Aa
All Good Except Viral Load
Had biopsy last Friday.Doc said the tissue appeared pink and healthy(will have formal results in a few days).The pre-biopsy labs all came back in normal ranges.So the question is if I'm doing so well why the 5 million + viral load and is this fatigue and general feeling bad all in my head.If all is well should I wait a while for treatment or should I treat now.Wouldn't mind a 0 viral load so I don't feel like a leper(afraid to have anyone close for fear of infecting them).Also still waiting for the genotype results.Anyway I dont mean to sound whiny,just curiuos.Would appreciate any input.Thanks,Tim
I was diagnosed w/hep c in 1980.At that time the Health Dept. Dr. said there was nothing to worry about & that I had just tested for the antibody.I ignored this for over 15 years.I was living in Fl. at the time.10 years ago I moved to Ga. after a very messy divorce.I`m also on methadone,120 mgs/day.Once in Ga. I went to a hospital & got in the care of a highly respected infectious disease Dr.He did his tests & also a biopsy.My geno type was 2 b.I was between stage 2 & 3 but closer to 3.He started me on interferon.That was worse than the virus.After 6-9 months,I had to have a triple bypass.My Dr. then told me I could no longer take the interferon tx.That was 5 years ago.3 months ago I went for a routine colonoscopy & it was learned that my enzymes were high enough to test further.My platelet count was very low so w/my history,he ran a CT scan of the abdomen & pelvic area.It showed that I now had cirrhosis & there was NO treatment available.I am suffering from terrible fatigue & it seems that I bleed & bruise very easily.I made an appt. w/my infectious disease Dr. for July 30th.This fatigue is killing me.I take my methadone now for chronic pain although it started out to help w/my addiction.Can anyone give me any advice or iis there anything that I should be doing that I`m not doing now.My appetite has dropped considerably & I wake up every AM feeling very nervous.Any help would be appreciated Stefin
Good info......i will look for your postings.......it may help me......It helps to understand when things are explained not so technical
Debbie in Ca
Debbie in Ca
My type is 1b. They wanted to wait 6m0s. and re-test me when first dx. since my load was so low. Didnt like that so I insisted on a bx as I knew that was the true way to find out what cond. your liver was in, needless to say when the bx results came back they got me on tx asap. If I had waited and gone there route I'd still be waiting for re-test, instead I'm on shot 5 moving right along. I read somewhere that you can go from stage 3 to cirosses in 12- 18mos and not knowing how long I had been stage 3 I needed to get on tx NOW!!!! sometimes you have to take the dragon by the horns!!!
I had a VL of 163,000 when I started TX but my BX came back at stage 3 w/occasional bridging so they started TX right away. My question is why such a low vl but my bx so far along. This is bugging me and have'nt gotten a real answer from anyone. I'm at wk 5 and my alt/ast are back in normal range. could it be that I've been carrying this for so long, I belive 25-30 yrs.
I have a similar viral load and my doc did not recommend bx. What is your genotype? Just wondering why the difference in bx recommendation.
Good Day ya all! Good to see you again Tuna! That was nice to read what you had to say meshell! I admire you being able to work that much! OMG, how CAN you do it?? Im lucky I can stay home although I had a Bad Dream last night, my hubby told me I had to go back to work, we weren't making the bills...I was thinking I would last half a day at any job and get fired for standing around/sitting around with a blank stare in my brain fog, or walking into walls cuz of my fatigue, accused of acting tipsy! It ought to be mandatory anyone on tx should get automatic SSI/short term disability, stay home and get well, rest when you need to!
DH BILL - I am from Arizona. Any other 'Zoners out there??
DH BILL - I am from Arizona. Any other 'Zoners out there??
Let me rephrase this.
A person with a viral load of 1,000 IU/ml (very low) is more infectious than a person with a viral load of 10 million IU/ml. However, lets define infectious: Blood-born risk...IV drug use, transfussion, tatoos, piercing, sexual (~3%), mom-baby at birth (<3%).
Second, a high viral load (I define this as >3 million IU/ML) is harder to treat than a low viral load (I define this as <1 million IU/ML)..but how much...probably 8-10% harder...(data still hard to draw conclusions from).
So you can see....if you are at either end of the spectrum (very high load or very very load), you can draw these conclusions but, if you are, as most patients, somewhere in between this difference is not clinically significant. For example, I would argue there is no difference in "contagousness" in a patient wiht a viral load of 1 million or 2 million. And there is no clinical difference in treatment success at 1 million vs 2 million IU/ML. And as has been proven again and again, viral load does NOT correlated at all with disese progression.
Hope this clarifies.
Erin
A person with a viral load of 1,000 IU/ml (very low) is more infectious than a person with a viral load of 10 million IU/ml. However, lets define infectious: Blood-born risk...IV drug use, transfussion, tatoos, piercing, sexual (~3%), mom-baby at birth (<3%).
Second, a high viral load (I define this as >3 million IU/ML) is harder to treat than a low viral load (I define this as <1 million IU/ML)..but how much...probably 8-10% harder...(data still hard to draw conclusions from).
So you can see....if you are at either end of the spectrum (very high load or very very load), you can draw these conclusions but, if you are, as most patients, somewhere in between this difference is not clinically significant. For example, I would argue there is no difference in "contagousness" in a patient wiht a viral load of 1 million or 2 million. And there is no clinical difference in treatment success at 1 million vs 2 million IU/ML. And as has been proven again and again, viral load does NOT correlated at all with disese progression.
Hope this clarifies.
