Aa
3a relapse on 4wk post tx pcr
I got the call from the NP yesterday about my 4 wk post tx pcr after 24 wks treatment and she said it was 125k IU/ml. I was saddened but not suprised Previous pcr's showed UND wk 12 through 24. The hep Dr said "treatment has to be stopped at 24 wks. Why he said "has to be stopped" I'm not sure but his report to the gastro seemed to indicate his concern about my elevated ALT-186 and AST-267 and drop in platelets-down to 77k. do to the "toxicity of the interferon".
A hep Dr, 2 gastros and 2 GPs all said 24 weeks would be ok. Apparently they are not as well informed as you all are.....considering my negative predictors...high VL 1.2M...non RVR....and no biopsy but according to the hep Dr's reading of ultrasound: "a coarsened liver echotexture probably related to fatty infiltration"
But to be honest, and I am almost embarrased to say, especially reading about some of you doing 48 and 72 wks of treatment that I don't think I could have made it past 24ks. It was just too severe for me to continue.
I don't know what I am going to do next but I really appeciate the help and guidance you all have given me.
Dominic
A hep Dr, 2 gastros and 2 GPs all said 24 weeks would be ok. Apparently they are not as well informed as you all are.....considering my negative predictors...high VL 1.2M...non RVR....and no biopsy but according to the hep Dr's reading of ultrasound: "a coarsened liver echotexture probably related to fatty infiltration"
But to be honest, and I am almost embarrased to say, especially reading about some of you doing 48 and 72 wks of treatment that I don't think I could have made it past 24ks. It was just too severe for me to continue.
I don't know what I am going to do next but I really appeciate the help and guidance you all have given me.
Dominic
I am so sorry for your bad news Dominic, it's heartbreaking. You don't have to feel embarrassed to say that you didn't think you could handle going longer...........treatment hits EVERYBODY differently and we all know that!
Our friend in here Kalio is a geno3 and she relapsed as well. You get so "taught" the "lucky geno's of 2 and 3" and doctors just about guaranteeing you success but you know what we've seen a LOT that have not gotten SVR.
You did the best you could and that is ALL your are expected to do - especially when it was their decision to pull the plug.
Our friend in here Kalio is a geno3 and she relapsed as well. You get so "taught" the "lucky geno's of 2 and 3" and doctors just about guaranteeing you success but you know what we've seen a LOT that have not gotten SVR.
You did the best you could and that is ALL your are expected to do - especially when it was their decision to pull the plug.
Very sorry for your news. Did you test positive for VL at 4 weeks? That's a caution sign for geno 3 for sure. The prevalence of fatty liver in geno 3 has been known for a while. Not to alarm you, but as I understand it - US can't distinguish between cirrotic scarring and steatosis. The echo texture could be either, and a biopsy (or possibly one of the other tests) is needed to distinguish.
Your lowered platelets on tx seem quite normal - and not all that low. Usually that wouldn't halt tx. The raised ALT/AST also strikes me as not uncommon - though your numbers do seem higher than most.
Your lowered platelets on tx seem quite normal - and not all that low. Usually that wouldn't halt tx. The raised ALT/AST also strikes me as not uncommon - though your numbers do seem higher than most.
This is very devistating to read about so many recent relapses. My heart goes out to each of you. I too, know the pain.
It reinforces to me so much that these doctors should throw the 2-log drop out the door and all order the 4 week tests. The 2-log drop should weed out the non responders, to be sure, but I can't see how it can be used for much else. If you are not clear by sensitive test at week 12, it is time to think overtime.
Myown -- you were RVR? Clear by sensitive test at week 4? What a deep blow. I am sorry.
dominic - that is a good article. One all 3as should read.
frijole
It reinforces to me so much that these doctors should throw the 2-log drop out the door and all order the 4 week tests. The 2-log drop should weed out the non responders, to be sure, but I can't see how it can be used for much else. If you are not clear by sensitive test at week 12, it is time to think overtime.
Myown -- you were RVR? Clear by sensitive test at week 4? What a deep blow. I am sorry.
dominic - that is a good article. One all 3as should read.
frijole
This particular piece came from hepatitis-central.com newsletter. At first glance it seems like a very commercial website but on closer inspection I found they have info on the latest clinical trials and news releases related to HVC.
