Aa
Should I stop Hepsera?
I been taken Hepsera 10mg daily for 6 years now and the virus is undetected. Today my doctor told me to stop to see my body could suppress the virus it self. Should I stop or keep taken it? will my condition get worse? what if it didnt work and I take hepsera or viread and develop resistant? Help or personal experience would be great. Thank you
if i were you i d just make sure to switch to tenofovir and take vit d supplements, for the switch i dont know if an add on period is needed between these two drugs because chemically similar.adv is both too weak and toxic to keep it anylonger
no just wasted money, they are only for liver cancer screening and also normal US is more than good for that
what about MRI and Ultrasound, can it detected liver damage. I recently go my MRI and US, it normal.
of course, as i keep posting, keeping patients without a fibroscan for a decade is criminal, i dont understand why can t you sue FDA
yes you may use vit d3 as in other posts, normal ast and alt should mean no liver damage at all but of course only a fibroscan monitoring during the years can confirm that 100%
Unfortunately US dont have fribroscan, no result on it. 6 years ago I have my biopsy done and it have some fibrosis but ast and alt are normal for 6 years. Should I still need fibroguard? What about Vitamin D3, what it use for?
it is expensive, google hepatitistechnologies.
if you have no liver damage you dont need all supplements, fibroguard is enough to prevent fibrosis.what is your fibroscan result?
all treatments are of course some kind of experimental monitored at an int'l research center
forgot to menthion i also had fatty liver and cleared it in 4 months by vitamins and diet
you ll see on my posts but here s a sum:
antivirals tdf+etv
anti fibrotic heptech supplements+vit d3
immune modulators gcmaf, trl7 agonist
healthy diet
antivirals of course just made hbvdna und and allowed best responce to antifibrotic.no effect on hbsag
immune modulator gcmaf: since started gcmaf hbsag in stable decline, rise of alt to 40-54
nagalase, abnormal enzym slowly getting normal.when normal macrophages activation will be at max
trl7 agonist just started to see if it boosts hbsag decline, not possible to report
antifibrotics heptech+vit d3+diet:
cirrhosis regressed from 16.3kpa to 5.6kpa in less than 2 years
last US even showed nodules less evident on part of the liver (previously they were the same).
Thank stef2011!
Hey you don't mind I ask what treatment u on? Are you on viread(brand) or tenvir(generic) plus peginterferon? How is your progress?
Hey you don't mind I ask what treatment u on? Are you on viread(brand) or tenvir(generic) plus peginterferon? How is your progress?
2009 is too old, just check 2011 if you like
also guidelines are just general guidelines for ignorant doctors, very expert doctors are able to personalize treatment and this is the news in hbv and hcv treatment (of course 90% of doctors are not good at this)
also guidelines are just general guidelines for ignorant doctors, very expert doctors are able to personalize treatment and this is the news in hbv and hcv treatment (of course 90% of doctors are not good at this)
http://www.aasld.org/practiceguidelines/Documents/Bookmarked%20Practice%20Guidelines/Chronic_Hep_B_Update_2009%208_24_2009.pdf
i just read this guideline for chronic hep B 2009.
"Among HBeAg-negative patients, viral suppression
was sustained in only 8% of patients who stopped adefovir after 1-year of treatment. The vast majority of patients who continued treatment up to 5 years maintained their response but there was minimal incremental response after the first year. HBsAg loss was observed in 5% of patients after 4-5 years of continued treatment. 206 In addition, long-term treatment was associated with a decrease in fibrosis score. Nonetheless,
3% of patients developed HCC indicating that longterm antiviral treatment does not completely prevent HCC. A preliminary report of 33 patients who had received adefovir for 4-5 years and had been followed up to 5 years off treatment showed that all patients had virologic relapse (redetection of serum HBV DNA) initially but 18 (55%) patients subsequently had sustained biochemical/virological remission and 9 of these 18 later lost HBsAg."
So doest this mean if i stop hepsera, I have 55% not need treatment or undetected HBV DNA and about 25% of HBsAg seroconversion to negative?
"Among HBeAg-negative patients, viral suppression
was sustained in only 8% of patients who stopped adefovir after 1-year of treatment. The vast majority of patients who continued treatment up to 5 years maintained their response but there was minimal incremental response after the first year. HBsAg loss was observed in 5% of patients after 4-5 years of continued treatment. 206 In addition, long-term treatment was associated with a decrease in fibrosis score. Nonetheless,
3% of patients developed HCC indicating that longterm antiviral treatment does not completely prevent HCC. A preliminary report of 33 patients who had received adefovir for 4-5 years and had been followed up to 5 years off treatment showed that all patients had virologic relapse (redetection of serum HBV DNA) initially but 18 (55%) patients subsequently had sustained biochemical/virological remission and 9 of these 18 later lost HBsAg."
