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Avatar universal

When to start treatment...

I am asian male 33 and have had chornic hep b probably from birth (adopted so no parental records to work off of).

I finally got to a specialist and am a litlte concerned because I get mixed feelings from different specialists... sometimes it's "oh definitely start medication right now" and sometimes more "well it's pretty early stages of damage, we can monitor and see, but it wouldn't be a bad idea to start treatment".

This has been going on and off for 3 years now as I battle between trying to get myself to start the treatment.

A big part of me has a problem with this though - current treatments have 0% tolerance after 7 years but I am told that if you ever stop your virus kicks back in super strong... this brings me to two fears:

1 I am not the most attentive person and as important as this deatil is I could easily see myself heading out for vacation to another country for a few weeks and forgetting/losing my pills

2 I appreciate that the tolerance for tenofovir is low but it's entirely possible that I develop a tolerance in my expected lifetime... at which point what?  The best my specialist can say is we can fall back on other drugs, but even then I may well outlive those drugs...

I am trying to dig up my history now but at one point a few years ago I was a stage 2 on a 6 stage scale of cirossis (very mild but starting) and liver enzymes were HIGH in the 200's sometimes.  Viral load in the 5 million plus I believe.  Really high on all counts anyway... (sorry about vagueness like I said trying to get my records online right now and going off memory).  

On top of regular hep b I apparently have mutated hep b also.  

I was very overweight at the time (5'10 and 240) and have since droped to 180 to fight high blood pressure... the result was that during a recent biopsy the doctor asked when I had started treatment... I told him I hadn't and he said my enzyme levels were way down (60-80 I believe) and he thinks I may have been suffering liver damage from fatty liver disease and not so much the hep.

Viral load has also been steading declining and is 1.2 mill last count.

Back to my hep specialist, he looks at it and says he still says I should start treatment.  He thinks also this last biopsy probably showed inacruately favorable scarring and scirocis...

This all makes me feel uneasy...

Add to this he is sponsoring a trial involving pegalated interferon and tenofovir and has me currently signed up for it(haven't started treatment yet) and assures me he has no interest whether I partake or not but it makes me uneasy too...

I actaully had another doc for a while because I wasn't wild about the way this guy works (always feels like he is explaining to me what he would want answered and not as much what I want answered) but that doc moved out of state and this guy is apprently still one of the best in the area for asian hep b.

My big concern is I have to wonder why it's a good idea to start treatment when damage is relatively low instead of monitoring and starting treatment when damage gets worse?

If I am going to develop a tolerance (it's a maybe and over a long enough time it seems likely) why would I start the clock ticking now rather than when things are bad?

Or is it the kind of thing that can get up on you so fast that it's not worth the risk?

I don't want to be penny wise pound foolish by trying to play the waiting and timing game, but on the other hand I don't want to start medication for no good reason possibly screwing myself down the road.

He is saying I need to decide which direction to go... he says he isn't irritated that he and his colegues have spent so long talking to me (he spends an hour a session sometimes which is quite long for a specialist I believe) and I am still flip flopping on whether I start treatment and has said I really need to decide which way to go.  He assure se they will do their best to help me no matter what (ie I chose to monitor and not treat or I choose treatment or I choose trial) and I have indeed been waffling for 3 year snow so I don't think that's particularly uncalled for bu tI can't shake these cold feet.

Is there a chance I should hold out?  I should play the timing game, get lots of blood tests and ultrasounds and stay off drugs as long as I can?

Or is that foolish and chasing dreams of self sero converting that is almost certain not to happen and risking my health?

I would love to becured of Hep B but I believe my demographic is very low on the likliehood scale to convert (asian with mutated hep b) so I am not really feeling the biggest selling point he is putting ou tthere (which is how great it would be at 33 to be "cured").

I saw a post a few down whihc mentioned taht someone in LA had to go without tinofovir for a few weeks due to drug shortage... that worries me too... anything is possible and I have heard of some pretty nasty drug shortages recently...