I also get "google alerts" daily press releases using the keywords hepatitis, teleprevar, intermune, etc. delivered to my mailbox. Some of it is useful and some not. But I have found some interesting and relative topics.
Dominic
I also get "google alerts" daily press releases using the keywords hepatitis, teleprevar, intermune, etc. delivered to my mailbox. Some of it is useful and some not. But I have found some interesting and relative topics.
Dominic
Thanks so much for this; I was trying to figure out why my doc suspected I had steatosis without an ultrasound and now I know. This is another piece of the puzzle that I now have an answer to. Thank You.
Thanks, Dominic, had not seen that article before. Keep coming to the forum, we need informed geno 3's here.
This may be of interest to 3a's or may be old news and just the first time I have seen it.
September 17, 2007
HCV Genotype 3 and Fatty Liver
Infection with Hepatitis C genotype 3 carries a greater chance of a fatty liver than other genotypes. Although this relationship is likely due to the strain's molecular structure, successful treatment can erase this extra burden.
by Nicole Cutler, L.Ac.
All of Hepatitis C’s genotypes are not created equally. Aside from differences in treatment response, one Hepatitis C strain carries a concern above and beyond damage from the virus itself. According to researchers, Hepatitis C genotype 3 (HCV3) is most likely to be accompanied by steatosis, or fatty liver.
Steatosis
As the most common liver disease in the United States, non-alcoholic fatty liver disease often accompanies Hepatitis C infection. Liver steatosis describes the accumulation of fat in liver cells. For those with Hepatitis C, steatosis is associated with more severe fibrosis progression.
Past studies have shown that various Hepatitis C virus (HCV) genotypes are associated with different forms of steatosis. In patients with genotype 1 and 4, steatosis is primarily due to metabolic factors such as obesity and diabetes. For those with genotype 3, the viral strain itself is suspected to cause fat accumulation in the liver cells.
The prevalence of steatosis is reported by a broad range of people, affecting anywhere from 34 to 81 percent of people with HCV. Variables predisposing someone with HCV to develop steatosis include:
· Alcohol consumption
· Obesity
· Diabetes
· Hyperlipidemia (high cholesterol)
· Viral type
Genotype 3 Dominance
By pooling together various bodies of research collectively examining over 6,400 people with HCV, those infected with HCV3 have a much higher chance of developing steatosis. Some statistics relating hepatitis with steatosis include:
· Overall, approximately 56 percent of those with HCV have steatosis.
· Approximately 17 percent of those with autoimmune hepatitis have steatosis.
· Approximately 27 percent of those with Hepatitis B have steatosis.
· Approximately 48 percent of those with HCV of a genotype other than 3 have steatosis.
· Approximately 74 percent of those with HCV3 have steatosis.
In the March 2004 issue of Gut, French researchers reported on the relationship between steatosis and HCV clearance after antiviral treatment. This study examined the liver biopsies before and after antiviral treatment of 151 participants. According to the authors:
· Steatosis improvement was seen significantly more often in patients who achieved HCV clearance from treatment.
· Among those who were successful in eliminating the virus with treatment, steatosis improvement occurred more often in those with HCV3 than those with other genotypes.
· Among those who were not successful in eliminating the virus with treatment, steatosis improvement did not differ by genotype.
Also published in the March 2004 issue of Gut, an internationally-based group of researchers confirmed that Hepatitis C genotype affects steatosis. By analyzing data from 755 people with chronic HCV, the authors advised that those with HCV3 and diagnosed steatosis should receive antiviral treatment.
As published in the March 2004 issue of the Journal of Hepatology, researchers from Scripps Clinic reported on the impact of steatosis on liver disease progression and treatment response in patients with chronic Hepatitis C. The researchers evaluated liver biopsies from 574 patients, and found the following:
· Steatosis severity was associated with body mass index, HCV3, older age and longer duration of infection.
· Among those with genotype 3, higher HCV viral load was associated with more severe steatosis.
· Steatosis improved markedly in genotype 3 patients who achieved viral clearance from treatment.
