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HBV, HCV Reactivation During Chemotherapy of Concern
HBV, HCV Reactivation During Chemotherapy of Concern
November 10, 2011 (San Francisco, California) — Two separate studies, performed at the University of Texas M.D. Anderson Cancer Center in Houston, demonstrate the potentially life-threatening impact of reactivation of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection in patients undergoing immunosuppressive chemotherapy.
The data, presented here at The Liver Meeting 2011: American Association for the Study of Liver Diseases (AASLD) 62nd Annual Meeting, suggest that greater surveillance for HBV and safer hematologic-sparing treatments for HCV are required.
In the first study, lead investigator Jessica P. Hwang, MD, MPH, and colleagues looked at HBV reactivation during cancer treatment using a retrospective dataset from her institution. "This is a topic that is gaining momentum in public health, oncology, as well as hepatology landscapes," she explained. However, because of the lack of large population-based studies, the current prevalence of HBV reactivation in patients undergoing cancer treatment is unclear. "Our goals were to determine the prevalence and predictors of HBV screening and reactivation in a comprehensive cancer center."
What is known is that HBV reactivation can occur at anytime during chemotherapy or after chemotherapy, during the recovery phase of the immune system's reconstitution. "This can lead to poor outcomes, hepatic flares, liver failure, and death," Dr. Hwang said. "It's important to identify these patients accurately so that effective oral antiviral therapy can be initiated."
The study by Dr. Hwang and colleagues explored 2 issues: the existence of inconsistent guidelines for screening cancer patients for HBV, and the lack of adherence to the guidelines that are in place.
The 3 entities that have addressed HBV and cancer are the Centers for Disease Control and Prevention (CDC), the AASLD, and the Association of Clinical Oncology (ASCO).
On screening and treatment, the CDC and AASLD recommendations are in agreement: All patients with cancer who are about to undergo immunosuppressive therapy should be tested for HBV and screened for hepatitis B surface antigen (HBsAg), hepatitis B core antigen (anti-HBc), and antibodies against HBsAg (anti-HBs). If there is a positive test result, HBV prophylaxis should be initiated.
Recommendations from ASCO are less comprehensive: Only those about to undergo "highly" immunosuppressive regimens (i.e., stem cell transplants or treatment with rituximab) and patients "at risk" for HBV should be tested, and screening should only be for HBsAg and anti-HBc (recommended treatment is the same).
"Although there is agreement on the importance of antiviral prophylaxis, ASCO does not advocate the use of all 3 screening tests," Dr. Hwang noted. Furthermore, the ASCO guidelines require that oncologists be aware of the risk factors for HBV infection, and that they take the time to actually perform HBV screening. The discrepancies in recommendations led Dr. Hwang's team to examine current practices at the M.D. Anderson Cancer Center.
The retrospective chart review gathered data on screening, positive tests, and HBV reactivation for all chemotherapy-naïve cancer patients seen at the M.D. Anderson over a 4-year period. Evidence of viral reactivation was defined as an alanine aminotransferase (ALT) level of at least 100 U/L plus total bilirubin of at least 2.5 mg/dL; detectable HBV levels when HBV was previously undetectable; or HBV DNA of at least 100,000 copies/mL.
The screening period was 2 months before the first or second round of chemotherapy. Both solid tumor and hematologic malignancies were considered. Risk factors for HBV prior to screening included International Classification of Diseases, Ninth Revision (ICD-9) codes for HCV, HIV, liver disease, and hepatitis.
Approximately 71,000 charts were reviewed. Of the 10,729 patients receiving potentially immunosuppressive chemotherapy, Dr. Hwang and colleagues found that only 1787 patients (17%) were screened for HBV. Tests used were HBsAg (1665 patients); HBsAg and anti-HBC (87 patients); and anti-HBc (35 patients). "If we just look at the patients with HBV risk factors, only 1 of 5 patients were screened," Dr. Hwang reported.
