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Genotype 3 Treatment
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Genotype 3 Treatment

We now know that geno 3 should not be treated like geno 2. Someone (sorry, I cannot remember who) on this forum gave me this valuable information, according to latest studies of:

Columbia University, MD, special research for G3

NOT   UND at       W 4 48 weeks tx
High VL UND     at       W 4        36 weeks tx
Low VL UND at       W 4        24 weeks tx

If anyone has more information and experience treating genotype 3, I would be very thankful to hear about it.

Marcia
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57 Comments Post a Comment
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Avatar_m_tn
I am a G3a non responder and that Tx formular seems about right to me.
The other thing to throw into the mix is Fibrosis.
Maybe treat longer if Stage is F3 or F4
but RVR seems to trump all the other negatives.

CS
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476246_tn?1310999221
Thanks a lot for the input. I hope you will be able to treat again, with success. It is always so heart breaking to hear about non responders. And then there is the fear that one might be one.

Marcia
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Avatar_m_tn
You will know with a week 4 PCR test whether you are heading down the difficult to treat parth or not. Just make sure you have a 4 week PCR test.
UND @ week 4 = really good SVR odds.

All the Best
CS
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96938_tn?1189803458
The 'if not und by 4, do 72' was the simple rule the liverhead gave me.  That went along with all the necessary time planning around pcr's and the prescriptions pre-dated to get them done.  But, with a prior failed tx and early cirrhosis and age (about 56) the formula was adjusted to the 48/72.  But, the criteria you mentioned seems to make sense for a 1st time tx'er who has not demonstrated 'difficult to treat' traits. Having done a prior 24 (G3) week relapsing tx, motivation was high to get to und as soon as possible.  Which is why we were aggressive early in tx (pre-dose riba and double Peg for 4 weeks).  One thing I've wondered about though - whether high or low VL, is if there is a difference assuming und is reached by week 4.  The Columbia folks seem to think yes.
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179856_tn?1333550962
I just wanted to say how great I think it is to see such important discussion going on. WE'VE all known that the cookie cutter approach 1 = 48 2 = 24 **** doesn't work but it's nice to see that FINALLY the liverheads are getting the facts too!

I just don't understand why it seems such a hardship for them to tailor treatment to a persons specific numbers.  I would advise any newbie who is in here to really learn these facts and how iMPORTANT being UND at week 4 really really is.  A lot of doctors still don't even know it.

Dr J was the first one I know of who was really onto this bandwagon (but that makes sense).  If anybody needs a second opinion in order to get their doctor to work with extensions.........even if you have to pay out of network to get one of the good guys - DO IT.  I paid $600 (and I'm a broke single mom type) cash and it was worth EVERY SINGLE PENNY and ounce of mac and cheese for dinner that I had to eat ;)  Anything that leads you to achieve SVR is.

Don't worry about having to do "more time" - get the SVR the first time if you can.
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388154_tn?1306365291
As you maybe remember Im on a study (danish) for relapsers geno 2, 3 and are given weight based riba and pegasus which always is 180mcg.

My first tx i started in september 2006 they didn`t check for baseline vl and first pcr wasn´t made until week 12, and 95 or maybee it was 98% of all geno 2and 3 are UND at week 12.
I was also on the old protocol 800ml riba for everyone and not weightbased peginteferon.

I´m gonna try to get to what I wanna say, I have a  friend geno 3 he started to tx 13weeks ago and is getting a new protocol weightbased riba but not weightbased peginterferon, hes got a 4w pcr.

He had a low baselin vl result 76000iuml (yea they gave him that aswell)
and they want him to extend to 48weeks since he had a borderland vl result week 5( he was sick w4 so he made the test one week later)

Finally this is what I´m wanna say to you!!
I checked up the prices for peginteferon verces pegasys and the price is very much the same due to amount of medecin, but if you on peginteferon and are thin, or like my friend dosen´t get the proper amount there is money to save for the hospital.

I dont dare to recomend what you gonna chose peg or pegasus,
the sx on pegasus is much less for me then on peg.

But I felt so very good post tx how knows how I´m gonna feel after this one?


your friend ca

ps my friend is treating in gothenburg but i think his on the new protocol for 3s probebly pretty much the same world wide
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476246_tn?1310999221
Thanks so much for the input!

Marcia
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476246_tn?1310999221
Thanks!

Yeah the prices, I checked them on sundhed.dk, they have all the meds, side effects and prices noted there. It's quite cool, so easy to access info. I hope they will not try to make me go for a less, because of the costs. I just found out from my GP, that they give you the meds at the hospital, don't even have to involve you insurance or anything. They just plain give the stuff to you. I love it!

According to my weight, I definitely do NOT want weight based. I weigh 56 kg.

It would definitely be better for me to do Pegasys, as I would get the 180mcg. I have already made up my mind ages ago, to push the doctors to put me on Pegasys.