From a laboratory perspective, scientists agree about the association between HCV3 and liver steatosis. In an in vitro model published in the January 2007 issue of Gut, Hourioux and colleagues compared lipid levels in sections of cells producing genotype 1a or genotype 3 core proteins. They found that the cumulative lipid droplet area was significantly greater in cells producing genotype 3 core proteins; lending this strain more amenable to fat accumulation. Another study comparing HCV proteins found that the genotype 3a core protein induced significantly greater enzyme activity that is required for the development of hepatic steatosis.
To further understand this pathological difference between HCV genotypes, scientists have been closely examining each genotype’s molecular structure variances. One possible explanation may involve HCV3’s obstruction of the liver’s release of very low density lipoprotein (VLDL) particles to the bloodstream. This theory rests on the foundation that dietary fat becomes trapped in the liver of those with HCV3.
When cumulatively examined, the evidence supports the premise that Hepatitis C genotype 3 exerts a specific effect on the genesis of hepatic steatosis independent of metabolic risk factors such as obesity. Although linking steatosis to genotype 3, the evidence also shows that those with this strain who are successful with antiviral treatment have a greater chance of liver recovery. It is clearer now than ever that the divergence between HCV genotypes exert more disparities than previously thought, and is likely due to the virus’ molecular structure.
References:
C Hourioux, et al., The genotype 3-specific hepatitis C virus core protein residue phenylalanine 164 increases steatosis in an in vitro cellular model, Gut, January 2007.
Hissar SS, et al., Hepatitis C virus genotype 3 predominates in North and Central India and is associated with significant histopathologic liver disease, Journal of Medical Virology, April 2006.
http://clinicaloptions.com, Insulin Resistance and Hepatic Steatosis in Patients With Chronic Hepatitis C, Stephen A. Harrison, MD, LTC, MC, Clinical Care Options LLC, 2007.
J. Westin, et al., Impact of Hepatic Steatosis on Viral Kinetics and Treatment Outcome During Antiviral Treatment of Chronic HCV Infection, Journal of Viral Hepatology, March 2007.
Sharma, Pratina, et al., Hepatic Steatosis in Hepatitis C Virus Genotype 3 Infection: Does It Correlate with Body Mass Index, Fibrosis, and HCV Risk Factors?, Digestive Diseases and Sciences, October 2004.
www.hcvadvocate.org, Liver Steatosis, Liz Highleyman, Hepatitis Journal Review, March 2004.
www.hivandhepatitis.com, Liver Steatosis in Genotype 4 Patients Is Mainly Due to Metabolic Factors, Liz Highleyman, hivandhepatitis.com, 2007.
www.medscape.com, Hepatitis C and Steatosis: A Reappraisal, A. Lonardo, et al, Journal of Viral Hepatology, March 2006.
Posted by Editors at September 17, 2007 10:40 AM
September 17, 2007
HCV Genotype 3 and Fatty Liver
Infection with Hepatitis C genotype 3 carries a greater chance of a fatty liver than other genotypes. Although this relationship is likely due to the strain's molecular structure, successful treatment can erase this extra burden.
by Nicole Cutler, L.Ac.
All of Hepatitis C’s genotypes are not created equally. Aside from differences in treatment response, one Hepatitis C strain carries a concern above and beyond damage from the virus itself. According to researchers, Hepatitis C genotype 3 (HCV3) is most likely to be accompanied by steatosis, or fatty liver.
Steatosis
As the most common liver disease in the United States, non-alcoholic fatty liver disease often accompanies Hepatitis C infection. Liver steatosis describes the accumulation of fat in liver cells. For those with Hepatitis C, steatosis is associated with more severe fibrosis progression.
Past studies have shown that various Hepatitis C virus (HCV) genotypes are associated with different forms of steatosis. In patients with genotype 1 and 4, steatosis is primarily due to metabolic factors such as obesity and diabetes. For those with genotype 3, the viral strain itself is suspected to cause fat accumulation in the liver cells.
The prevalence of steatosis is reported by a broad range of people, affecting anywhere from 34 to 81 percent of people with HCV. Variables predisposing someone with HCV to develop steatosis include:
· Alcohol consumption
· Obesity
· Diabetes
· Hyperlipidemia (high cholesterol)
· Viral type
Genotype 3 Dominance
By pooling together various bodies of research collectively examining over 6,400 people with HCV, those infected with HCV3 have a much higher chance of developing steatosis. Some statistics relating hepatitis with steatosis include:
· Overall, approximately 56 percent of those with HCV have steatosis.