Of those screened, 34 patients were found to have HBV reactivation. Fourteen of the 34 were found to have chronic HBV infection, and anti-HBc was detected in 20 patients. Of the total reactivation cohort, 23 patients had hematologic cancers, 11 had solid tumors, and 10 had been treated with rituximab.
Predictors of those chosen for screening were being male, having HBV risk factors, having a hematologic malignancy, and the use of rituximab. Predictors of HBV reactivation were being male, being Asian or black, and having HBV risk factors. "Interestingly, Asian and black race did not predict screening, yet they were more often testing positive," said Dr. Hwang.
Most striking was the lack of use of HBV therapy after a positive test. Of the 34 patients, 9 received prophylaxis (2 later died), 11 received treatment after HBV reactivation (8 died), and 14 received no treatment (10 later died).
"It does not appear that we are following the CDC and AASLD recommendations," Dr. Hwang pointed out, adding that M.D. Anderson is not even adhering to ASCO recommendations.
"Preventable reactivation does occur, is occurring, and prophylaxis has been shown to dramatically reduce mortality in cancer patients with HBV," she explained.
HCV Reactivation
A study from the same institution looked at HCV reactivation in patients who had undergone treatment with rituximab and gemcitabine. In this retrospective chart review, investigators looked at the records of 308 HCV-infected patients treated at M.D. Anderson over a 1-year period. HCV exacerbation was defined as a greater than 3-fold increase in ALT in the absence of hepatotoxic drugs, systemic coinfection, recent blood transfusions, and tumor infiltration of the liver.
"We found that 11% of patients who received this chemotherapy developed reactivation of HCV," reported coinvestigator Harrys Torres, MD, assistant professor of infectious diseases at M.D. Anderson. "Interestingly, none of these patients died with liver failure, which is different than with HBV reactivation."
What concerns Dr. Torres is that HCV reactivation necessitates discontinuation of chemotherapy. "We have to stop chemo in 50% of cases," he said. "It seems that HCV reactivation does not compromise the patient from the biologic standpoint, but from the oncologic standpoint, with treatment interruptions," it does.
Treating HCV concurrently with the administration of chemotherapy is not an option. "Current HCV agents are associated with anemia and neutropenia, and these patients already have some sort of hematologic toxicity with the chemotherapy," Dr. Torres said. "In the near future, we're hoping to see new drugs that can be given orally once a day that would allow chemotherapy to continue."
Dr. Hwang reports receiving grant funding from Bristol-Myers Squibb. Dr. Torres reports consulting for Merck, Astellas, and Vertex.
The Liver Meeting 2011: American Association for the Study of Liver Diseases (AASLD) 62nd Annual Meeting: Abstracts 172 and1732. Presented November 7, 2011.
http://www.medscape.com/viewarticle/753313
November 10, 2011 (San Francisco, California) — Two separate studies, performed at the University of Texas M.D. Anderson Cancer Center in Houston, demonstrate the potentially life-threatening impact of reactivation of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection in patients undergoing immunosuppressive chemotherapy.
The data, presented here at The Liver Meeting 2011: American Association for the Study of Liver Diseases (AASLD) 62nd Annual Meeting, suggest that greater surveillance for HBV and safer hematologic-sparing treatments for HCV are required.
In the first study, lead investigator Jessica P. Hwang, MD, MPH, and colleagues looked at HBV reactivation during cancer treatment using a retrospective dataset from her institution. "This is a topic that is gaining momentum in public health, oncology, as well as hepatology landscapes," she explained. However, because of the lack of large population-based studies, the current prevalence of HBV reactivation in patients undergoing cancer treatment is unclear. "Our goals were to determine the prevalence and predictors of HBV screening and reactivation in a comprehensive cancer center."
What is known is that HBV reactivation can occur at anytime during chemotherapy or after chemotherapy, during the recovery phase of the immune system's reconstitution. "This can lead to poor outcomes, hepatic flares, liver failure, and death," Dr. Hwang said. "It's important to identify these patients accurately so that effective oral antiviral therapy can be initiated."
The study by Dr. Hwang and colleagues explored 2 issues: the existence of inconsistent guidelines for screening cancer patients for HBV, and the lack of adherence to the guidelines that are in place.
