biggest mistake of most liver specialist do not treat with interferon if hbvdna is und
this is obvious to stupids, hbvdna und with hbeag neg means there is immune control of hbv and sometimes even low hbsag
at last a study shows highest seroconversion rates in this phase of cronic hbv, looks like most doctors try to keep the infection rather than cure it
HIGH RATES OF HBSAG SEROCONVERSION AFTER TREATMENT WITH INTERFERON ALFA IN CHRONIC HEPATITIS B VIRUS-INFECTED PATIENTS WITH UNDETECTABLE HBV DNA
H.B. Yu1*, Z.H. Cao1, Y.H. Zhang1, L.N. Ma1, B. Ma1, Y.L. Liu1, Y. Jin1, X.D. Zhang1, H. Wu2, X.Y. Chen1
1International Medical Department, 2Department of Infectious Diseases, Beijing You'an Hospital,Capital University of Medical, Beijing, China. ****@****
Background and aims: The patients infected by hepatitis B virus with undetectable HBV DNA, HBeAg negative/anti-HBe positive are not recommended to receive antiviral therapy currently. However, HBsAg seroconversion is considered the closest outcome to clinical cure and associated with the good long-term prognosis in chronic hepatitis B (CHB). The immune characteristics of B cells and their clinical implication during this treatment in those patients remain unclear. The aim of this study is to investigate the efficacy of antiviral therapy and immune characteristics of B cells in those patients .
Methods: Patients with undetectable HBV DNA, HBeAg negative/anti-HBe positive and HBsAg positive were enrolled, and treated with interferon (peginterferon alfa-2a 135µg/week (n=53) or 180µg/week (n=14) or peginterferon alfa-2b 100µg/week (n=16)). When HBsAg titer300 IU/L) was set to the terminal of the therapy .Flow cytometric was performed to analyze the peripheral total B cell percentages in 3 patients who achieved HBsAg seroconversion and 2 HBsAg-vaccinated healthy controls.
Results: Of the 83 patients received interferon treatment, 26 (31.3%) achieved HBsAg clearance(n=1) and seroconversion(n=25). HBsAg seroconversion occurred after a median of 30 weeks after the treatment (range: 12-132 weeks). Eight patients had completed treatment and were followed for a median of 30 weeks post-treatment (range: 24-60 weeks). All of them sustained HBsAg seroconversion (mean anti-HBs 473.1±298.7 IU/L) during the post-treatment following up. 18 patients are still undergoing treatment (mean anti-HBs 411.2±461.7 IU/L ). The data (3 patients achieving HBsAg seroconversion and 2 HBsAg-vaccinated healthy individuals) indicated that circulating B cell percentages were close to healthy controls at baseline(range:5-7%)and were increased after the HBsAg clearance(range:16-19%).
Conclusions: Patients whose HBV DNA are undetectable in plasma, HBeAg negative/anti-HBe positive and HBsAg positive should be treated, because they can achieve high rates of HBsAg seroconversion. B cells may play an important role in HBsAg clearance /seroconversion.
The paper is interesting and encouraging. I like to give you my view on this. I can be wrong.
The current thinking is that Interferon is most successful when the patient has low hbvdna and elevated ALT (indicating immunactive, I think). In the past, this had led to some doctors suggesting that patient with high hbvdna should be treated with lamivudine( only antiviral available at the time) first, sequentially or concurrently, then followed by Interferon. Indeed, some trials were done but the results showed no difference to mono interferon treatment.
The abstract of the paper did not say how the patients achieved low hbvdna, if by antiviral whether this was used concurrently with interferon. I don't know how recent is the paper, but it is definitely worthwhile to revisit the idea.