· Approximately 17 percent of those with autoimmune hepatitis have steatosis.
· Approximately 27 percent of those with Hepatitis B have steatosis.
· Approximately 48 percent of those with HCV of a genotype other than 3 have steatosis.
· Approximately 74 percent of those with HCV3 have steatosis.
In the March 2004 issue of Gut, French researchers reported on the relationship between steatosis and HCV clearance after antiviral treatment. This study examined the liver biopsies before and after antiviral treatment of 151 participants. According to the authors:
· Steatosis improvement was seen significantly more often in patients who achieved HCV clearance from treatment.
· Among those who were successful in eliminating the virus with treatment, steatosis improvement occurred more often in those with HCV3 than those with other genotypes.
· Among those who were not successful in eliminating the virus with treatment, steatosis improvement did not differ by genotype.
Also published in the March 2004 issue of Gut, an internationally-based group of researchers confirmed that Hepatitis C genotype affects steatosis. By analyzing data from 755 people with chronic HCV, the authors advised that those with HCV3 and diagnosed steatosis should receive antiviral treatment.
As published in the March 2004 issue of the Journal of Hepatology, researchers from Scripps Clinic reported on the impact of steatosis on liver disease progression and treatment response in patients with chronic Hepatitis C. The researchers evaluated liver biopsies from 574 patients, and found the following:
· Steatosis severity was associated with body mass index, HCV3, older age and longer duration of infection.
· Among those with genotype 3, higher HCV viral load was associated with more severe steatosis.
· Steatosis improved markedly in genotype 3 patients who achieved viral clearance from treatment.
From a laboratory perspective, scientists agree about the association between HCV3 and liver steatosis. In an in vitro model published in the January 2007 issue of Gut, Hourioux and colleagues compared lipid levels in sections of cells producing genotype 1a or genotype 3 core proteins. They found that the cumulative lipid droplet area was significantly greater in cells producing genotype 3 core proteins; lending this strain more amenable to fat accumulation. Another study comparing HCV proteins found that the genotype 3a core protein induced significantly greater enzyme activity that is required for the development of hepatic steatosis.
To further understand this pathological difference between HCV genotypes, scientists have been closely examining each genotype’s molecular structure variances. One possible explanation may involve HCV3’s obstruction of the liver’s release of very low density lipoprotein (VLDL) particles to the bloodstream. This theory rests on the foundation that dietary fat becomes trapped in the liver of those with HCV3.
When cumulatively examined, the evidence supports the premise that Hepatitis C genotype 3 exerts a specific effect on the genesis of hepatic steatosis independent of metabolic risk factors such as obesity. Although linking steatosis to genotype 3, the evidence also shows that those with this strain who are successful with antiviral treatment have a greater chance of liver recovery. It is clearer now than ever that the divergence between HCV genotypes exert more disparities than previously thought, and is likely due to the virus’ molecular structure.
References:
C Hourioux, et al., The genotype 3-specific hepatitis C virus core protein residue phenylalanine 164 increases steatosis in an in vitro cellular model, Gut, January 2007.
Hissar SS, et al., Hepatitis C virus genotype 3 predominates in North and Central India and is associated with significant histopathologic liver disease, Journal of Medical Virology, April 2006.
http://clinicaloptions.com, Insulin Resistance and Hepatic Steatosis in Patients With Chronic Hepatitis C, Stephen A. Harrison, MD, LTC, MC, Clinical Care Options LLC, 2007.
J. Westin, et al., Impact of Hepatic Steatosis on Viral Kinetics and Treatment Outcome During Antiviral Treatment of Chronic HCV Infection, Journal of Viral Hepatology, March 2007.
Sharma, Pratina, et al., Hepatic Steatosis in Hepatitis C Virus Genotype 3 Infection: Does It Correlate with Body Mass Index, Fibrosis, and HCV Risk Factors?, Digestive Diseases and Sciences, October 2004.
www.hcvadvocate.org, Liver Steatosis, Liz Highleyman, Hepatitis Journal Review, March 2004.
www.hivandhepatitis.com, Liver Steatosis in Genotype 4 Patients Is Mainly Due to Metabolic Factors, Liz Highleyman, hivandhepatitis.com, 2007.
www.medscape.com, Hepatitis C and Steatosis: A Reappraisal, A. Lonardo, et al, Journal of Viral Hepatology, March 2006.