The 3 entities that have addressed HBV and cancer are the Centers for Disease Control and Prevention (CDC), the AASLD, and the Association of Clinical Oncology (ASCO).
On screening and treatment, the CDC and AASLD recommendations are in agreement: All patients with cancer who are about to undergo immunosuppressive therapy should be tested for HBV and screened for hepatitis B surface antigen (HBsAg), hepatitis B core antigen (anti-HBc), and antibodies against HBsAg (anti-HBs). If there is a positive test result, HBV prophylaxis should be initiated.
Recommendations from ASCO are less comprehensive: Only those about to undergo "highly" immunosuppressive regimens (i.e., stem cell transplants or treatment with rituximab) and patients "at risk" for HBV should be tested, and screening should only be for HBsAg and anti-HBc (recommended treatment is the same).
"Although there is agreement on the importance of antiviral prophylaxis, ASCO does not advocate the use of all 3 screening tests," Dr. Hwang noted. Furthermore, the ASCO guidelines require that oncologists be aware of the risk factors for HBV infection, and that they take the time to actually perform HBV screening. The discrepancies in recommendations led Dr. Hwang's team to examine current practices at the M.D. Anderson Cancer Center.
The retrospective chart review gathered data on screening, positive tests, and HBV reactivation for all chemotherapy-naïve cancer patients seen at the M.D. Anderson over a 4-year period. Evidence of viral reactivation was defined as an alanine aminotransferase (ALT) level of at least 100 U/L plus total bilirubin of at least 2.5 mg/dL; detectable HBV levels when HBV was previously undetectable; or HBV DNA of at least 100,000 copies/mL.
The screening period was 2 months before the first or second round of chemotherapy. Both solid tumor and hematologic malignancies were considered. Risk factors for HBV prior to screening included International Classification of Diseases, Ninth Revision (ICD-9) codes for HCV, HIV, liver disease, and hepatitis.
Approximately 71,000 charts were reviewed. Of the 10,729 patients receiving potentially immunosuppressive chemotherapy, Dr. Hwang and colleagues found that only 1787 patients (17%) were screened for HBV. Tests used were HBsAg (1665 patients); HBsAg and anti-HBC (87 patients); and anti-HBc (35 patients). "If we just look at the patients with HBV risk factors, only 1 of 5 patients were screened," Dr. Hwang reported.
Of those screened, 34 patients were found to have HBV reactivation. Fourteen of the 34 were found to have chronic HBV infection, and anti-HBc was detected in 20 patients. Of the total reactivation cohort, 23 patients had hematologic cancers, 11 had solid tumors, and 10 had been treated with rituximab.
Predictors of those chosen for screening were being male, having HBV risk factors, having a hematologic malignancy, and the use of rituximab. Predictors of HBV reactivation were being male, being Asian or black, and having HBV risk factors. "Interestingly, Asian and black race did not predict screening, yet they were more often testing positive," said Dr. Hwang.
Most striking was the lack of use of HBV therapy after a positive test. Of the 34 patients, 9 received prophylaxis (2 later died), 11 received treatment after HBV reactivation (8 died), and 14 received no treatment (10 later died).
"It does not appear that we are following the CDC and AASLD recommendations," Dr. Hwang pointed out, adding that M.D. Anderson is not even adhering to ASCO recommendations.
"Preventable reactivation does occur, is occurring, and prophylaxis has been shown to dramatically reduce mortality in cancer patients with HBV," she explained.
HCV Reactivation
A study from the same institution looked at HCV reactivation in patients who had undergone treatment with rituximab and gemcitabine. In this retrospective chart review, investigators looked at the records of 308 HCV-infected patients treated at M.D. Anderson over a 1-year period. HCV exacerbation was defined as a greater than 3-fold increase in ALT in the absence of hepatotoxic drugs, systemic coinfection, recent blood transfusions, and tumor infiltration of the liver.
