Aa
large study on patients clearing hbsag
900
LARGE SCALE LONGITUDINAL STUDY OF CHRONIC
HEPATITIS B PATIENTS WITH HEPATITIS B SURFACE
ANTIGEN SEROCLEARANCE
Danny Wong, Ching Lung Lai, James Fung, David But, Ivan Hung,
John Yuen, Frederic Fung, John Young, Man-Fung Yuen; Medicine,
The University of Hong Kong, Queen Mary Hospital, Hong Kong
SAR, China
Background and Aim: Seroclearance of hepatitis B surface antigen
(HBsAg) is a rare event in chronic hepatitis B patients. We
conducted a large scale longitudinal study investigating the
virological, histological and clinical aspects, including the risk
of development of hepatocellular carcinoma (HCC) in patients
with HBsAg seroclearance. Patients and Methods: Two hundred
and ninety-eight patients (211 male and 87 female;
median age on presentation: 43.1 years) with HBsAg seroclearance
were recruited and followed up every 3 – 6 months
for clinical assessment. Intrahepatic HBV DNA and covalently
closed circular DNA (cccDNA) were measured by real-time
PCR. Serum HBV DNA was measured by the Artus HBV RG Test
(QIAGEN, Germany). Liver stiffness was assessed by FibroScan
(Echosens, France). Results: The median age of HBsAg seroclearance
was 49.6 years. The median follow-up duration was
108.9 months and the median follow-up duration after HBsAg
seroclearance was 36.4 months. Liver biopsies were performed
on 29 patients (median time of biopsy: 48.6 months after
HBsAg seroclearance). All have detectable intrahepatic HBV
DNA (median: 1.68 copies/cell), and cccDNA were
detectable in 23 patients (79.3%, median: 0.03 copies/cell).
Of the 29 patients with liver biopsy, 9 and 16 patients had sera
available within 1 year and between 5 – 10 years after HBsAg
seroclearance, respectively, for HBV DNA analysis. All 9
patients had undetectable HBV DNA (<1.1 IU/mL) within 1
year of HBsAg seroclearance, and 4/16 patients had
detectable HBV DNA levels between 5 – 10 years of HBsAg
seroclearance (median: 2.37 IU/mL). Of the 26 patients with
adequate liver tissues for histological examination, 4 had mild
fibrosis (F1) and 5 had minimal necroinflammation. FibroScan
was performed on 76 and 78 patients who had HBsAg seroclearance
at age 8.1 kPa) was observed only in 7.9%
(6/76) patients with HBsAg seroclearance at age <50 compared
to 29.5% (23/78) patients with HBsAg seroclearance at
age ≥50 (p = 0.001). Seven patients developed HCC (median
age: 69.3). Kaplan-Meier analysis showed that the chance of
HCC development in patients with HBsAg seroclearance at age
<50 was significantly less than those with HBsAg seroclearance
at age ≥50 (p = 0.004). Conclusion: Although serum
HBV DNA was detectable in only a small proportion of patients
with HBsAg seroclearance, intrahepatic HBV DNA was still
present in all patients. Nevertheless, patients who cleared
HBsAg at age <50 had significantly less fibrosis and lower
chance of HCC development than those with HBsAg seroclearance
at ≥50 years.
LARGE SCALE LONGITUDINAL STUDY OF CHRONIC
HEPATITIS B PATIENTS WITH HEPATITIS B SURFACE
ANTIGEN SEROCLEARANCE
Danny Wong, Ching Lung Lai, James Fung, David But, Ivan Hung,
John Yuen, Frederic Fung, John Young, Man-Fung Yuen; Medicine,
The University of Hong Kong, Queen Mary Hospital, Hong Kong
SAR, China
Background and Aim: Seroclearance of hepatitis B surface antigen
(HBsAg) is a rare event in chronic hepatitis B patients. We
conducted a large scale longitudinal study investigating the
virological, histological and clinical aspects, including the risk
of development of hepatocellular carcinoma (HCC) in patients
with HBsAg seroclearance. Patients and Methods: Two hundred
and ninety-eight patients (211 male and 87 female;
median age on presentation: 43.1 years) with HBsAg seroclearance
were recruited and followed up every 3 – 6 months
for clinical assessment. Intrahepatic HBV DNA and covalently
closed circular DNA (cccDNA) were measured by real-time
PCR. Serum HBV DNA was measured by the Artus HBV RG Test
(QIAGEN, Germany). Liver stiffness was assessed by FibroScan
(Echosens, France). Results: The median age of HBsAg seroclearance
was 49.6 years. The median follow-up duration was
108.9 months and the median follow-up duration after HBsAg
seroclearance was 36.4 months. Liver biopsies were performed
on 29 patients (median time of biopsy: 48.6 months after
HBsAg seroclearance). All have detectable intrahepatic HBV
DNA (median: 1.68 copies/cell), and cccDNA were
detectable in 23 patients (79.3%, median: 0.03 copies/cell).
