increasing alt flare with hbvdna undetactable and hbsag decrease.this last status reflects the killing of infected cells without any escape for the virus which cannot infect new cells and lose the infected cells which produce hbsg and cccdna
I am glad your ALT has decreased. I would say you are no longer in the Immune tolerance phase because you are HbeAg negative. Are you still in the Immune Clearance phase?
I don't know because I lack the clinical experiences of a doctor. In the Immune Clearance phase, ALT and hbvdna will flunctuate, and you may be in this phase for a number of years. Others may like to comment.
Thanks for your Comment. Regarding Immune Clearance Phase , I understood in other way around. I thought that Immune clearance phase - becoming more chronic . In sense , usual cycle of HBV where Immune System sees Virus attacks Liver cells. Still I don't understand clearly the HBV phases - Immune tolerance phase & Immune Clearance phase
Yes, in the immune clearance phase, the immune system no longer tolerates the virus and start attacking the virus infected cells. This battle can be fought many times, each time doing some damage to the liver. Therefore a prolonged period of clearance (attempts to clear) is not desirable. Before the age of 40 (if infected at birth), most hbvers will finally win the clearance war - HbeAg is negative, viral load is very low and ALT is normal - the immune system is keeping the virus under control. The hbvers is then in the inactive phase. with luck, this phase lasts forever, but after a period of time, the virus mutates into a form that escapes the immune control and starting replicating again, ALT will rise and the liver is being damaged. This is the so called HbeAg negative hepatitis. Treatment is then needed again.
It is obvious that during the immune clearance phase, there is a chance that the patient may achieve victory simultaneously without any treatment, but on the other hand, the battles may be too hard and too frequent that medical treatment is needed to prevent severe fibrosis/cirrhosis developing. Whether and when to treat during this phase is a difficult decision to make and best left to experienced Hepatitis
doctors to make.
The above is a very simplified explanation and may not be completely accurate. That is, don't use it to decide your treatment.
Yes, in some cases when the patients show signs of liver diseaase, treatment should be started. In other cases, it may be prudent not to rush to treatment, the patients may seroconvert simultaneously. Only an experienced liver doctor should make the call.
The immune clearance phase is characterized by the presence of HBeAg, high levels of serum HBV DNA, and active liver disease (ie, elevated ALT and moderate/severe necroinflammation on liver biopsy).
Not all biochemical exacerbations lead to HBeAg seroconversion or persistently suppressed serum HBV DNA levels, a phenomenon termed abortive immune clearance. These patients may develop recurrent exacerbations with intermittently undetectable serum HBV DNA with or without transient loss of HBeAg. Such repeated episodes of hepatitis may increase the risk of cirrhosis and HCC.
Source : http://www.clinicaloptions.com/Hepatitis/Management%20Series/Chronic%20Care/Modules/chroniccare_lok/Pages/Page%205.aspx
1) Do you think that Immune clearance phase is always accompanied by Positive HbeAg ? In my case ,Do you feel that it might had been positive for some time before and it has become negative now? I checked HbeAg Status before 1.5 years and it was negative at that time .
2) Is possible , one can be negative for HbeAg in all phases of HBV?
within the immune clearance phase, I am not sure whether the HbeAg staus can flip flop between positive and negative. But as your quote suggested, transient loss of HbeAg and hbvdna are possible within the clearance phase.
my latest blood report
AST - 121
QHbsAg - 895 iu / ml
kindly tell your advice. again my ALT has increased.
whether my liver is attacked heavily. whether anti viral is inevitable. I accept that there is decrease in QHbsAg but ALT is continuously high for past 4 months. worried please help.
first thing for every member of the forum:
high alt is good, always good when hbvdna and hbsag go down, it means you have an immune response while a normal alt is useless because it means you have no immune response.
if hbeag has become negative you are clearing hbv and before mutants can escape this immune response i d start intf+ntz as soon as possible.chances are you clear hbv very fast
waiting with no immune modulators......hbv will escape your immune response like in most of the cases and alt will become lower or normal
I am sorry, your e-Antigen was negative over a year ago and also in April this year. In this case, you may consider whether you have HBeAg negative chronic hepatitis. Your viral load should tell you more. Tenofovir treatment is also effective for e-Antigen negative hepatitis.
i forgot he was hbeag neg, i thought he just seroconverted hbeag neg.....
tenofovir is not indicated on hbeag neg at all because he can clear hbv he should not treat for simply hbvdna und, tenofovir will likely rise hbsag and lower alt now making hbv clearance much less possible
his best treatment is intf now because hbsag less than 1000iu/ml boosted by ntz, vit d and maybe simvastatin too
Hi your reports suggests that earlier you were in immune clearance phase ( i.e when all your statistics were high). Now with your qHbsAg coming down to 895 is really a good news. But i think HBV DNA is also an imp indicator so you should check that too.
But can you please tell that you are under which medication from last six months? Alinia or Liv 52 HB. and what are your dosages per day. I am asking this bcoz I am also on Liv 52 HB from last 04 months and can perhaps extrapolate our results.
high alt are followed by hbsag decline while lowering/low alt are followed by hbsag increase
as regards immune system as hbsag declines interferon gamma in the liver increases, the key of evrything is getting hbsag to lower continuatively, if it goes up and down there is no effect.
abbott architect manual diluition test can have an error of 500iu/ml and more, once hbsag is less than 250iu/ml there is no diluition for sure, if the lab is very updated it is possible they are already using the kit with no diluition and results are without error
Could you fiil out ALT / AST and HVB DNA ? (also could you found any other relation betwen qHBsAg and life stile .... e.g. sport, or diet, or ....)
Jan 2011 ?
March 2011 1088
May 2011 606
June 2011 652
August 2011 733
Nov 2011 1091
Feb 2012 1789
April 2012 1576
June 2012 895
July 2012 672
August 2012 461
Sept 2012 925
651801 copies/ml is a lot of replication, my guess is your immune system is not able to block reinfection to keep stable decrease of hbsag, intf is the best option here or intf+alinia+simvastatin
the use of an antiviral is not good because making hbvdna totally und it may suppress the immune response you already have because hbcag in virions is the strongest stimulant for immune response, may on and off tdf+intf might be ok but in this case you need expert doctors or researchers with experinece on this on and off vs hbsag and hbvdna response
i dont think you ll ever solve this status in other ways
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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