Posted by Editors at September 17, 2007 10:40 AM
They would not do a pcr at 4 wks and at the time I didn't know that it was important. I did insist on a seven week pcr which turned out to be 134 VL and sometime between there and wk 12 I was und. I think they are living is the stone ages at this office. They just kept beating the drum about a 2 log drop at 12wks as being important. i never heard them say anything about rescue drugs...I've not seen any indication that they even knew what they are. You guys here are light years ahead of this office. I will try to get a biopsy when I am feeling better if I have to drive up to the teaching hospital.
The gastro said 24 wks for g 2's and 3's is all they would do and when the hep Dr sent his report that "treatment has to be stopped at 24 wks" it kind of sealed my fate. After reading this forum for the past few months I think I now know what qustions to ask the Dr's...If I treat again.
Again I appreciate all the encouragement. God bless you all.
Dominic
The gastro said 24 wks for g 2's and 3's is all they would do and when the hep Dr sent his report that "treatment has to be stopped at 24 wks" it kind of sealed my fate. After reading this forum for the past few months I think I now know what qustions to ask the Dr's...If I treat again.
Again I appreciate all the encouragement. God bless you all.
Dominic
Sorry Dominic,
i didn't see your original post.
I agree with Zazza and others that you should try to have a biopsy once you feel up for it.
My WBC and ANC have been low for 40 weeks: Dr. put me on neupogen to keep them at 2.5 or so. Did your Dr. discuss using those meds?
wyntre
i didn't see your original post.
I agree with Zazza and others that you should try to have a biopsy once you feel up for it.
My WBC and ANC have been low for 40 weeks: Dr. put me on neupogen to keep them at 2.5 or so. Did your Dr. discuss using those meds?
wyntre
Sorry to hear your news, thats something we all worry about and hate to hear. Likes been said nothing to be embarrassed about. Any please don't blame yourself. Hey were all in the same boat here. Will have my first pcr in November, 3 months post tx. Just didn't want one after a month.
Wishing you the best, and take care.
Wishing you the best, and take care.
"I guess some things you think are in your past can follow you into the present."
This is so true. This is actually one of the reasons I want to rid myself of the virus, to be able to leave the past in the past where it belongs.
This is so true. This is actually one of the reasons I want to rid myself of the virus, to be able to leave the past in the past where it belongs.
Oh no, Dominic, I am so sorry. But don't blame yourself. You did more than most by writing in here and having an open mind about what is cutting edge today, understanding that geno 3 slow responders need extended treatment. Studies are being done right now to verify this. It is not easy when all the doctors say 24 weeks is enough.
I don't really understand their reasons for saying your treatment had to be stopped. Platelets of 77000 does not seem too low to me. But I don't know that much about platelets. I suggest you get a biopsy as a next step to find out whether or not your need to retreat is urgent.
Again, I am so sorry that you had to join the geno 3 relapsers. And if you decide to retreat, I am confident that you will have the strength to treat for as long as you and your doctors find necessary.
Zazza
I don't really understand their reasons for saying your treatment had to be stopped. Platelets of 77000 does not seem too low to me. But I don't know that much about platelets. I suggest you get a biopsy as a next step to find out whether or not your need to retreat is urgent.
Again, I am so sorry that you had to join the geno 3 relapsers. And if you decide to retreat, I am confident that you will have the strength to treat for as long as you and your doctors find necessary.
Zazza
guaf and FM........I too am sorry to hear of your relapse. Hope the future works out ok for you.
wyntre......My stats other than I put in my original post is: 54 yr male...contracted hcv I think anywhere between 22 and 32 yrs ago. The gastro I see says they don't biopsy g 2's and 3's because they are so "easy to clear". After I started treatment I found out this was not very sound advice but my wbc dropped to 2 and they said that I could develope an infection so no biopsy.
I have since learned to choose your Dr. carefully and do a lot of research.
I cleaned up my act 16 yrs ago...started living right...working out...eating right. And I have 2 wonderful grandkids. Dx'ed hvc in 2005. I guess some things you think are in your past can follow you into the present.