"We found that 11% of patients who received this chemotherapy developed reactivation of HCV," reported coinvestigator Harrys Torres, MD, assistant professor of infectious diseases at M.D. Anderson. "Interestingly, none of these patients died with liver failure, which is different than with HBV reactivation."
What concerns Dr. Torres is that HCV reactivation necessitates discontinuation of chemotherapy. "We have to stop chemo in 50% of cases," he said. "It seems that HCV reactivation does not compromise the patient from the biologic standpoint, but from the oncologic standpoint, with treatment interruptions," it does.
Treating HCV concurrently with the administration of chemotherapy is not an option. "Current HCV agents are associated with anemia and neutropenia, and these patients already have some sort of hematologic toxicity with the chemotherapy," Dr. Torres said. "In the near future, we're hoping to see new drugs that can be given orally once a day that would allow chemotherapy to continue."
Dr. Hwang reports receiving grant funding from Bristol-Myers Squibb. Dr. Torres reports consulting for Merck, Astellas, and Vertex.
The Liver Meeting 2011: American Association for the Study of Liver Diseases (AASLD) 62nd Annual Meeting: Abstracts 172 and1732. Presented November 7, 2011.
http://www.medscape.com/viewarticle/753313
Best Answer
you are welcome, it is my pleasure unfortunately hbv is very complex and i studied it myself because most liver specialists have no clues of the complexity behind this infection and every little risk worths at least knowledge
if you have insurance coverage for this you might check from time to time hbvdna with the sensibility 6iu/ml or little lower if available.yearly should be enough, these are also european guidelines to detect occult hbv
research has shown that the first 10 years from seroconversion hbsag negative/hbsab positive there might be some residual hbvdna detactable which will decrease to totally und after 10-15years
guidelines in europe are going towards this direction especially of hbvdna monitoring and US monitoring after clearance especially for those with severe fibrosis
Thanks very much, Stef. I would have been clueless. This is timely for me. I thought I don't have to think about HBV ever again...but clearly I'm not getting off that easy. Guess I better catch up on my reading. Thanks again, Stef.
be very carefull of all immune suppressive drugs, they can all reactivate hbv.you can find data on this searching our community or easily online on scientific publication
the most important thing is not to have t together with hcv because in that case, even if rare, there is a very small risk of occult hbv.the hbsg mutates and infection goes on with no hbsag, almost no hbvdna and a lot of liver damage because of the hbsag mutants (the virus is able to damage liver cells directly even without replication).any way this is not meant to scare and occult hbv is ver rare and common only in hbv+hcv coinfection for long time
unfortunately hbv is like herpes and it is a actually something in between retrovirus and dna virus (it has both rna and dna), very similar to hiv.it has a very stable short dna integrated in our dna called cccdna
reactivation is impossible if immune system stays ok but in case of immune suppression of any kind it can come back
it is not possible to measure real complete eradication because even few cccdna hidden in our dna can reactivate the whole thing, so even a biopsy will find no cccdna while there can still be some
a indirect measure of eradication can be the loss of hbsab antibody by decades or its level becomeing very low, less than 10miu/ml.
if this antibody gets so low or lost it is obvious there is no virus left, hbsab antibody funtion is: block entrance of hbv to liver cells and block its replication, neutralize hbsag which suppress immune system by inactivating dentric cells and macrophages and making immune tollerance.the real antibody to clear and control hbv is hbcab which is needed in high levels and hbsag neutralizes immune system to protect the hbcag (the core antigen) and keep hbcab antibodies very low
anyway do not worry too much about all this, just good to know to have a list of all drugs that suppress immune system to avoid them whenever possible.
in case you have to use some of these it is good to use tenofovir or entecavir antivirals to block virus reactivation.in this case be careful because drug makers tried to make virus mutants of hbv in the past by using weak antivirals (we share the same antivirals as hiv), only tenofovir has no resistance and entecavir only 1.2%.