Ribavirin I would get 800 mg.  I don't think I can get them to give me more Ribavirin than 800mg. Shouldn't that be enough for me?

My VL is 580.000, according to that and the Columbia University Study, I should be doing 36 weeks, provided I'm UND at 4weeks.

To sum it up:

At least 36 weeks tx, with 180mcg Pegasys and 800 mg Ribavirin.

Please correct me, if it is incorrect.

your friend, Marcia
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476246_tn?1310999221
I forgot to mention, that I haven't had a biopsy, yet. I can't wait to get it done, but it will probably still take a while. I have my first appointment at the hospital on June13th. They will do all the blood tests again and some additional ones I haven't had yet, check my heart, etc. They are keeping me the whole day. And I will finally see the hepatologist. They are not doing the biopsy the same day, though.

I want to be as much informed as I possibly can and I am so glad that all you great people are here, you are such a big help.

Thank you all, Marcia
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217229_tn?1192766004
OK - maybe I'm a throwback to the dinosaur era... Or just a medical freak.

I didn't go UND until the middle of my TX.

I'm a 3a.

I only did 24 weeks last shot was end of February - last Riba start of March of 2007. So I'm UND/SVR 14 months so far.

At 4 weeks, my PCR showed viral load had barely moved down and was still detectable.

But at 12 weeks it was UND.

So if what you guys are saying is true --- then I'm one lucky duck.

LOL!

Quack the heck on!

LOL!

No seriously - I'm in total agreement - the more I've learned - the more I've realized that most doctors don't know ANYTHING about this disease, the treatment --- and the side effects from both the disease and the TX.

I also think that if some folks had been allowed to go 48 to 72 instead of 24 alone - that there would be a lot more UND/SVR going on.

And 1a group if not UND at 72 - try for 24 more weeks. I mean WHY the heck not --- IF THEY ARE RESPONDING?

If not responding - then well - I don't know what to say --- but WHY take people OFF TX --- at 72 if they have shown some sort of response?

I think a lot of the issues have to deal with insurance, money and that's the bottom line for most of us.

I think that's sad.

Meki

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Avatar_m_tn
At 4 weeks, my PCR showed viral load had barely moved down and was still detectable.
But at 12 weeks it was UND.
So if what you guys are saying is true --- then I'm one lucky duck

Yes Meki you are one of the 40% who manage to SVR in spite of a poor early response.
G3s are like that. Turn it around and you tend to cure.

Its the turn it aroun bit thats hard.
CS
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144210_tn?1273092382
You got mail.
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476246_tn?1310999221
So meki's tactics is not something one should count on, right. Meki, you really are one lucky duck. But your tx was hard, wasn't it. Wow, lots of sx. Bozo the scratching dog, etc. I love your stories, they make me crack up, but there was a lot of suffering. You just make it sound so funny.

Marcia
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96938_tn?1189803458
The range of dosing for riba is about 13-15 mg per kg of weight.  At 56kg, 800 mg riba puts you about in the middle.  If it were me, I'd be pretty firm if the doc attempted to prescribe less. And, if you have an adequate supply you might consider taking it for a week before you start the Peg. Even if the advantage is small, any edge you can possibly get might be helpful.
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476246_tn?1310999221
Thank you...

I will ask the doctors what they thing about predosing with Riba. It's the hospital who supplies me with the medications, so there is not much I can do on my own. I hope they will be cooperative. Maybe I can convince them to take me as an experiment of the 'new studies'. Never know, they might bite on it, as it is a University hospital.

Marcia

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387294_tn?1207623785
Well I am genotype 3a, and did what was standard protocol of 800 riba and pegasus.  I have done 24 weeks and still clear 8 weeks off treatment. I was under 615 at week four but still detected by Qual. TMA, tests week 8 and subsequent have been clear.  I am waiting and hoping it worked.  Many indicate that relapses usually occur in the first 4-6 weeks and I hope so.  I will keep you posted.
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387294_tn?1207623785
Oh I failed to add I was high viral load (9 million) to start so I went down about 5 logs by week four.  Also, I do agree that your fibrosis level is a consideration in amount and time to treat type 3's.
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387294_tn?1207623785
Oh I failed to add I was high viral load (9 million) to start so I went down about 5 logs by week four.  Also, I do agree that your fibrosis level is a consideration in amount and time to treat type 3's.
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217229_tn?1192766004
You know - there has been a discussion that I think warrants merit.

The below is just my opinion on what I've read and kind of put together in my head.

I think Genotype 3a hits harder, faster and does quicker damage - but is "wispy" compared to the hardcore Genotypes 1 and 2.

I think 1 is a hardy, strong strain that does not need to destroy everything in it's path - so does not take over the host in an effort to gain ground.

2 is hardy - but has flaws in it - it gets hold - but seems to be broken much easier than 1.

3 seems to wriggle in fast and hard - doing hardcore damage, seeking it's way in to the host but it seems to dissipate faster than the other 2.