Thanks for any help and advice!
76 Responses
Avatar universal
BTW I should mention that I have had several ultrasounds, lab tests and a few biopsies and as far as I can tell overall the results seem to match up to my weight/general health... that may be coincidence but it does make me wonder.
Avatar universal
You are giving us very "confused" information, we would like to know
1. your HbeAg status
2. your most recent ALT
3. your most recent hbdna(viral load) in iu/ml or copies/ml
4. your most recent biopsy result (grade of inflammation and stage of fibrosis)

You are wrong about this "7 year tolerance for Tenofovir". Tenofovir has only been approved as a treatment for Hepatitis B for about 7 years. During these 7 years, no case of drug resistance has been reported. Because of its high genetic barrier to resistance and its high potency in suppressing viral replication, it is likely that Tenofovir may have no drug resistance for a very long time.

Yes, you are right that Tenofovir may have to be taken for a long time. But successful cases of patients stopping Tenofovir after several years of undetectable viral load have been reported. Also, there is a treatment protocol of adding Interferon to Tenofovir after several years of undetectable viral load that has a high success rate of clearing the virus.

If you dislike taking a pill daily for a long time, you may like to consider the 48 week treatment with pegylated interferon. Under ideal conditions, such as low level of HBsAg, this treatment offers a chance of a cure, it can also lead to your Hepatitis coming under control if you are a responder.

Whether you can wait depend on many factors and must be balanced against the benefits of treatment.
Avatar universal
You are giving us very "confused" information, we would like to know
1. your HbeAg status
2. your most recent ALT
3. your most recent hbdna(viral load) in iu/ml or copies/ml
4. your most recent biopsy result (grade of inflammation and stage of fibrosis)

You are wrong about this "7 year tolerance for Tenofovir". Tenofovir has only been approved as a treatment for Hepatitis B for about 7 years. During these 7 years, no case of drug resistance has been reported. Because of its high genetic barrier to resistance and its high potency in suppressing viral replication, it is likely that Tenofovir may have no drug resistance for a very long time.

Yes, you are right that Tenofovir may have to be taken for a long time. But successful cases of patients stopping Tenofovir after several years of undetectable viral load have been reported. Also, there is a treatment protocol of adding Interferon to Tenofovir after several years of undetectable viral load that has a high success rate of clearing the virus.

If you dislike taking a pill daily for a long time, you may like to consider the 48 week treatment with pegylated interferon. Under ideal conditions, such as low level of HBsAg, this treatment offers a chance of a cure, it can also lead to your Hepatitis coming under control if you are a responder.

Whether you can wait depend on many factors and must be balanced against the benefits of treatment.
Avatar universal
Thanks for the fast response!  

I am realize and am sorry for my shoddy info... it all seems so clear when I am in my docs offic discussing but now I realize I really need my lab results to go off of.  I am trying to get my results from my online portal and will post details ASAP.

I was told that I am not a good candidate for interferon alone as I have been infected for a long time and have very high viral load (it was 10^8 at one point but has dropped to 10^6 recently). Is that not correct?

Also in general how do you feel about treatment at 33?  It just feels really early to me a nd makes me worried about the long term ramifcations....

If I was 50 or 60 no problem, but at 33... that's a long time of taking drugs assuming I don't clear and my doc has been very clear with me that the chances of me clearing are pretty low...

Again I will get detailed lab and biopsy results ASAP.
Avatar universal
Oh also the trial is Pegilated interferon for 6 months along side Tinofovir and then continue tinofovir for however long after.

The idea being that the two combined increases the chance for sero conversion...  All I see around here is talk about tenofovir for a long time then interferon to "finish it off" so to speak... do the two ideas conflict?  

I suppose I could do both for 6 months, then a few years of tenofovir and then another round of interferon?
Avatar universal
Hey got my info!:

So Biopsies fibrosis (leaving out a lot of the report as fibrosis is what's asked for):

Jan 2011: Knodell 1, Ishak 2
Dec 2011: Knodell1, Ishak 1
Dec 2012: Ishak 2

Liver panel:

May 2011: BEAG Reactive  
April 2011: HBVDNA 640100000 copies/mL 110000000IU/mL
Oct 2011: AST 82 ALT 243
Oct 2011: HBVDNA 6520000 copies 1120000 IU that's not a typo, double checked...
Nov 2012: AST 28 ALT 80

I know I have labs going back further but they must b e only in my other hospital file so I will have to ask for them tomorrow from the site.