Thanks all for the encouragement. I hope for all the best that God has to offer.
Dominid
wyntre......My stats other than I put in my original post is: 54 yr male...contracted hcv I think anywhere between 22 and 32 yrs ago. The gastro I see says they don't biopsy g 2's and 3's because they are so "easy to clear". After I started treatment I found out this was not very sound advice but my wbc dropped to 2 and they said that I could develope an infection so no biopsy.
I have since learned to choose your Dr. carefully and do a lot of research.
I cleaned up my act 16 yrs ago...started living right...working out...eating right. And I have 2 wonderful grandkids. Dx'ed hvc in 2005. I guess some things you think are in your past can follow you into the present.
Thanks all for the encouragement. I hope for all the best that God has to offer.
Dominid
Sorry to hear this. I too relapsed and was RVR - 0 damage 24 weeks. Sometimes even when it appears that all should go well, it doesn't. I haven't decided what I will do either at this point.Still taking other tests.
Hang in there and one thing all of us relapsers have to remember is that some of the others on forum that have relapsed went on to clear when they tx again.
wish you the best.
Hang in there and one thing all of us relapsers have to remember is that some of the others on forum that have relapsed went on to clear when they tx again.
wish you the best.
Sorry to hear the news. And, nothing to feel embarrassed about - tx is tough. As to next steps, no quick decisions. Feeling better and recovery while you assess your position seems like a good idea. Getting a more definitive ides of the condition of your liver may help in future decisions. Did you have a 4 week pcr, or was 12 the first? I'm not far behind you, I'm pretty sure that I might have my first post-tx pcr tomorrow. I really don't want to do it yet but the doc wants to see enzymes, cbc and tsh so I might as well do the pcr while they're in there plumbing anyway. Good luck Dominic.
so sorry to hear both of your news....but don't give up hope...regroup...and know you have lots of support here!!! Blessings
So sorry to hear your news.
What are your stats and why didn't you have a biopsy?
Best of luck in future tx.
wyntre
What are your stats and why didn't you have a biopsy?
Best of luck in future tx.
wyntre
I too am a 3a and 2x relapser. I know how you feel. I did 24 weeks and now looking at 48. I tell myself I will do it, but I really did stumble across the 24 week finish line. A 4 wk pcr would have been really helpful about now; I didn't get a 4 wk pcr either, but will next time. I am stage 4 so got to go again; hope you have more time to wait on teleprevir and or alinia. There is still plenty of hope so stay close and educate yourself here....you WILL clear! GodSpeed.
I sooooooo feel for you. It just doesn't seem to be a good week for heppers. I just got my news on Monday about my relapse. It doesn't matter if someone does tx for 1 week or 100 wks. It's still difficult and still an accomplishment.
Good luck from one relapser to another.
Mouse
Genotype 1a, Stage 3, Grade 3
Finished 48 wks of tx on 4/13/07
Relapsed 9/20/07 (6 mos. post)
Good luck from one relapser to another.
Mouse
Genotype 1a, Stage 3, Grade 3
Finished 48 wks of tx on 4/13/07
Relapsed 9/20/07 (6 mos. post)
Not at all. I know the text sometimes doesn't express what one is really saying. I have read this forum a lot and I appreciate your views and unselfish efforts to help. Thank you.
Dominic
Dominic
I hope you don't think I was second guessing your treatment decision because I certainly wouldn't ever do that. Again, I wish you luck. Mike
You may be right but they would not let me go longer so the choice was out of my hands anyway. I should have done my homework and came to this sight before I started treatment so I could have known and found a Dr who would have been up to date on his facts. I have found that there is a lot of misinformation out there...even among Drs.
I am very sorry about this news. I admire your honesty in assessing whether you could have done loner but I doubt that very few people who've done extended TX would have thought they could do it - until they did. Sometimes it's as simple as one day at a time or one foot in front of the other. My intent certainly isn't to instill any self incrimination within you but only to suggest that you're not that different from anyone who has done 48 or 72 weeks of TX. Those who have done it believed that they had to and,had they believed that 24 weeks would have been enough, they wouldn't have done a day longer. I wish you good luck. Mike
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