Was sharing my status and though I should maybe share my current experience with IFN.
I'm currently 29. First diagnosed 2012 January. First HBV DNA June2012 was about 214000 IU.
I was HBeAg Negative then. For some reason at baseline I became HBeAg Positive.
DNA ~170000 IU
qHBsAg 4500 IU
Fibroscan 6,6 Kpa
DNA 67000 IU
qHBsAg 4700 IU
DNA 6000 IU
qHBsAg 3900 IU
DNA 3000 IU
qHBsAg 4700 IU
My ALT/ASP is generally unchanged, DNA keeps dropping but HBSaG is really scaring me. Doc says we need to wait for a pattern to take out any conclusions and consider stopping treatment.
One thing I can think of is before that Week 12 visit I went to a gym a few times and skiing where I got tired like crazy.
Should it be already undetectable on IFN or is it normal its still there ?
it is normal, intf doesn t act directly on hbvdna but acts on cccdna, hbsag and also on hbvdna in the end.
of course it d best having hbvdna und but your result at 2000iu/ml is good anyway, it is hbsag kinetics that counts now, be aware that max intf effect on immune system is reached at 48weeks and that you can keep intf even for 2 years if it has a constant hbsag decline so that you can make it totally und
the intf response at 2 years is much higher with same sides as in the first 48weeks
stopping rules for pegintf are:
no hbsag decrease by week 12 hbeag+ or 24 hbeag-
hbvdna decrease less than 1-2logs
it is best to wait for the 24th weeks results because most have an increase of hbsag till week 24ths on hbeag - and the decrease happens between week 24th and 48th.this increase always happens on peg add on to nucs and can be a purging effect on infected cells especially if hbvdna keeps going down
if there is no decrease after 24 weeks of treatment it is best to stop and start tdf to try again peg add on aftter few years
some examples on hbsag kinetics
Thanks stef,I guess the trial coordinator would terminate my treatment by now if there was no point. Thanks again for your knowledge, it is too bad there arent many hbsag kinetic trials on the net, hopefully after this trial they will publish more results over net.
Had 32W results over phone. DNA fluctuating at 4000IU and hbsag still at 5000IU levels. Seems like its time to give up ...
Doc said to keep it going and we will evaluate the case at 40Week as hes on holidays now.
Just had my 40week visit. DNA continues to rise from 2000 at week 18, through 4000 week 24 and 6000 (IU/ml) in week 32. HBsAg still standing at 5000 IU/nl levels.
Strange thing is that I seroconverted .Why is this switching so often in my case ? I was Hbe- Jan'12 and turned + on baseline of TX around Oct'12. During TX i saw it tuned - for a while and now its back +.
I actually thought that they will stop my TX but they gave me the last 8 shots to finish 48weeks.
Combo results don't show any news in HBsAg drop. Do I benefit in any way from finishing 48w as a non responder?
I knew the TX might be a failure from the beginning so I knew this could happen. Its just few % success rate after all. This is my first treatment attempt and its IFN mono.
I handled IFN pretty good until recently. I must admit I feel tired like hell since a few weeks.
ALT is around 60 all the time. Will check neutrophils level, but generally the rest was close to within norm, thats why I write only about platelets.
My hematology was all very good within norm until week 32. Its 7 injections to go, I will complete it for the sake of science.
the max immune strength under peg is reached after 48weeks so this is the reason probably
you should start tenofovir as soon as possible and retry peg after 1-3years, this will rescue peg responsiveness with little chances of failure especially if we can reach hbsag levels around 1500iu/ml although few patients had response despite about 7000iu/ml of hbsag
Yeah Calebz, just judging by your ALT level that IFN did not work on you. That's why I wonder how Paris2013 can reduce his HBSaG to near 0 with normal ALT. It's a science we can't figure out. Oh well, I hope the best for you in your future treatment.
Otan, AsianMale1985 all have elevated ALT while on IFN. Not sure about April9903 and Cyrus.
Hello just completed my 48 week Interferon mono therapy treatment. My week 40 results are :
DNA ~170000 IU
qHBsAg 4500 IU
Fibroscan 6,6 Kpa
DNA 200 IU/ml
qHBsAg 6000 IU
ASP/ALT 50/99 (finally some ALT activity ?)
HBSaAg is disappointing. Got scared with the DNA raise in week 32 but it appears I end my treatment with a small light in the tunnel.