But basically I have been riding really high DNA and enzyme levels for years... I droped about 60lbs in 2012 and there are corresponding drops in enzymes and viral load... liver has not shown any progression in damage and the last biopsy says "no significant steatosis respresenting an improvement to the prior"...

So question is:

Is that correlation or causation and do I still warrant treatment or was damage likely due to fatty liver (which it was identified at one point as roughly 25% fatty) and despite high viral load there is no ongoing damage so treatment can/should wait?
Avatar universal
Sorry there was a typo, ignore above and go with these numbers:


May 2011: BEAG Reactive  
April 2011: HBVDNA 640100000 copies/mL 110000000IU/mL
Oct 2011: AST 82 ALT 243
Oct 2011 HBVDNA 640200000 copies 1100000000 IU
Nov 2012: HBVDNA 6520000 copies 1120000 IU that's not a typo, double checked...
Nov 2012: AST 28 ALT 80

Sorry...
Avatar universal
So in Nov 2012:
ALT 80
HBVDNA  1.12 log 6 iu/ml
Fibrosis: Ishak 2, (2 in 0-6)

What is not clear is your HBeAg status (it was positive in May 2011). But your doctor signed you up for a clinical trial and from your description, it seems you are still HBeAg +ve.

I am not a doctor, so these are just my opinions.

It seems you are in the immune clearance phase. Since your fibrosis score is relatively low, you can wait to see whether you can seroconvert your HBeAg on your own.

The clinical trial you describe is interesting. I wonder what the endpoints are? It seems it will use Interferon to ensure a rapid seroconversion of HBeAg, then continue with Tenofovir to reduce viral load to undetectable. I wonder whether then Tenofovir will be stopped?
There is no conflict with the idea of adding Interferon after long term use of Tenofovir. Different ideas are being tested.

Finally to your question. Fatty liver can elevate your ALT and may also lead to fibrosis in the long term. However, your elevated ALT and mild fibrosis are also consistent with transition from immune tolerant phase to the immune clearance phase.
Avatar universal
Sorry to be unclear... I am still reactive, I didn't post more recent findings because they didn't change.

The doc signed me up for a triall but I have not had any medications...

My hope was that somehow the recent 100 fold decrease in viral load and lower ALT meant something good in terms of my risk levels.

As I understand it, nothing good happens until you sero convert and I have not so I don't know what exactly I was hoping for but was still hoping (I really don't want to start on life long meds).

From what I was told inteferon alone is not a good fit for my situation (high viral load/long infection time) so the choices I have all involve some kind of drug that introduces a dependence...

That scares me on so many fronts.

But then so does potential liver cancer.

So I am battling between chosing to go onto a drug which locks me in until who knows what with very small hope of forcing a seroconversion (That doens't then revert) in an effort to prevent potential cirhosis and thus liver cancer

or

Risking it on monitoring and hoping that I don't get a freak HCC and that when firbrosis becomes more pronounced I can then step forward and start treating in an attempt to reverse fibrosis and defend against liver cancer.

I am correct that fibrosis can be reversed right?

My concern is I just don't know enough about liver cancer and how fast it can set on and how nasty treatment really is (since as I noted all documentation likes to point to fatality rates for unmonitored and untreated or late detection cancer) to really feel comfortable making that call...

On one sideI don't want to lock into potientailly 50+ years of daily pill popping with the fear of resistance hanging over my head when it's entirely possible I go the rest of my life just fine untreated but on the other boy would I be kicking myself if I have to get surgery for liver cancer or worse yet try to get on a transplant list...

Why can't it be easy :(

Fromw what you say and what I am reading it sounds like I may have gone from tolerant, to clearance and am in a quiecent phase right now...

My doc described it as coming in waves where the immune system chases the virus so to speak and as the viral load succumbs, so does the immune systems effects making peaks and valleys....

If this is accurate it seems I am looking at the upside of a low viral load for a while with the downside of potential flairs and the resultant damage that comes from them... another hting I am having trouble evaluating risk wise...

Sorry to be rambling with my typing... just feels better to put it down in writing for some reason.

BTW The endpoints of the trial are 6 months of inteferon and tenofovir with tenofovir continunued until the viral load is low enough (I assume under 200 or undectable) with a monitored end to tenofovir to see if load stays low.