Not so in those who have somehow managed to grab a variant of 3a that seems to have mutated a little bit --- to what I kind of call 3b (like CockSparrow's).

Now - maybe I'm way off --- but those are the kind of things I've been watching in the writing everyone has done.

I'm no biologist - I'm just putting together pieces of conversations... I may be right --- but probably not... Just observations I'm making --- OK?

Part of that observation is that it seems that 1a 1b 2a all seem to have long times living with the virus in their systems without much noticeable effects...

But 3a's they seem to get damage or symptoms faster than the other 2 genotypes. It seems (maybe only in my mind) that 3a's start feeling unwell - very quickly --- I was getting sick within 7 years of last known HCV clearance for me.

There are 1a's who have had HCV for 20 or 30 years.

In that amount of time - I would have been dead.

So --- whatcha think of my musings?

Meki


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217229_tn?1192766004
"biologist"

Snicker --- egads... OK - I'm no scientist - doctor - anything that requires MEDICAL to it... LOL!
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387294_tn?1207623785
I have probably had hep c for 20 or 30 years, which is a guess, with stage 1 liver damage.  In all my research about type 3 I have heard that fatty liver can be common but no acceleration of fibrosis.  Type 3 can be easy to treat, but variables like fibrosis level...  can make it difficult. I don't think there are strict variables but with type 3 race, weight, fibrosis level and viral load can impact treatment strategy.  Again I think the 4 week viral load is important to doctors today.  I have grilled my doctors and some of the information stated her about rules to extend type 3 due to viral load.... is not accepted by qualified hep doctors at this point.  I do think the 4 week viral load test is very commonly used at this point.
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387294_tn?1207623785
I have probably had hep c for 20 or 30 years, which is a guess, with stage 1 liver damage.  In all my research about type 3 I have heard that fatty liver can be common but no acceleration of fibrosis.  Type 3 can be easy to treat, but variables like fibrosis level...  can make it difficult. I don't think there are strict variables but with type 3 race, weight, fibrosis level and viral load can impact treatment strategy.  Again I think the 4 week viral load is important to doctors today.  I have grilled my doctors and some of the information stated her about rules to extend type 3 due to viral load.... is not accepted by qualified hep doctors at this point.  I do think the 4 week viral load test is very commonly used at this point.
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476246_tn?1310999221
Thanks for your input. Just wanted to ask, did the 800 mg Riba correspond to your weight, or was is more or less. I am asking it this way, as it might not be appropiate to ask straight out how much you weigh.

Marcia
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476246_tn?1310999221
I agree that there is something fishy about geno 3. Unfortunately I do not know my subtype.

I have read that geno 3 is prone to having NASH, actually 71%. Not so nice. ;-(

I have been wondering why I have had such aversion to fats for so many years, and wonder if there is any correlation. I get really sick, if I have heated butter on food. Once I had it in a restaurant. They had put it on the rice. It made me so sick, I head cold sweat outbursts and was sick for a whole week.

Lets see about your theory that 3 does quicker damage, when I get my biopsy. I hope you are wrong about that one, as I might have had this since 26 years or so. According to that, my liver should be in a pretty bad state. But then again, I haven't touched any pot for 20yrs, alcohol and cigarettes for 10 years. And I have been vegetarian and partial health freak since year 2000. I hope all that counts towards damage control.

Since my daughter has it, I assume she got it since birth. I think there is a greater possibility she got it that way, than using one of my razors. I hardly ever cut myself, and always use them under the shower, so no blood left on them. We always had each our own razors, but it could be she might have used mine at some time. The chances of her having contracted it from a razor of mine that she used after I had cut myself and she also cut herself are much smaller than her having contracted it at birth.

What I'm getting at is, that according to that I must have at least had it for 18 1/2 years. I wish I had kept all the Rhogam vials. Maybe one would be able to check them. I really started having heavy symptoms only a few months ago. But looking back, menstruation problems started in 2004, my hormone levels are all fine, so pre-menopause is ruled out. So I don't know how all this it justifies your theory about feeling symptoms earlier than the other genos. But definitely I do have symptoms of fatigue, joint aches, messed up periods, muscle aches and brain fog. All this has gotten better, since I eliminated all toxins and dairy products from my diet and my skin.

Marcia

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Avatar_n_tn
Everything I read about genotypes is that one cannot predict disease progression by them. There has been some studies that SUGGEST that 1a is worse than 2 or 3 when it comes to progression but the studies themselves state it there be a statistical problem with that theory because there were so many more 1as than 2 and 3s in the study. NOTHING I've seen says 3s have a more virulent virus. I think length of infection, gender, fibrosis stage, alcohol consumption are the most agreed upon reasons for progression.
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Avatar_m_tn
    Lots of good info on this. But in the end I am still confussed. I guess that is part of just being scared. 3 wks ago I finished 24wk tx 3a. I cleared the virus at 3 1/2wks but I do have significant liver damage. No one seems to know anything for sure. Damn viruses are amazing. I just don't want to die of this disease. It looks nasty. Treatment just wiped me out and got worst I would have liked to do 48wks but I just couldn't do it. Its in Gods hands right
     Red
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476246_tn?1310999221
So you must be waiting for your next test to see, if you're still UND. It must be nerve wrecking, but great to be finished with tx. I wish you all the best on your way to SVR. I hope you will find a way to build up your liver again. I thought that the liver is able to repair itself, if taken well care of. Don't know much about it though. I think that you would be able to find out a lot about that.