Its too bad I can't continue IFN more as it seems my ALT started to show some traces of response.
total failure of treatment as expected, peginterferon doesn t work if hbsag and hbvdna are high, tenofovir should have been used first to lower at least hbvdna and allow some response despite the high hbsag
the best thing to do is start tenofovir right away and add on peginterferon after 3 years
My experience with interferon is similar. The positive part of the treatment is the following: a) interferon is an immune modulator and it has a longterm positive effect, b) I think your fibroscan value is improved (mine is from 6.8kpa -> 5.8kpa), c) HBV DNA decreased to a very low level.
Please keep your DNA level as low as possible, so "the best thing to do is start tenofovir right away". (I quote it from Stefano :)
this has nothing to do with having children, tenofovir has no effect both on men and women and it must be used in pregnancy if the mother is infected.i think that high hbvdna is much worst onhaving children
The results of this study suggest that the addition of a vitamin D supplement to current standard therapy can significantly improve the rate of RVR, EVR and SVR in treatment-naïve patients with HCV genotype 1 compared the rates with standard therapy alone. The observed SVR in the control group (42%) was consistent with previous reports[2,3]. Overall there was a marked increase in the virologic response at week 4 (44% vs 17%), week 12 (94% vs 48%), and week 24 after the cessation of therapy (86% vs 42%), and a low rate of relapse (8% vs 36%) with vitamin D supplementation compared with no supplementation. The rate of relapse in the control group was within the reported 18%-40% range for current standard HCV antiviral therapy[2,22].
There are only two reports examining the association between vitamin D status and outcome of antiviral therapy in patients with chronic HCV viral infection. Petta and co-workers retrospectively analyzed a cohort of 167 patients treated with Peg/RBV for hepatitis C, and detected an association between lower vitamin D serum levels and failure to achieve SVR. Our results provide further support for that data. The second study by Bitetto and co-workers showed that vitamin D supplementation improved the response to antiviral treatment for recurrent HCV in liver transplant recipients. Several differences between those two studies should be noted. Bitetto and co-workers’ HCV patients were immunocompromised, and they were supplemented with low-dose vitamin D (800 IU/d) after liver transplantation. In addition, most of their HCV patients (75%) had low vitamin D levels despite treatment. Finally, that study was retrospective and focused on the prevention of osteoporosis, not on the treatment of hepatitis C.
The exact mechanism of action leading to improved RVR, EVR, and SVR in patients receiving vitamin D is unknown. Vitamin D is metabolized by the liver and converted to 1,25-dihydroxy-vitamin D3, which is the active form of the vitamin[6,7]. Individuals with chronic liver disease may have poor conversion from vitamin D3 or any of its other biologically active metabolites. 1,25 vitamin D3 appears to modulate immunity principally via regulation of T-cell function. The vitamin D receptor (VDR) is expressed on virtually every type of cell involved in immunity. The immunomodulatory actions of vitamin D are elicited through its direct action on T-cell antigen-presenting cell function. T helper cell type 1 (TH1) actions are intensified when vitamin D is insufficient, as in the majority of our patient population, or when signals through VDR are weak. Regulatory T cell and TH2 cells are diminished, thus favoring an autoimmune TH1 response. This is a pro-inflammatory response which may impair IFN and insulin signaling, thus decreasing the viral response[29,30]. A recent study on 120 patients with chronic HCV genotype 1 infections reported that a TH1 to TH2 ratio of 32 ng/mL increased the response to antiviral therapy to the same extent in patients with vitamin D deficiency as well as those with vitamin D insufficiency. Multivariate analysis revealed that viral load, advanced fibrosis and vitamin D supplementation remained as independent predictors. Thus, it can be concluded that vitamin D supplementation is responsible for a higher SVR, rather than the baseline vitamin D level. It remains to be determined whether the addition of vitamin D acts by a mechanism other than improvement of insulin resistance or immune function such as the upregulation of toll-like receptors involved in the immune response in HCV-infected patients
Limitations of the present study include the small number of patients, lack of vitamin D level assessment during therapy for the treatment and control groups, and that this prospective and randomized study was not placebo-controlled, thus the patients knew whether or not they received a vitamin D supplement. Another limitation is the lack of data on the TH1 and TH2 immune response. The identification of determinants of the response, such as polymorphisms of the IL28B gene, polymorphism of the VDR and immune function[13,35], may help explain the difference in response rates between patients with different ethnic backgrounds. This was not done in our study since data on IL-28B and on VDR polymorphism were not available at the time the study was designed.