The desired result is a sero conversion making the patient effectively "cured" and the idea is that the interferon and tenofovir together inncreases the likelihood of seroconversion.

But again as it's explained to me due to high viral load and having mutated virus my results are not likely to be rosey as evne if I sero convert agains the wild Hep B I will not against the mutated and so will not really be "cured" even anyway...

The hope being that I sero convert and then we find my mutated viral load is so low that I still count as "cured"...

So you can see why I am hesitant...

The way I am looking at it right now is "Am I ready to go on tenofovir" and if I am then I will toss the interferon on as well, but if I am not then I think I am saying no to the whole package...

Thanks again for any input... I don't know why but input from someone else who isn't my (or even A) doctor is really helpful!
Avatar universal
BTW what's the +ve?
Avatar universal
positive +ve  negative-ve

when you found out you're hbv carrier?
Avatar universal
Thank you for your information regarding the endpoints of the clinical trial. So the trial is testing the viability of a finite period of treatment involving Tenofovir + PegIFN. Very interesting.

For your information, there are two types of seroconversions: HBeAg +ve to HBeAg -ve, and HBsAg +ve to HBsAg -ve.

You keep mentioning that you have a mutated virus, I don't see any evidence for that. I think you are still in the immune clearance phase and have not yet transitioned to the immune control phase.
Avatar universal
Dear Stephen,

i'm wondering how at mid 30's still eag+... when eag serocovnersioen normally occurs in eag+ carrier?

i'm also still eag+ on ifn mono tx (i quit TDF after 1 year combo with IFN) and now on IFN mono week #49..
Avatar universal
Yes I recall discussing the difference between e antogen and surface antogen... but at this point forget the difference... I belive the surface antibody was the more desireable of the two?

I say I have mutated virus because my doctor tol me I tested positive for muttated.  I think it showed up in a test result somewhere (I have scores of test resuilts over the last few years, I left all that out for brevity in my posts).

So if I am in the immune clearance phase that is shen the most damage occurs correct?  That is when the liver is actively being attacked as the body fights the virus that lives in the liver?

I'm just so confused and not sure which I am more scared of - potential liver cancer or getting onto a drug with a lifetime dependency and no fault tolerance.

Avatar universal
So you went off tenofovir?  Was your viral load really low?  I have always heard there is no going off tenofovir until your viral load is undetectable...
Avatar universal
It is not uncommon to still be HbeAg+ve in your 30's. I believe Genotype C takes longer to seroconvert. Anyway, most hbvers should seroconvert before the age of 40.
Avatar universal
HBsAg seroconversion is the closest to a cure, so that is what we are aiming at.

It is not a routine test that tests for mutations. Usually, if you are HBeAg-ve with a high viral load, then doctors may test whether you have the pre-core or bcp(basal core promotor) mutations.
As I am assuming that you are still HBeAg+ve, that is why I cannot see evidence of mutations.

Yes, damage is being done during the immune clearance phase, especially if it is prolonged.

You are still thinking that antivirals have to be taken for life. This is the current thinking, but in truth, the two most potent antivirals, Entecavir and Tenofovir, were only FDA approved in 2005 and 2008 respectively, so no-one has taken them for life. The other treatment, PegIFN is a finite length treatment.
Avatar universal
Thanks again for your input Stephen... I am very sure my doctor mentioned that I have mutated HBV and did indeed talk about pre core mutations... is there a certain test I would see that result in?  I have boatloads and only pasted the info directly pertaining to viral load and liver enzymes so I can always look for more to be sure.

I am going with the theory that antivirals have to be taken for life becuase I am under the impression that seroconversion rates are very low (especialy in Asians with high viral load) and as that is the only "cure" realistically there is no expected end point.  

I don't hold much hope for any actual cures (ie Tcell therapy) as I have seen too many come and go with no actual viable product so don't want to get my hopes up.

Is your point that I should not consider it a life long commitment or that there is no evidence it won't develop a resistance long before I expire?

I take it from your above comment that most people seroconvert by the time they are 40 to mean that at 33 I am still in reasonable range to seroconvert on my own (despite that group being a very small group).

I have to wonder does going on medication in anyway prevent my own seroconversion or can it only help?