all other antivirals are still used by ignorant or pushed by drug makers liver specialists even if out of guidelines, and lamivudine is still used to block hbv reactivation while on chemio and so on.lamivudine is extremely dangerous and can make hbv mutation that makes hbsab immunity antibody useless or infect people vaccinated, so lamivudine is absolutely to avoid
that is still being used on pregnancy hbv positive mothers too sometimes, with all the dangers you can imagine
Stef...I don't want to hijack this thread into an HBV discussion but that wasn't what I was told. I'm anti-HBs positive and it was explained to me that I'm immune AND non-contagious. Never has anyone said that my HBV could come back, I've been under the impression this is a permanent cure. It seems contradictory to be immune and still be at risk for re-activation if undergoing chemotherapy or taking arthritis drugs, etc. I would have thought my Hepatologist would have had something to say about that.
I will have some reading to do.
I will have some reading to do.
Exactly right , HCV is a RNA virus and HBV is a DNA virus.
HCV can be eradicated in the true meaning of the word
whereas a DNA virus such as HBV will always stay in the human DNA.
thanks for confirming that stef2011
b
HCV can be eradicated in the true meaning of the word
whereas a DNA virus such as HBV will always stay in the human DNA.
thanks for confirming that stef2011
b
Thanks Mike....I found the last section of results on the following document a bit unclear to me, your information helps. The combination of results means cured but not immune then and only anti-HBs being positive indicates immunity. Thanks again.
http://www.cdc.gov/hepatitis/hbv/PDFs/SerologicChartv8.pdf
http://www.cdc.gov/hepatitis/hbv/PDFs/SerologicChartv8.pdf
hbv has also another bad thing, those who never got it in their life have the lowest risk of liver cancer
while those who had acute hbv and cleared, and those who are cronic carriers but hbvdna undetactable by antivirals, share the same risk of liver cancer
unfortunately hbv integrated in human dna (which is called cccdna) remians but as long as immune system is working normally it can never reactivate an hbv infection, chemio probably destroys immune system complitely.....
this happens with steroids, artritis drugs, entercept, all immune suppressive drugs reactivate a cleared hbv infection.of course hbv antivirals can prevent this if taken before starting immune suppressive drugs
i dont know if entercept and artritis drugs can reactivate a clered hcv infection too
i can clear all abou hbv because i am very expert, hbv is almost never cleared only immune controlled.the word learance from acute hbv is scientifically wrong, hbv like herpes will always stay in the human dna of infected persons even if they cleared the virus
so hbv carriers, both cronic carriers or those who cleared the infection anytime in their life, are a risk of death with chemio without antivirals because they get a lethal type which most of the time leads to death
hcv should be different but i am not expert enough to say, i just know it is easier to clear because it doesnt integrate in human dna like hbv
It is my understanding that HCV unlike HBV and HIV does not enter
the cell nucleus to leave a reservoir. What this means is that
HCV can be completely eradicated whereas HBV does only get
suppressed to a ponit where ones own imune system can keep it
that way. I could therefore see the likelyhood of HBV being
reactivated a lot more than HCV.
the cell nucleus to leave a reservoir. What this means is that
HCV can be completely eradicated whereas HBV does only get
suppressed to a ponit where ones own imune system can keep it
that way. I could therefore see the likelyhood of HBV being
reactivated a lot more than HCV.
"...Instead, the NCCN says in its Prevention and Treatment of Cancer-Related Infections guideline, that, "in patients undergoing intensive immunosuppressive therapy, evaluation of HBV surface antigen, core antibody, and surface antibody should be considered at baseline." Patients with a surface antibody only (HBsAb+) are effectively immunized against HBV, noted Dr. Ludwig...."
Test All Chemo Patients for Hepatitis B, Says NCCN Presenter
http://www.medscape.com/viewarticle/739169
Test All Chemo Patients for Hepatitis B, Says NCCN Presenter
http://www.medscape.com/viewarticle/739169
I agree...poor terminology in the use of the word "reactivated" and left open to interpretation. With regards to the portion referring to HBV (I know this is an HCV forum but some of us have been exposed to both) - it says:
"On screening and treatment, the CDC and AASLD recommendations are in agreement: All patients with cancer who are about to undergo immunosuppressive therapy should be tested for HBV and screened for hepatitis B surface antigen (HBsAg), hepatitis B core antigen (anti-HBc), and antibodies against HBsAg (anti-HBs). If there is a positive test result, HBV prophylaxis should be initiated. "
However, it fails to differentiate if the positive result refers to any of these tests being positive or if the results of these tests in combination indicate a positive result for HBV. You can be immune or cured/immune and have a positive result for either anti-HBs or anti-HBc from what I understand.