So doest this mean if i stop hepsera, I have 55% not need treatment or undetected HBV DNA and about 25% of HBsAg seroconversion to negative?
carrier state is something from a decade ago it doean t exsist anymore and was a totally wrong thinking.
today we have, and only off therapy of course, inactive virus, which can be confirmed only by:
hbsag<500iu/ml
hbvdna<2000iu/ml
alt<30 men 19 woman
only for genotype D
inactive virus can reactivate any moment and just means there is an immune response which can be boosted by interferon to clear hbv very fast
only genotype D has been studied on large number of patients by brunetto pisa, some studies were done on genotype B and C in asia with less patients and hbsag level was around 100iu/ml if i remember correct.no studies on genotype A
so the word carrier state was used, without any study to prove its meaning, around 2000-2004, it can tbe used today and has no meaning.
also note that in those years there was no way to monitor closely liver damage, it was pure fantasy the fact doctors used to think hbeag neg was a good prognosis it is actually the opposite
brunetto in a congress made a story of all the mistakes done in the past of hbv, hopefully these mistakes are over
hey i just read one of the topic online indicate my lab work is carrier states? it confuse:
Hsbag Positive
anti-hbs Negative
anti-hbc igm Negative
anti-hbc IgG+ igm Positive
hbeag Negative*
anti- hbe Positive
Chronic infection but low risk of liver damage — carrier state
I thought carrier state no treatment needed.
I remember 6 year ago, Hvb viral DNA
hep b viral dna iu/ml 12600
hep b viral dna copies/ml 204,932
I hate my doctor, I think he dont have updated information on treatment because he is a GI not hepatology.
http://labtestsonline.org/understanding/analytes/hepatitis-b/tab/test
Hsbag Positive
anti-hbs Negative
anti-hbc igm Negative
anti-hbc IgG+ igm Positive
hbeag Negative*
anti- hbe Positive
Chronic infection but low risk of liver damage — carrier state
I thought carrier state no treatment needed.
I remember 6 year ago, Hvb viral DNA
hep b viral dna iu/ml 12600
hep b viral dna copies/ml 204,932
I hate my doctor, I think he dont have updated information on treatment because he is a GI not hepatology.
http://labtestsonline.org/understanding/analytes/hepatitis-b/tab/test
ship samples by fedex to the indian labs willing to make the tests or if you happen to travel to europe, asia or some african countries you can check hbsag in that occasion
we posted indian labs because very good and cheap
To bad for me, I live in the US and ask you said qhbsag are not available. So what are my option testing for more accurate of the virus?
that hbvdna is obsolete, too poor sensibility, you need a test with hbvdna<10iu/ml but if you combo with peginterferon this has no importance
if you are in US, US is 10years obsolete on tests and for market reasons dont allow use of hbsag quantification which are available every where in the wrold (UK,US, australia excluded)
no switch tdf+intf but you need a lab for hbsag quant otherwise you can see if you are clearing hbv
what are the rate of clear hbv in asian tdf+interferon? how long is the treatment?
see other posts in the forum.one study with peg add on on stable long term nucs had:
40% hbsag clearance at 48weeks
10% non response
50% with hbsag at very low levels like 30-300iu/ml (which is nothing) after 72 weeks on the combo.the combo, if responder, is meant to be kept until hbsag und
thank stef2001 for the reply.
I dont understand the difference between hbsag quant and hbv dna?
my lab
hepatitis B viral DNa
hep b viral dna iu/ml <100 in range
hep b viral dna copies/ml <160 in range
my other lab
Hbv, Qualitative PCR hbv Dna not detected
both lab work perform by two difference lab.
So what your recommend stop and see couple month to see the the virus progress or just switch to TDF+interferon?
what are the rate of clear hbv in asian tdf+interferon? how long is the treatment?
I dont understand the difference between hbsag quant and hbv dna?
my lab
hepatitis B viral DNa
hep b viral dna iu/ml <100 in range
hep b viral dna copies/ml <160 in range
my other lab
Hbv, Qualitative PCR hbv Dna not detected
both lab work perform by two difference lab.
So what your recommend stop and see couple month to see the the virus progress or just switch to TDF+interferon?
what are the rate of clear hbv in asian tdf+interferon? how long is the treatment?
hbvdna checking is useless, it must be und but it means nothing to curing hbv
you should check both hbsag quant in iu/ml and hbvdna and then switch to tdf+interferon to clear hbv
Have an Answer?
You are reading content posted in the Hepatitis B Community
A list of national and international resources and hotlines to help connect you to needed health and medical services.
Herpes sores blister, then burst, scab and heal.
Herpes spreads by oral, vaginal and anal sex.
STIs are the most common cause of genital sores.
Condoms are the most effective way to prevent HIV and STDs.
PrEP is used by people with high risk to prevent HIV infection.