Of the 29 patients with liver biopsy, 9 and 16 patients had sera
available within 1 year and between 5 – 10 years after HBsAg
seroclearance, respectively, for HBV DNA analysis. All 9
patients had undetectable HBV DNA (<1.1 IU/mL) within 1
year of HBsAg seroclearance, and 4/16 patients had
detectable HBV DNA levels between 5 – 10 years of HBsAg
seroclearance (median: 2.37 IU/mL). Of the 26 patients with
adequate liver tissues for histological examination, 4 had mild
fibrosis (F1) and 5 had minimal necroinflammation. FibroScan
was performed on 76 and 78 patients who had HBsAg seroclearance
at age 8.1 kPa) was observed only in 7.9%
(6/76) patients with HBsAg seroclearance at age <50 compared
to 29.5% (23/78) patients with HBsAg seroclearance at
age ≥50 (p = 0.001). Seven patients developed HCC (median
age: 69.3). Kaplan-Meier analysis showed that the chance of
HCC development in patients with HBsAg seroclearance at age
<50 was significantly less than those with HBsAg seroclearance
at age ≥50 (p = 0.004). Conclusion: Although serum
HBV DNA was detectable in only a small proportion of patients
with HBsAg seroclearance, intrahepatic HBV DNA was still
present in all patients. Nevertheless, patients who cleared
HBsAg at age <50 had significantly less fibrosis and lower
chance of HCC development than those with HBsAg seroclearance
at ≥50 years.
also, I failed to mention I was born with HBV as was my brother, sister, mother and 3 aunts. My grandfather was a carrier but they knew nothing back in the 30's
None of us make antibodies for hep B. lucky for us none of us ever had liver damage or elevated liver markers, just the virus.
My granfathers father must have been the 1st one to get it as he died in his 30's back in 1935. They did not know what he had but he was very sick and had yellow skin before he died.
None of us make antibodies for hep B. lucky for us none of us ever had liver damage or elevated liver markers, just the virus.
My granfathers father must have been the 1st one to get it as he died in his 30's back in 1935. They did not know what he had but he was very sick and had yellow skin before he died.
At the time of the Hep A vaccination my VL was 10,400,000 (million) 7.02 RNA LOG Jan-7-2009
I was confirmed hbeag neg and chronic carrier. All other liver enzymes were at normal range.
3-6-2009 I wanted to test to see if I had built an immunitly against hep A from the vaccine and also complained of liver pain from the vaccine. Another test showed that the VL went down to 358,000 (thousand) IGM was high in response to the vaccine. I was still hbeag neg at that time and the doctor was confused so he sent me to a specialist in Beverly Hills. Now that I think of it I am going to get those reuslts faxed too.
That was the 1st time they tested me for cancer but did not PCR. I did not like that doctor because he claimed I had Hep A becuase of the high IGM at the time even though I told him I was just vaccinated for that 2 months ago!
I am still not making antibodies for Hep B. I going to go get another round of tests on 3 weeks. I'll post the results as an image.
IF it was not the vaccine it was the herb.
I was confirmed hbeag neg and chronic carrier. All other liver enzymes were at normal range.
3-6-2009 I wanted to test to see if I had built an immunitly against hep A from the vaccine and also complained of liver pain from the vaccine. Another test showed that the VL went down to 358,000 (thousand) IGM was high in response to the vaccine. I was still hbeag neg at that time and the doctor was confused so he sent me to a specialist in Beverly Hills. Now that I think of it I am going to get those reuslts faxed too.
That was the 1st time they tested me for cancer but did not PCR. I did not like that doctor because he claimed I had Hep A becuase of the high IGM at the time even though I told him I was just vaccinated for that 2 months ago!
I am still not making antibodies for Hep B. I going to go get another round of tests on 3 weeks. I'll post the results as an image.
IF it was not the vaccine it was the herb.
no it weakens immune response because you have to make many more antibodies since the viruses are very different, not even the same family i believe but anything can be in the single case.....
what was your situation before taking the tea as hbeag/hbeab and alt?hbcab igm quantitative would be very helpful but i am sure it is not used in normal hospitals
one thing is probable in case of immune tollerant phase and hbeag positive the phyllanthus triggered your immune response to hbeag negative/hbeab positive but as i said earlier this also happens naturally, i ve seen similar riductions even in some posts in this forum
what was your situation before taking the tea as hbeag/hbeab and alt?hbcab igm quantitative would be very helpful but i am sure it is not used in normal hospitals
one thing is probable in case of immune tollerant phase and hbeag positive the phyllanthus triggered your immune response to hbeag negative/hbeab positive but as i said earlier this also happens naturally, i ve seen similar riductions even in some posts in this forum
Hey, I also want to mention, I had a Hep A vaccine JAn of 2009.