So are they saying ANY positive result could mean potential "reactivation" (whatever that means) of HBV if undergoing chemo? Likely not.....but I sure wish they'd state this much clearer.
Thanks for posting this, Mike. Good info. I'll want to read further just to be sure I'm not mistaken about the HBV interpretation on this.
Trish
"On screening and treatment, the CDC and AASLD recommendations are in agreement: All patients with cancer who are about to undergo immunosuppressive therapy should be tested for HBV and screened for hepatitis B surface antigen (HBsAg), hepatitis B core antigen (anti-HBc), and antibodies against HBsAg (anti-HBs). If there is a positive test result, HBV prophylaxis should be initiated. "
However, it fails to differentiate if the positive result refers to any of these tests being positive or if the results of these tests in combination indicate a positive result for HBV. You can be immune or cured/immune and have a positive result for either anti-HBs or anti-HBc from what I understand.
So are they saying ANY positive result could mean potential "reactivation" (whatever that means) of HBV if undergoing chemo? Likely not.....but I sure wish they'd state this much clearer.
Thanks for posting this, Mike. Good info. I'll want to read further just to be sure I'm not mistaken about the HBV interpretation on this.
Trish
Thanks for posting Mike, and (surprisingly ;-) I completely agree with DD. What the hell are they talking about? It sounds like the HCV "reactivation" cohort are people who are actively infected (perhaps at low levels) and have normal enzyme levels. Nowhere is the word SVR used and nowhere do they mention actual PCR testing either before, during or after the chemo events. So...WTF are they talking about?
DD - I've been out of the loop. What do you mean when you say "And, remember all the major medical bodies are now stating that SVR is equivalent to eradication?" Has the occult/viral persistence thing (even in SVR's) been laid to rest in favor of eradication? And no, I'm not going to lay the "I told you so" on you if it has. ;-)
DD - I've been out of the loop. What do you mean when you say "And, remember all the major medical bodies are now stating that SVR is equivalent to eradication?" Has the occult/viral persistence thing (even in SVR's) been laid to rest in favor of eradication? And no, I'm not going to lay the "I told you so" on you if it has. ;-)
I read it like you did.
I thought it was terribly sloppy and confusing and not very illustrative of anything other than chemo can exacerbate HCV's effects.
I also concluded that "reactivation" did not refer to SVR patients.
I haven't ever used the word "reactivation" in a HCV context so that was what got my attention.
I think we all reacted the same. This looks like BS to me and that's why I posted it.
Mike
I thought it was terribly sloppy and confusing and not very illustrative of anything other than chemo can exacerbate HCV's effects.
I also concluded that "reactivation" did not refer to SVR patients.
I haven't ever used the word "reactivation" in a HCV context so that was what got my attention.
I think we all reacted the same. This looks like BS to me and that's why I posted it.
Mike
Thank you DD this had bugged me all night last night and now I feel better. I love it when someone smarter than me can read right thing the mumbo jumbo and pick out the grains that need to be looked at!!!!!!!!!!!!!!!!!!!!
And yes if I had cancer that needed to be treated I agree with you Bali my hcv standing probably would not be the first and foremost thing on my mind.
But this thread is a great thing to read in the morning, it cheered me up!
And yes if I had cancer that needed to be treated I agree with you Bali my hcv standing probably would not be the first and foremost thing on my mind.
But this thread is a great thing to read in the morning, it cheered me up!
I read about studies from Europe where SVR was durable despite chemo
unfortunately I did not save the article (can`t save everythng I read.....)
But for all practical reasons if you get diagnosed with inoperable cancer
that needs chemo your priorities might just shift a little........