Marcia
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217229_tn?1192766004
It could be based on each individual and their genetics as well.

I mean - like how good their immune system is, etc.

Because I know from date of last HCV testing where I was clear - to point of my getting sick ---- and showing serious signs were less than 10 years.

In all - it's only possible IF I got HCV the day after the test --- for me to have had it since 1992/1993. (methinks I got it in 1996 -- January 4th/5th, to be exact... LOL)

So I know that it worked it's hardcore magic on me... LOL! Fast.. really fast.

Yet I've heard of 1a and 1b folks not knowing they had it for YEEEEEEEARS... We're talking 20 - 30 years.

Me - if I follow my med records - I started getting sick within 2 years of what I believe was my transmission. That's pretty fast. I started getting really sick in 2004 - to the point that they were searching out other issues (cancer, etc. for my symptoms because I had only slightly elevated ASTs and ALTs so no one thought to check my liver.)

Weird --- I kind of assumed that I was normal - but seeing how I didn't go UND in the first 4 weeks --- hardly moved... I must be abnormal for SVR and maybe for disease progression overall.

Just a thought.... I honestly don't know the answers --- I wish I did folks...

Meki


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Avatar_m_tn
I've had it 25 years and am Grade 1 Stage 2. Hasnt worked real fast on me.

What happened to you actually occurs with any Geno.
There was a theory that because of steatosis G3 progress faster but like G1b being faster progressing its not really true.

There is one thing about G3s. Has anyone seen a G3 with really high Viral Load 30-50million or more. Happens with G1s and occasionally with G2s, does it happen with G3s. I havent seen it.

CS
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451988_tn?1209915425
i understand that gt3's are mostly needlesticks; junkies, tatoos, razorblades and such; lot of gt1's are blood transfusions; before the nineties, they didn't screen the blood; here in the USA, medicine is not efficient; US trained doctors tend to throw the works at you, they have the money; my wife, who works in the field, worked before in france and argentina; she says here in the US if you scrape your pinky the first thing they do is give you some blood; it's a business; that's why most gt1's are here and have high vl's anyway it's a thought...
ciao
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Avatar_m_tn
G1a and G3a worldwide are associated with drugs.
They are the 2 genos that seems to have gotten into the drug user community.
Its also why G3a is on the increase in many countries.
Sorry but they are just the stats. Doesnt mean thats how you actually go it.

CS
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387294_tn?1207623785
Well I learn something I would have rather not known everyday.  I am type 3 and didn't realize that it was associated with drugs.  I don't know how I got it, no drugs, tattoos, blood transfusions....  so its a mystery to me.  So it goes.  mary ellen
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Avatar_m_tn
I am also g3 and no drugs or transfusions. Stage 3 fibrosis at first diagnosis. ALT has not touched normal in last 4 yers despite Tx
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446474_tn?1404424777
Below is a link to a debate between leading US Hepatologists about optimizing treatment for genotypes 2/3. (You may have to sign up on their site to get this doc but it is free).

http://www.medicalcrossfire.com/onlineLearning/cme/2006/06-LC-27-M-100.pdf

Chronic Hepatitis C
"Strategies for Optimizing Current Treatment and the Potential Impact of Emerging Therapies"

PANELISTS
Adrian M. Di Bisceglie, MD - Saint Louis University Saint Louis, Missouri
Michael W. Fried, MD - University of North Carolina at Chapel Hill Chapel Hill, North Carolina
David R. Nelson, MD - University of Florida Gainesville, Florida
Mitchell Shiffman, MD - Virginia Commonwealth University Medical Center Richmond, Virginia

SPECIAL EDITION
Release Date: February 12, 2007 • Expiration Date: February 12, 2008
This activity is supported by an educational grant from Roche Pharmaceuticals.

MODERATOR
Emmet B. Keeffe, MD, MACP Stanford University School of Medicine Palo Alto, California
Jointly Sponsored by The American Academy of CME, Inc. and
Medical Crossfire®/Liberty Communications Network.

****( Text starts on Page 7 of PDF)****
"Genotype 2 and 3 Patients:
Presenting the Data"


All the best for SVR!!!
Hector
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476246_tn?1310999221
Hector, you amaze me each time with the info you are supplying to this forum. Thank you so much, I will get to it immediately.