It would be terrible if I was going to seroconvert on my own and start taking meds only to block my recovery and lock myself into meds...
Avatar universal
In May 2011, you were still HBeAg+ve. May be you should check your HBeAg status now, otherwise all the discussions about seroconversion will not apply to you.

My point about having to take antiviral for life is as you say, a theory at the moment. It can be overturned by new discoveries. But most important,  it is possible to stop taking antiviral after several years, without a cure, BUT the virus will then be kept in control by the immune system. These stopping rules are in place now and success rate is about 50%. So your "life long commitment" is not set in stone.

It is a fine balance between waiting to seroconvert or start treatment during the immune clearance phase. Many factors need to be considered, the most important being the state of your liver. An experienced liver doctor would be most helpful here.

Whether treatment will hinder the HBeAg seroconversion is unclear to me. But again this is not the point - when you need treatment then you need treatment, you don't wait. HBeAg seroconversion is just a signpost in the long journey that is Hepatitis B, many people still need treatment after they have seroconverted.

Avatar universal
As off Nov 2012 HEP BE AG Reactive (A)

Can you clarify for me how HBEAG effects seroconversion?  

I thought unless you seroconvert, getting viral load low enough to control was mostly a temporary thing (I am aware seroconversion can revert also) so I ahdn't really considered it an endpoint...

I have taken my results to 2 hep specialists and both bluntly said "start treatment" based on viral load, enzyme levels and fibrosis.

While it is probably stupid to second guess two specialists, I often feel they may prioritize things differently than an actual patient (ie in my job I tell people to do things to a level I don't hold myself to in my personal life because I am ok with the risks I take but don't want to be responsbile for someone else taking the same risk as low as that risk may be).

For instance I don't think anyone not actually faced with hopping on drugs for potentially the rest of their life can really understand the value and desire of delaying treatment.

I feel that a stage 2 fibrosis seems low and I have 2 or 3 stages to go through before things get bad... it seems based on previous comments you and I are on the same page about that, but the specialists do not seem to agree... somehow though I feel better about responses from others like me than from the speicalists kind of how you feel better about reviews of a car from a driver than from a dealer...

As for seroconversion being just a signpost, I thought until it reverted, you were pretty much good to go?  I am incorrect on that?

Thanks again so much... your informitive posts bring a lot to this forum!
Avatar universal
Can you clarify for me how HBEAG effects seroconversion?

I am confused by your question. HBeAg is a protein produced inside an infected liver cell when the virus is replicating and then secreted into the blood. In a blood test, if they can detect this protein, you are HBeAg positive(+ve) or reactive. This generally means the virus is replicating. When the blood test cannot detect the presence of HBeAg, you are HBeAg negative(-ve) or nonreactive. Over 10 years ago, this was generally taken to indicate that the virus is not replicating and is a good sign. Since then, they discovered in some people, the virus has mutated such that when it replicates, it does not produce HBeAg. So even though HBeAg is negative, the virus is still replicating.
Nowadays, whether a virus is replicating or not, can be determined by the viral load (hbvdna). So HBeAg-ve and very low hbvdna indicate immune control and no treatment is needed, but HBeAg-ve and elevated hbvdna indicate immune escape and treatment is usually indicated.

Seroconversion is just a fancy word to mean they cannot detect HbeAg in your blood whereas previously they can do so (technically, a true seroconversion also involves the presence of HBeAb, the antibody).
Avatar universal
OK so when you were asking if I was still +ve you wanted to make sure I wasn't chasing something I had basically already gotten?

Basically -ve is good, -ve and low viral load is better and -ve and low viral load with HBeAb is about as good as it gets...

I'm off to see my PCP tomorrow and see what she says about delaying treatment... she isn't a speicalist but I trust her a lot (long relationship).

You have helped me a lot in terms of lining my ducks up!
Avatar universal
HBeAg-ve and very low hbvdna is good.
HBeAg-ve  and elevated hbvdna (> 2000 iu/ml) is no good.
Avatar universal
With your viral load and fibrosis you need treatment by all guidelines.
I would go to the doctor who offers the combo treatment, it gives the best chance of hbsag seroconversion and since the doctor offers it he seems to be well educated about the Hbv, unlike most of the others who just follow the clinical guideline. I would check if the doctor can arrange hbsag quantitive test for you, it is generally not available in the US but needed to monitor interferon treatment progress.
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