Don`t think my successfully treated HCV would be first thing on my mind......
b
unfortunately I did not save the article (can`t save everythng I read.....)
But for all practical reasons if you get diagnosed with inoperable cancer
that needs chemo your priorities might just shift a little........
Don`t think my successfully treated HCV would be first thing on my mind......
b
I take a lot that comes out of the medical community with a grain of salt. This is the same community that let people they knew where high risk for hep c wait 21 years before they started testing them for hep c or even telling us there may be an epidemic out there and the blood supply is not safe. The lives they could have saved if we knew we had a liver disease and a life style change would have made all the difference in the world. When someone can tell me why they let the HIV epidemic known but not the Hepatitis C epidemic known I'll stop questioning every written word they come out with.
And also note they refer to EXACERBATION of HCV from the chemo treatments, which to me indicates they ARE referring to already infected patients...but with stable signs and markers. You are right, it is highly doubtful that they found 308 SVR's from HCV treatment who also had Cancer, and undertook Chemo!!!!! I think this is a terminology issue, and they mistakenly give the impression they are discussing those who have become SVR...but really are just talking about HCV infected patients with little or no abnormal blood markers, other than being positive for HCV. This study needs to be explored in full, not just a short synopsis. I will bet they are NOT studying an SVR group!!!! That's my take.
Any other opinions...anyone wish to chime in????
Any other opinions...anyone wish to chime in????
I suppose that unless they had like 50-100 SVR'd patients that subsequently developed cancer which required chemotherapy, then those patients in fact reactivated, then, it's kind of hard to know for sure. I mean, shingles is basically a reactivated chicken-pox virus. It's the same virus. I never knew this until I developed shingles at age 28. My mother said that neither my younger sister, nor I had ever had a noticable case of chicken pox, in other words, she never saw a single pox on either of us. My younger sister ended up breaking out with chicken pox in her 30's when she was pregnant with her 2nd child, and she grew up right next to me when we were kids (14-months apart in age), so it stands to reason that if I had chicken pox as a kid, that she would have gotten them then. Like I said, my mom never remembered us having chicken pox. Then, I come down with shingles at 28. I told my doctor, how can that be when I've never had chicken pox? The doctor said, 'well you HAD TO HAVE had chicken pox, or you could not have gotten shingles because shingles is a reactivated chicken pox virus', he said, 'you could have have 1 pox on the bottom of your foot and your mom didn't know it and you didn't know it, but it would have been enough for your body to recognize it'. I was surprised and I never knew any of that stuff. My point is, that until enough patients with long standing SVR develop cancer (which of course we don't want that to happen!), then, how will the doctors really know for sure? Susan400
This is a little confusing to me but interesting
Do they mean people who have SVR?
Does this mean after SVR , reactivation can occur?
I've never read this kind of article before, thank you
Mike, (I think)
Do they mean people who have SVR?
Does this mean after SVR , reactivation can occur?
I've never read this kind of article before, thank you
Mike, (I think)
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"investigators looked at the records of 308 HCV-infected patients treated at M.D. Anderson over a 1-year period. HCV exacerbation was defined as a greater than 3-fold increase in ALT in the absence of hepatotoxic drugs, systemic coinfection, recent blood transfusions, and tumor infiltration of the liver."
What does this mean??? They looked at the records of 308 HCV INFECTED patients???? Were they only looking at "exacerbation" of an existing HCV infection in patients? It sure sounds this way. Nowhere do they mention studying certified, long standing SVR patients...only HCV INFECTED patients. I am not sure they are looking at true SVRs. Maybe HCV positives with normal ALT's, or something like that. I need more info on this study!!!!!
And, remember all the major medical bodies are now stating that SVR is equivalent to eradication. Why would they expect 'reactivation???'.
I think this is a different sort of patient group....again, where is the discussion of SVR status...etc??? I think it may be 'stable' HCV infected serum positive patients with low normal ALT's and no evidence of damaging disease process.
Anyone else out there know anything more on these studies????
DoubleDose