Marcia
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146021_tn?1237208487
I've learned a lot from this discussion, which always leads to more questions.....
First, I was surprised when you stated:
We now know that geno 3 should not be treated like geno 2.
I didn't know!
Also, I didn't know the formula for clearing or length of tx. My viral load was 11 million to start, but I had cleared by week 3. I think I was just extremly lucky, blessed to still be und  6 months after a 16 week tx. (would never advocate shortened tx to anyone else)
Here's the part that is really a mystery to me:

"G1a and G3a worldwide are associated with drugs.
They are the 2 genos that seems to have gotten into the drug user community. "
OK, what does that mean?
If you can explain this comment I would really appreciate it. Obviously, I don't spend enough time on the "brainy" side of the forum:)
Bug
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387294_tn?1207623785
I am concerned that people do read this forum and while there are some interesting pieces of information shared from what people have learned along the way, it should not be confused as a medical forum for physicians and researchers.  I would hate anyone to rely to heavily on any information but use it to ask good questions when dealing with their own qualified doctor.  

Also, many people who become SVR with type 3 or other types are not on this forum.  People who are treating for the first time or determining whether to retreat are often times on message boards to gain new information and treatment strategies.  So those of us here do not represent a valid cross section of hep c patients.
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217229_tn?1192766004
Interesting. I didn't know that genotypes were more prone to being from specific transmission routes.

Very interesting.

I know I didn't get mine from IVDU --- or any other drug usage --- so I think that it's interesting that the medical community has associated any genotype with drug usage.

But --- I've never researched the amounts or percentages.

Maybe I'm naive in my thinking - but I don't think everyone or even a large portion of the HCV community obtained the virus through IVDU.

I just don't believe that.

I think more of it is from the medical treatments people have obtained.

I truly believe that everyone who has HCV probably obtained it from some sort of medical operation or injection.

Meki
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419309_tn?1326506891
My understanding of genotype distribution was that it was mostly geographically linked:  1a & 1b most common in the US, genos 2 & 3 most common in Europe, and genos 4 most common in Asia/Africa.  I've started seeing more investigation into the *nature* of each genotype, but I don't think there are any conclusive agreements ... yet.

My husband's hx fits your theory, though... we guess that he's probably had the disease close to 40 years, just diagnosed last year (asymptomatic, geno 1, stage 4).  There's been some conjecture that HCC is more common in geno 1s, but like I said, there's a dirth of info on the subtypes.

I tend to think that the disease (and also its treatments) affects individuals so very differently because of all the variables:  (1) the varying types (2) the varying states of health of the host (3) the length of infection and (4) the contributory environment.  

I often wonder why docs focus studies only on the "actively infected" population?  I've entertained the idea that the medical community might have some more success if they researched the population that contracts AND clears hepatitis WITHOUT treatment.  If we could only figure out what makes those ~30% who are exposed to HCV  "spontaneously" clear it, we'd be golden!

eureka
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Avatar_m_tn
Heres a study from Iran
http://www.comparative-hepatology.com/content/5/1/4#B28
Distribution of hepatitis C virus genotypes in patients infected by different sources and its correlation with clinical and virological parameters: a preliminary study

Genotypes 3a and 1a are more prevalent in IVDU in Europe and USA. In the present study, 18 (40%) and 17 (37.8%) patients with IVDA had genotype 1a and 3a respectively. It seems that there is a high similarity between the pattern of genotype in IVDU in Europe and United States when compared with Iran. However, it can not be due to migration of these people to these countries because the history of travel abroad was only seen in 6 cases (13.3%).

From http://www.wjgnet.com/1007-9327/14/1237.pdf
Hepatitis C virus genotypes distribution and transmission risk factors in Luxembourg from 1991 to 2006

Genotype 3 was significantly associated to IVDU

One pattern, characterized by high genetic diversity, involves geographically discrete areas where HCV has been endemic for a long time such as
West Africa with types 1 and 2,
Central Africa with type 4, and
Asia with types 3 and 6.

Another pattern involves areas with a few subtypes circulating in specific risk groups, e.g. subtype 3a in drug addicts.

The third pattern involves areas where a single subtype is present, such as in Egypt with subtype 4a and South Africa with subtype 5a.


Other molecular epidemiology studies have shown that HCV subtype 3a is significantly associated with transmission through injecting drug use in industrialized countries[22-24] and explain the prevalence of subtype 3a in many North and South American and European countries. HCV subtype 3a originates from Asia and has spread widely among injecting drug users[25,26].

Mechanisms of subtype 3a transmission remain poorly defined. Genotype 3 was not associated with a high level of HCV RNA as compared to the others genotypes in our cohort. Nevertheless, the relative homogeneity of NS5B sequences of injecting drug users from France, South America, Australia and California have indicated that HCV subtype 3a has been transmitted from a common origin through a unique worldwide epidemic among the drug user communities[27].