In conclusion, the addition of vitamin D to Peg/RBV combination therapy in treatment-naïve patients who were infected with HCV genotype 1 significantly increased the rates of rapid, early, and sustained viral responses.
we can compare hcv and hbv in this setting since pegintf just boost immune system response and virologic response at 24 weeks from 42% to 86% is a huge difference, i also bet the serum levels achieved by supplementation are minimal
i saw another study on immune cells i dont find now and there is a big **** in intf gamma production and Tregs decline by vitamind added to pegintf
another important note, response to pegintf increases serum vitamin d when not taking supplements, this confirms viruses damage vitamin d pathways/immune system modulation and when cleared this pathways is restored
I know that this is a little bit inconsistent with the actual research...
“Our data confirm an association between low levels of vitamin D and high concentrations of HBV in the blood," lead investigator Dr. Christian Lange from Johann Wolfgang Goethe University Hospital in Frankfurt said in a statement. “These findings differ from previous research of patients with chronic hepatitis C, which found no connection between vitamin D levels and concentration of HCV in the blood."
Hell to ******* uselss insurances......words to be polite
you should buy generic tenofovir in india or vietnam, supply for few years, that ll be about 20usd per month, no need of insurance and even if you go there by flight you still save
sorry but you dont have results to stay off drugs and the effort of pegintf go wasted
lam is to avoidmlike plague, it would ruin you definitively if used
Hello, my week 54 update as fallows:
DNA still raising now at 2000 IU
HBsAg down to 3700 IU
ALT stays at 45
I guess this means a relapse to baseline levels soon but at least i didn't flare up after stopping the TX. Interesting thing is that trial sponsor has an additional program for relapses that consists of 2 years of Tenofovir for free but you need to meet some special scenarios of hepatitis flare up after TX.
Another thing i found out by sitting and chatting at lobby is that some sort of three pill trial for hepatitis C works very well - info from three different participants.
lastest fallow up for week 56
DNA stopped at 2400 IU (exactly the same as week 54)
HBsAg down to 3400 IU
ALT at 49
week 54 update as fallows:
DNA still raising now at 2000 IU
HBsAg down to 3700 IU
ALT stays at 45
DNA ~170000 IU
qHBsAg 4500 IU
stef my doc told me that its a NO GO for TDF + trying to conceive a child.
Since my current result don't indicate a flare they won't give me free TDF anyway.
I think I will postpone my fight with HBV untill this is resolved for me.
Im thinking to get TDF generic abroad and try to take it for some time and add IFN but the insurance program for HBV treatment requires my HBV DNA to be detectable before start of treatment and certain drop in DNA within 24 weeks - they discontinue treatment otherwise or not qualify me for it (DNA UND). I'm thinking how to bypass this. Second insurance option is lamivudine for HBE- as I already mentioned.
I don't know about the child thing - I searched the web and it only says there are no studies regarding the subject so I guess they say no out of the box.
Regarding treatment options no other country will cover your treatment for HBV just like that and this is not his choice of treatment but ****** insurance health program for treatment of HBV/HCV. There are organizations that try to force it on government to change this outdated program.
tenofovir must be given to infected mothers to prevent reinfection and this is done since 2000 on hiv too so just imagine how well and safe the thing is....i dont think the doctor is so stupid and ignorant, they surely have a budget per patient because fo insurance
insurances should be outlaw on healthcare, it just can t work, hopefully europe will keep public healthcare and one day maybe patents and insurances will be outlaw, making money on people's life is just disgusting
hi cale.. same situattion here.. NUC's will not be a choice due to the young age (same of mine!)... in any case I beliver you'll do agaign modno ifn in some months (at least 10/12 months since the end of the tx)..
Just had my week 72 visit, my DNA completely rebound to 110000iu/ml and hbsag increased from 3300 to 4000 so I'm back where I was at start. At least my Fibroscan stays at 6.8Kpa.
I think I will go on NUC's. My public health care changed treatment guides and I think it opened up Baraclude (and I think tenofovir too) for Hbe-.
Haven't seen the program details cause its fresh news.
Too bad its almost a permanent medicine and I'm still trying for a child.
Anybody had any experience in Tenofovir in men trying to conceive ? Label says it had no issues with rats...
Stef, here we have a lot of discussion on the therapy you advocate (A few years NUCs then combo IFN). To be honest, we still have concerns on that, not about the negative effect, but about current situation. We know it's a wonderful way to cure the patient, but so far no doctors know about that, no wide publish of that, and no medicine journals talk about that. Can you give us more info about the therapy? We need more positive power.
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