Do you think it could have also stimulated an imune response agains HBV with the Chanca Piedra.
97% reducion from Jan to Mar is HUGE and I have not heard of such a rapid decline in a short amount of time of VL anywhere?
Do you think it could have also stimulated an imune response agains HBV with the Chanca Piedra.
97% reducion from Jan to Mar is HUGE and I have not heard of such a rapid decline in a short amount of time of VL anywhere?
ok very well said. thanks for sharing your thoughts and researches. they really elucidated some things i am not cleared about the pathogenesis of the hepatitis b virus.. hope for more knowledge sharing.
what do you think in men's physiology caused this?
they found genetic male links to HCC and this maybe the same link for more cronic hbv
there maybe also hormonal links, they found testosterone boosts hbe seroocnversion between 15-20yo, i had an acute hbv while being inactive carrier and made hbe seroconversion at 19yo
i saw researches about those who clear hbsag it is related to age mainly and cirrhosis or inactive carriage.a little hbvdna detectable in very low amounts makes also more hbsag seroconversion
after hbsag seroconversion it is important to check hbvdna for occult hepatitis because some of these developped HCC
no those studies have been proven wrong, they are too old, they have made the mistake that you can read the low cholesterol in 2 ways since viruses and cancer are related to low cholesterol but not with lowering cholesterol.
it is the virus/cancer using big amounts of cholesterol that makes the severity of disease and not the low cholesterol activating the virus/cancer
the same has been found with hcv, so if the low cholesterol is made by the virus/cancer it means disease is very severe while if it is you to make low cholesterol you weaken the viruses/cancers
they found genetic male links to HCC and this maybe the same link for more cronic hbv
there maybe also hormonal links, they found testosterone boosts hbe seroocnversion between 15-20yo, i had an acute hbv while being inactive carrier and made hbe seroconversion at 19yo
i saw researches about those who clear hbsag it is related to age mainly and cirrhosis or inactive carriage.a little hbvdna detectable in very low amounts makes also more hbsag seroconversion
after hbsag seroconversion it is important to check hbvdna for occult hepatitis because some of these developped HCC
no those studies have been proven wrong, they are too old, they have made the mistake that you can read the low cholesterol in 2 ways since viruses and cancer are related to low cholesterol but not with lowering cholesterol.
it is the virus/cancer using big amounts of cholesterol that makes the severity of disease and not the low cholesterol activating the virus/cancer
the same has been found with hcv, so if the low cholesterol is made by the virus/cancer it means disease is very severe while if it is you to make low cholesterol you weaken the viruses/cancers
excellent research on seroconversion.
i would like to ask among all the members here who are very well informed in the HBV (especially stevenNYers, stefano170669, zellyf and cajim), if they have encountered anything through their research that say something about the demographics of those who cleared the virus.
interesting to note that 95% of the population would have the ability to totally eradicate the HBV upon initial acute encounter while unfortunately for the rest of the members here suffer chronicity.
just asking those people here who did many research: is there a common pattern or characteristic for those who suffer the chronic infection?
i did some research and i found out that males are somewhat more predisposed to chronicity than women. what do you think in men's physiology caused this?
H W Zhang. doi:10.1136/gut.2008.157149. Risk factors for acute hepatitis B and its progression to chronic hepatitis in Shanghai, Chin. Gut 2008;57:1713-1720
another study would account the abnormality related to cholesterol.
Z Chen. Prolonged infection with hepatitis B virus and association between low blood cholesterol concentration and liver cancer.BMJ 1993; 306 : 890. (Published 3 April 1993)
- does this study contradict with your observation stefano170669 regarding the applicability of simvastatin in reducing the HBsAg?
i would like to ask among all the members here who are very well informed in the HBV (especially stevenNYers, stefano170669, zellyf and cajim), if they have encountered anything through their research that say something about the demographics of those who cleared the virus.
interesting to note that 95% of the population would have the ability to totally eradicate the HBV upon initial acute encounter while unfortunately for the rest of the members here suffer chronicity.
just asking those people here who did many research: is there a common pattern or characteristic for those who suffer the chronic infection?
i did some research and i found out that males are somewhat more predisposed to chronicity than women. what do you think in men's physiology caused this?
H W Zhang. doi:10.1136/gut.2008.157149. Risk factors for acute hepatitis B and its progression to chronic hepatitis in Shanghai, Chin. Gut 2008;57:1713-1720
another study would account the abnormality related to cholesterol.
Z Chen. Prolonged infection with hepatitis B virus and association between low blood cholesterol concentration and liver cancer.BMJ 1993; 306 : 890. (Published 3 April 1993)
- does this study contradict with your observation stefano170669 regarding the applicability of simvastatin in reducing the HBsAg?
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