In this study, the authors reported region specific HCV 3a variants suggesting local transmission among intravenous drug users from the same geographical area. Therefore, the intrinsic characteristics of the transmission network of IVDU (unsafe injecting practices, drug preparation materials, needle or syringe exchange) together with the importance of the social context of drug injections may explain the efficiency of HCV genotype 3 transmission in Luxembourg.

Our study shows that the main risk factor for infection by genotype 3 is IVDU whereas the main risk factor for infection by genotype 1 is medical-related transmission.

The age of infected individuals may be a direct variable for the genotype distribution. Nevertheless, our data did not show that patients infected by genotype 1 were older than 40 years. This would mean other routes of infection by genotype 1 such as IVDU.

One from France
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1233931
The epidemiology of HCV infection in southeast France changed radically during the study period in relation to modifications in the etiology of infection. We observed the emergence of new epidemic subtypes (subtypes 1a and 3) linked to intravenous drug use and a decrease in the types linked to blood transfusion and nosocomial infection (epidemic subtype 1b and endemic type 2).

Replacing G1b and 2 with 1a and 3a is occurring worldwide. In the West anyway.
Its what is happening here in Aust.

All the Best
CS
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Avatar_m_tn
Bug
the link below gives a really account of what is happening in Europe.
You will have to register with elsevier but it is free

http://download.journals.elsevierhealth.com/pdfs/journals/0168-8278/PIIS0168827807005739.pdf

It was already known that genotype distribution was associated with the mode of transmission, with subtypes 1a, 3a and 4 being mostly IDU-related and
genotypes 1b and 2 associated with blood transfusion and unsafe medical procedures

CS
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476246_tn?1310999221
Just wanted to comment  on a few things.

Distribution of certain genotypes in IV drug users. This does not mean that you must have gotten it though IV drug use. So please, anyone who has never done IV drugs, don't get offended. It is just that these types at a certain times where introduced into that specific group of people and was easily spread though out that group. It makes perfect sense, as often utensils for using the drugs are shared. One does not even have to share the actual needle. Sharing spoons and cotton wool is already enough to get infected. So this is the spread seen locally.

Then one can look at the geographic situation.

Geno 3 and NASH. I read in a medical report, that fatty liver has been found in 71% of Hep c geno 3s.  I cannot find it now, but had taken notes of, as it might be in my interest to get this matter checked. After what I researched on it, I found out that I am at low risk considering that my bmi is usually around 20.8 and has never been higher than 23.4. My normal blood pressure is low. And I don't have any other of the possible causes listed.

It's unclear exactly what causes nonalcoholic fatty liver disease. But many researchers believe that metabolic syndrome — a cluster of disorders that increase the risk of diabetes, heart disease and stroke — likely plays an important role in its development. Signs and symptoms of metabolic syndrome include:

    * Obesity, particularly around the waist (abdominal obesity)
    * High blood pressure (hypertension)
    * One or more abnormal cholesterol levels — high levels of triglycerides, a type of blood fat, or low levels of high-density lipoprotein (HDL) cholesterol, the "good" cholesterol
    * Resistance to insulin, a hormone that helps to regulate the amount of sugar in your blood


mar148....  Andiamo1 started a thread called 'Should forum members offer diagnosis?' on the Hepatitis Social/Living with Hepatitis Forum a couple of days ago . Check it out, there is some good discussion going on.

Marcia
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The study came up as pdf file straight from your link. Very interesting!

It is a little contradictory to the  suggestion of the Columbia University MD, suggesting to treat 36 weeks for High VL, if UND at week 4. it does suggest to prolong tx in certain cases, but unfortunately doesn't mention any time frames. Obviously they are still treading in muddy waters, concerning 'custom tx' for geno 3s. Considering dosing of meds, the studies done in Italy, could probably not really be applied to the US, as ppl are generally smaller in Italy. It could be applied to me, as I am about average Italian size.

Anyway, i will hopefully get a biopsy soon and then will be able to put down all the data and discuss how to attack this dragon.

Marcia
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Steatosis is associated with G3a. Dont need any other risk factors for it.
Other 3 subtypes are also prone to it but not to the same extent.
Us 3s are lucky re the Fatty Liver It goes away with successful Tx.
It does slow down the viral kinetics somewhat though.

Thanks for clarification. 1a & 3a can be caught in a number of ways. IVDU just being one.
It was more about genotype distrubition changing and its being blamed on drug use.

CS
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or even a large portion of the HCV community obtained the virus through IVDU.
I just don't believe that.
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Oh I do. The stats for IVDU are just too high.

I think more of it is from the medical treatments people have obtained
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I also think that IVDU gets the blame for a lot of medical transmission.
Saves a lot of money and red faces, saying you got it from IVDU and not medical treatment.

CS
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Thanks for the verification on this one. Was just wondering, did they consider overweight, hypertension, diabetes etc... when they made the statistics that 71% of geno 3's have steatosis? I believe that being geno 3, one is more prone to it than other genos, but how much more, as all those other factors play a big role, too. Especially since there is a big tendency to those other illnesses.