Erin
Again, there is just NO corrleation between viral load and damage. It is probably a combo of your body, your genetics, your liver and your specific strain of virus.
GI.PA
GI.PA
You have entered into the large grey MYSTERY area of Hcv with your question. I too had some problems with all this and it took me a long time to sort it all out in my head. I'll try to help ya.
Spme things can be studied and some things can't. We can't get Hcv to live outside the human body long so we can't put it into a dish and observe it under a mocroscope and/or "play with it". This limits what can know about it. We have to depend on measurements taken from individuals and we are all clinically different in so many ways. Most viruses are that way. Ever have everyone in your house get colds all at the same time? Some get the same cold much worse than others. Why? Who knows? It's because we are all so different. So...why do some folks have major damage with low loads and some have minimal damage with high loads? It's all due to the differences in each other that have nothing to do with the virus. We all eat different,sleep different,exercise different,handle stress different, and on and on.... Too many things to decipher there.
Our individual immune systems are the big key to most of this. We all depend on our own systems to kill this. The meds are not what we depend on for this. They help stimulate or systems to produce more killer cells to accomplish this. The Riba mainly helps to protect our livers from invasion and so hold down replication. This is all a buncha chemical stuff that goes on inside of us. Before we start tx we all still have all of these same chemical things going on but it happens at different rates for each individual. 20% of all folks infected with Hcv kill it off on their own. The rest of us manage to hold it down but at different rates. There is no way to measure all the things needed to do this. It takes a buncha chemical things to happen for the virus to replicate too. We can show a buncha virus but that doesn't mean that it's doing a lot of critical damage to replicate. The liver has the ability to regenerate itself....to a point. So it follows that if your liver is regenerating at a good rate and the damaged area is not critical to the regeneration you could have a major load and still show little damage. Some people may not regenerate as fast. Still others may be relatively slow.
The liver is not the only place this stuff replicates either. It's just the "Preferred" housing addition. They are still trying to figure that one out.
You will drive yourself crazy if you try to figure out WHY Hcv does what it does when even the best researchers can't. We just need to accept that this is the way things are. Pay attention to the things that we DO know and accept the things we don't know the WHY for. It helps that little man in your head to keep from hurting himself while he looks for answers that aren't in there.
Did any of that make sense to you? I try not to get too technical when I talk about this stuff.
Spme things can be studied and some things can't. We can't get Hcv to live outside the human body long so we can't put it into a dish and observe it under a mocroscope and/or "play with it". This limits what can know about it. We have to depend on measurements taken from individuals and we are all clinically different in so many ways. Most viruses are that way. Ever have everyone in your house get colds all at the same time? Some get the same cold much worse than others. Why? Who knows? It's because we are all so different. So...why do some folks have major damage with low loads and some have minimal damage with high loads? It's all due to the differences in each other that have nothing to do with the virus. We all eat different,sleep different,exercise different,handle stress different, and on and on.... Too many things to decipher there.
Our individual immune systems are the big key to most of this. We all depend on our own systems to kill this. The meds are not what we depend on for this. They help stimulate or systems to produce more killer cells to accomplish this. The Riba mainly helps to protect our livers from invasion and so hold down replication. This is all a buncha chemical stuff that goes on inside of us. Before we start tx we all still have all of these same chemical things going on but it happens at different rates for each individual. 20% of all folks infected with Hcv kill it off on their own. The rest of us manage to hold it down but at different rates. There is no way to measure all the things needed to do this. It takes a buncha chemical things to happen for the virus to replicate too. We can show a buncha virus but that doesn't mean that it's doing a lot of critical damage to replicate. The liver has the ability to regenerate itself....to a point. So it follows that if your liver is regenerating at a good rate and the damaged area is not critical to the regeneration you could have a major load and still show little damage. Some people may not regenerate as fast. Still others may be relatively slow.
The liver is not the only place this stuff replicates either. It's just the "Preferred" housing addition. They are still trying to figure that one out.
You will drive yourself crazy if you try to figure out WHY Hcv does what it does when even the best researchers can't. We just need to accept that this is the way things are. Pay attention to the things that we DO know and accept the things we don't know the WHY for. It helps that little man in your head to keep from hurting himself while he looks for answers that aren't in there.
Did any of that make sense to you? I try not to get too technical when I talk about this stuff.
Thanks so much both of you for your response to my question. I belive I got it now!! Indiana thanks for talking non-tech I can understand that a lot better. You made it quite clear, thanks again.
You mentioned VL has nothing to do with being contagious. I am going to copy here exactly what it says on my RNA lab reults by Specialty laboratories, Onoquest inc. It says here higher concentration make HCV more infectious. Is VL the same as RNA? Any comments welcome. LL
HCV RNC is detectable within one week of exposure to HCV. Patients with higher concentrations of HCV RNA are more infectious and more resistant to interferon therapy. The use if Interferon is associated with a decline in HCV, RNA. Decline of HCV RNA to undetectable concentrations is associated with a sustained response, even after the dicontinuation of interferon therapy.
HCV RNC is detectable within one week of exposure to HCV. Patients with higher concentrations of HCV RNA are more infectious and more resistant to interferon therapy. The use if Interferon is associated with a decline in HCV, RNA. Decline of HCV RNA to undetectable concentrations is associated with a sustained response, even after the dicontinuation of interferon therapy.
You MAY feel bad because of the Hep C but be sure your primary care doctor looks for other reasons that cause fatigue before everyone assumes it is just the Hep C.
The results of your biopsy and genotype will help guide you through the treatment decision.
GI.PA
The results of your biopsy and genotype will help guide you through the treatment decision.
GI.PA
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