I have also posted a paper indicating, to me, that current Pegylated interferon may not be manufactured properly. If this is true and corrected, combining with the low hbvdna achieved by antiviral, we may already have a good cure already. This is my wishful thinking, at least.
i think combo trials int+lam were done very bad, maybe to dscourage this treatment, reading all research about it with correct views there are some points
interferon doesn t work on many at all because hbv can suppress both interferon injected and natural interferon produced by the body.i don t remember exactly but hbx is linked to this.hbx is linked to glucose/lipids methabolism so maybe changing that we can impair hbx production
the other problem is interferon half life, peginterferon doesn t stay in the blood all the time but dicrease fast so actually peginterferon is not the best solution while more pratical (one injection per week)
the best article i have read was using a insulin pump to keep the level of interferon always active.this is for sure the best method but it scares me actually.try to lokk for this article on google and let me know what you think
in cases where interferon is not suppressed we have many parameters to henance its activity:
low fat/low bmi body, high fat in the body is linked to less circulating interferon and higher sides effect (the fat cells absorbs interferon)
low glucose and no insulin resistance, better response
no fatty liver, no severe fibrosis, better response to interferon, less sides effects
vitamin d higher than 50ng/ml, SVR or hcvrna suppression for HCV more than doubled and on some genotype close to 90%, hcvrna suppression also very very fast.trials for hbv are still on progress but i think there is no need to see results, optimal vit D is ok anyway and extremely cheap (in my country vit D is free)
now i don t remember other factors, the good oitn of the article is that hbv suppression by antivirals before interferon can reverse suppression of interferon
the lack of all studies on these combo is the use of hbvdna in the blood which is absolutely useless.they must check cccdna, pgrna and total intreepatic dna (possibly hbx too) in the liver to see what is the difference between those who gained back response to interferon and those who have interferon suppressed by hbv
my guess is the lower intreaepatic hbvdna, cccdna the more difficult for hbv to suppress interferon.but this needs proff
they should also concentrate research make interferon response better on more patients with higher SVR
now we know that wen hbsag decreses there is response to iterferon and that longer treatment 2-5 years, have much better results and svr
combo with alinia will surely improve svr but no research planned on this....also off label clinical cases would be good
another guess is interferon lambda has higher response and mild sides, maybe it will be possible to treat continuatively for 5-10 years, who knows
my guess is the lower intreaepatic hbvdna, cccdna the more difficult for hbv to suppress interferon
sorry more clear this way:
my guess is the lower intreaepatic hbvdna, cccdna the better response to interferon is achieved anyway
from many research, especially dr.brunetto, hbsag less than 1500iu/ml is linked to hbv eradication.and of course hbsag 16iu/ml makes seroconversion by interferon, that's extremely low
another thing to consider is how weak hbsag suppression is by interferon, it is extremely rare to gain more than 1500iu/ml reduction by 1-2 years of interferon so since alinia is much more potent on this it should always be comboed off label
the minimum to increase levels with severe deficency is 4000-5000iu daily, if your liver has no cirrhosis the safe levels are up to 10000iu daily and sunbed 3 times a week
i have see on cronic fatigue syndrom that we have exactly the same problems for vitamin D.today i have seen a post and they check for both 25OH (too low) and 1.25 (too high), one said it can reflect immune system impairment
see discussion here
cccDNA in infected liver cells are hard to measure - only by biopsy(?). Nucleoside Analogues antiviral suppresses production of hbv dna but not HbSag inside infected liver cells. Therefore, low hbvdna in the blood indicates few new hbv virions produced, but amount of HBSag in the blood may not go down, as they are still being produced by cccDNA inside infected liver cells and released into the blood..
SO HERE IS MY THEORY (possibly wrong): Amount of HbSag in the blood is an indication of many liver cells are infected with cccDNA.. Interferon is supposed (my guest) to enter infected liver cells and cause it to destruct. So amount of HbSag in the blood should be an indicator of whether you will get a complete cure.
ALL THESE ARE OF COURSE TOO SIMPLE AND TOO SIMPLISTIC.
well i tell you even researchers are guessing on interferon but they told me there is something wrong or missing with immune system which is corrected by interferon (about 11% patients), so better give it a try always
another thing we know for sure we have no immune response towards virus and some (like me) have only immune response towards infected cells and this just makes damage to liver and nothing to the virus
the kinetics they know is: with nucs low replication goes on so hbvdna in the liver is not blocked at all, production of hbsag/cccdna increase on hbeag negative
only on 19% patients there is a slow decline of hbsag/cccdna by the years
they know one thing for sure immune system is blocked like said in gcMAF studies from the eraly macrophage presenting antigens to denstric cells, plus probably many other ways so dentric cells do not allow lympho making hbsag to duplicate to have enough hbsab and hbcab to eradicate hbv
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