Another thing, I tried to find out about the symptoms of NASH. They are all the same as hep c. So no way to tell. I just wonder, if aversion to fatty foods could be a symptom of steatosis or a symptom of being prone to it. Maybe the body just tells you, stay away from that stuff, cause I can't digest it properly....
I'm very sensitive, and can most times just look at food, to know if I'm gonna be able to take it.

My GP told me that aversion to fatty foods has to do with the gall bladder and can be an indication to gall bladder stones. I had an ultra sound scan, and no gall bladder stones.

Marcia
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Thanks so much for the info. I had always read about the geographical distribution of hepc genotypes which still left me wondering where I got hep c.
It doesn't matter, and I will never know.

I have several risk factors, one of which is working in the medical community since '82, and performing sharp debridement on wounds. Pulled off those darn gloves at times maybe when I shouldn't have. They always get in the way, but I leave them on nowadays!

I have always wondered if my time spent in the Air Force had something to do with the geographical distribution, (not that I thought you had to travel to Asia of Europe to get hep c) I never went out of the states during my 4 yrs, but perhaps shared blood tainted materials with those who did.
Thanks again for all the info,and thanks Marcia for starting this thread.
Nice of you to point out Adiamos post to mar too.
Can I just give one big group hug?:)
Bug
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"I also think that IVDU gets the blame for a lot of medical transmission.
Saves a lot of money and red faces, saying you got it from IVDU and not medical treatment."

Also stops a lot of lawsuits.

I'm checking into my batch of Rhogam - and waiting for the medical record papers - when I was down in Anchorage - I got the exact date and time - and it completely correlates with what I believe was an ACUTE phase (which I had attributed to being pregnant and on a cruise ship).

I also am getting the batch number and I specifically let the records person KNOW that I had HCV - type 3a - that I was researching to see if I could have obtained it through that means --- AND that I was going to attempt to contact others who may have taken that batch during that time frame. I advised them that I was going to take out a personal's ad in the Anchorage Newspaper... Once I knew the batch number -  And spread the word around that the possibility exists - that if someone got a shot of Rhogam during that time frame - they MAY have HCV and should be checked.

My way of thinking is that:

A) either the batch was contaminated ...but - keep in mind that I was given that in 1996/January so it was either an OLD batch,

B)one that had been re-used with a syringe that had already been injected --- like maybe the first person's shot wasn't enough and they re-used the same syringe....

OR....

C)Maybe they really weren't following clearance procedures.


Just so you know - she advised me I would have my records and the batch number by MONDAY --- ahem... It's now Sunday the following week past that Monday.

Methinks Providence Hospital is seriously checking into it.

Which --- to me --- means a lot -- because there could be several other folks out there that have 3a here in ALASKA --- which they have told me is a pretty uncommon genotype here.

And I think those folks need to be aware that it is a possibility that they could have it too.

It's IMPERATIVE to me that people know they should be checked out. This disease needs to be stopped - and people who do not know they have it may be engaging in behavior which could transmit this disease to others.

If it's not the Rhogam - I certainly have no other earthly idea where it could have come from... I didn't have any transmission factors --- no cuts, except with family --- no transfusions - no major dental work... Nothing that could point to it. No outside the marriage unprotected sex --- no kissing anyone else... NADA... No needle sticks from EMT work --- no blood on me -- I was mostly the transporting crew --- so I was there just to read guages and pat people on the back --- no really serious blood scenes...

Just absolutely NOTHING that could point to a transmission route except that - in that amount of time --- since knowing I was clear.

So - yeah ---- I can see where doctors or the medical industry would want to say it comes more from IVDU than their practices.

I don't blame anyone tho --- I mean - people are just now learning how things are spread --- how contamination starts -- how to kill this disease and others.

We're a very young society medically - and we're learning more every day.

So there is no blame.

For me --- there is just a need to make sure that anyone else who may have been infected can take care of themselves and not pass it on.

This disease needs to be eradicated from the world.

Love to you all... thanks for listening... LOL!

Meki







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Thanks for the verification on this one. Was just wondering, did they consider overweight, hypertension, diabetes etc...

Yes. Alcohol, being overweight etc the only statistically significant factor with steatosis and G3 was being G3.

We can get both type of steatosis though.
The G3 one goes away with svr. The life style form has to be gotten rid of thru diet and excercise

CS
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Wow, I sure don't want to hear that.

The life style NASH, I cannot have, the alcohol one neither, as I don't drink

So if I had the G3 one, I could get rid of it through tx. Well, only the biopsy will tell that one. Does it have to do with how long you've had the virus or is it just as random as with the grade and stage.

Sorry I'm buggin you with all these questions, but it is getting darn interesting.

Marcia
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Cant say for sure but length of infection doesnt seem to come into it much either.

I had steatosis after being infected 13 years, which was when i found out.
Low Cholesterol is related to steatosis at least with us 3s so that might be an indicator.

CS
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Thanks. Wow, do you mean low cholesterol...as in lower than lower limit? My cholesterol is 4,0 mmol/l, (154.44mg/dL) normal range here is 4,0 - 7,3.

(I think I have been infected for 25 years.)

Where do you find all the info about steatosis and g 3

Marcia
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I have finally been able to find some stuff on this subject. This is the conclusion of one of them. They also talk about hypocholesterol in this study. It's good to know though that viral steatosis it goes with tx, if SVR is achieved.

CONCLUSION
The relationship between HCV and steatosis in terms of fibrosis and disease progression is unclear. HCV genotype 3 is clearly associated with steatosis ("viral steatosis"). It seems that in some patients, steatosis may be associated with fibrosis progression. The mechanisms underlying this association are unknown. The challenge for the clinician in care of patients with chronic HCV infection and steatosis is to be able to differentiate between those with pure steatosis alone and a benign course from those with progressive disease (the same challenge in separating NASH from NAFLD).

There remain many unanswered questions and there is a need for large prospective studies on hepatitis C patients, using multivariate analysis, which take into account confounding factors for steatosis, insulin resistance, fibrosis, and response to treatment. A meta-analysis of individual patient data (the HCV MAID Study) is ongoing to investigate the relationship between steatosis, inflammation, and fibrosis in chronic hepatitis C. Moreover, we need to develop experimental models using different HCV genotypes in order to understand the mechanisms leading to steatosis.

Thanks for getting me onto this wagon, I love this forum and all you people who make it so great!

Marcia
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Marcia
A couple of articles for you

Hepatocellular fat accumulation and low serum cholesterol in patients infected with HCV-3a

The American Journal of Gastroenterology
Volume 97 Issue 11 Page 2880 - November 2002

OBJECTIVE:
The aim of this study was to prospectively investigate the prevalence of hepatic steatosis in chronic hepatitis C patients with respect to viral genotype, hepatic iron concentration, total body iron, body mass index, and serum lipid parameters. Furthermore, the effect of hepatitis C virus (HCV) eradication by antiviral therapy on serum cholesterol levels was studied.

METHODS:
Hepatocellular fat and hepatic iron were determined in liver biopsies obtained from 137 interferon-naïve patients with chronic hepatitis C (100 men, 37 women, mean age 40.8 ± 10.7 yr) enrolled in two prospective clinical trials of interferon/ribavirin therapy. Body mass index and fasting cholesterol levels were determined at baseline, during, and after therapy.

RESULTS:
Marked steatosis (>20% of fat-containing hepatocytes) was found in 74.5% of patients infected with HCV-3a compared with 17.9% in HCV-1 and 21.7% in HCV-4-infected patients (p< 0.01). Steatosis in HCV-3a-infected patients did not correlate with the body mass index, hepatic iron content, ferritin, or transferrin saturation. At baseline, serum cholesterol was lower in patients infected with HCV-3a (147 ± 42 mg/dl; p< 0.01) compared with HCV-1 (188 ± 36) or HCV-4 (172 ± 35). In contrast to HCV-1- or HCV-4-infected patients, serum cholesterol increased in HCV-3a virological responders at the end of treatment and 6 months after therapy (baseline 146 ± 38, end of treatment 166 ± 29, p< 0.05, sustained virological response 200 ± 34, p< 0.01). However, serum cholesterol remained unchanged in HCV-3a nonresponders.

CONCLUSIONS:
Our data suggest that, in addition to inducing steatosis, HCV-3a lowers serum cholesterol. This metabolic effect is fully reversible after successful HCV-3a eradication. This unique property is not shared by other HCV genotypes.


Here are a couple of links from MedScape. They are free but you have to register

Impact of Hepatic Steatosis on Viral Kinetics and Treatment Outcome During Antiviral Treatment of Chronic HCV Infection
http://www.medscape.com/viewarticle/553011_print

Hepatitis C and Steatosis: A Reappraisal
http://www.medscape.com/viewarticle/525585

If you search Medscape for steatosis you will find quite a bit

CS
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Thank you so much. Now I am even more anxious to get the biopsy.

Now another question, are there any special symptoms associated with viral steatosis? Like I was talking about aversion of fatty foods. I actually feel quite off when I have fatty foods. Heated butter is the worst, I can't even look at it. Milk makes me really sick. All kinds of heated oils I avoid, as they also make me nauseas. I can tolerate raw cheeses in moderation. Virgin Coconut Oil I can heat. Virgin Olive Oil is good in it's fresh form, but I don't tolerate it as well when heated. Do you have any of these problems?

Marcia
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Nah dont think you can blame fatty liver for those symptoms.
Its funny just had a G2 complain about the same thing after having a Junk food weekend.

More a symptom of HepC than anything else. Its quite common.
But nah i dont have that problem. I live on Cheese.

CS
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476246_tn?1310999221
K. thanks
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