HBsAg quantitative and HBV DNA levels

[4est]

One study say that a correlation of quantitative assay of HBsAg and HBV DNA levels during chronic HBV treatment was found (http://www.ncbi.nlm.nih.gov/pubmed/18409002) and I want to ask you, to post your results of HBsAg quantitative and HBV DNA levels to see if this correlation is present or not.

Unfortunately I don't have my HBsAg quantitative, but when I will have the results I will post on this topic.

thanks!

[4est]

even if we let out immune tolerant phase, we still have to compare 84 Pisa vs 4318 Hanover and this are not even closer :)  

[4est]

I know that I ask this question before, but I'm still confused by the values presented in table 2 (http://www.natap.org/2011/APSL/APSL_05.htm)

Pisa reported a median value of 84 IU/ml for inactive carriers and Hannover reported a median value of 4318 IU/ml for low replicative phase and  12920 IU/ml for immune tolerant phase.
patients in Immune tolerant phase and Low Replicative phase are considered Inactive cariers, so I expect that the value to be at least in the same range, but I see 84 vs 4318 (or 12920), so I'm confused on this one.

any explanation ?

[StephenCastlecrag]

Hope this help:

A new role for an old marker, HBsAg , 01 February 2010
Maurizia Rossana Brunetto
Journal of Hepatology
April 2010 (Vol. 52, Issue 4, Pages 475-477)
Full Text | Full-Text PDF (441 KB)
Background & Aims

The quantifiable level of HBsAg has been suggested as a predictor of treatment response in chronic hepatitis B. However, there is limited information on HBsAg levels considering the dynamic natural course of HBV-infection. This study aimed to determine HBsAg levels in the different phases of HBV-infection in European HBsAg-positive patients.
Methods

226 HBV-monoinfected patients, not undergoing antiviral therapy, were analyzed in a cross-sectional study. Patients were categorized according to the phase of HBV-infection: HBeAg(+) immune tolerance phase (IT, n=30), immune clearance phase (IC, n=48), HBeAg(−) low-replicative phase (LR, n=68), HBeAg(−) hepatitis (ENH, n=68), and acute hepatitis B (n=12). HBsAg was quantified and correlated with HBV-DNA, HBV-genotypes and clinical parameters. In addition, 30 LR-patients were followed longitudinally.
Results

HBsAg levels were higher in IT-patients and IC-patients compared to LR-patients and ENH-patients (4.96/4.37/3.09/3.87-log10IU/ml, p<0.001). HBsAg showed a strong correlation with HBV-DNA during acute hepatitis B (R=0.79, p2000IU/ml) showed >3-fold higher baseline HBsAg levels with a NPV of 95% for an HBsAg cut-off of 3500IU/ml.
Conclusions

HBsAg levels show significant differences during the natural course of HBV-infection and between HBV-genotypes. These findings may have important implications for understanding the natural history of HBV-infection and for using quantitative HBsAg as a diagnostic tool, i.e. as a marker for predicting HBV-reactivation.

[4est]

Baraclude is the commercial name for entecavir and is use in treatment of hepatitis b lin order to block the viral replication. I suggest to discuss this option  with a doctor and not to take it without medical approval.
I don't know about the price in philiphines, or if supported by the state or not, but, I've check over the internet and i saw that the price is around 650$.

[nhix]

does anybody knows the medicine baraclude? how much is it here in the philippines?

[4est]

one interesting presentation reagrding hbsag quant http://www.md2010.org/files/presents/s2/c2-1.pdf

[4est]

from: http://alliance.hepatitis.org.au/uploads/HBV_Alliance/HepB_healthycarrier.pdf (a 2008 article)

"The majority of infected persons in the world, currently estimated at approximately 400 million, are thought to have acquired
infection at the time of birth or in early infancy.  From the time of infection, chronic hepatitis B passes through phases of
relative inactivity and phases of activity with progressive liver damage.  It is currently thought that there are 4 phases of
chronic hepatitis B. These include (1) an immune tolerance phase in childhood and adolescence, in which there are very
high levels of virus, but no accompanying active liver disease; (2) an immune clearance phase in which the immune
system attempts to clear the virus, resulting in liver damage; (3) an immune control phase characterised by low levels of
virus and no obvious liver damage and (4) an immune escape phase, during which the virus mutates, evades the immune
system and causes more liver damage.
During the first and third phases, patients have no obvious ongoing liver damage and in the past have been called “healthy
carriers” or “inactive carriers”. However, patients do not always stay in these states, as they move from one phase to
another, and are always at risk for hepatitis flares or progressive liver damage and the development of cirrhosis.
Patients in the first (immune tolerance) or the third (immune control) phases are generally not offered antiviral therapy, as
therapy has never been shown to result in benefit. Rather, patients in the second and fourth phases should be actively
monitored for antiviral therapy by assessment of liver enzymes, hepatitis B levels, and liver biopsy"

[4est]

you are wright :) - I had some discution with stef2011 and he told me that it is use for progress of medication or also that HbsAg with a low value is a indication for a possible seroconversion.

I don't had yet my HbsAg qunat (nobody ask for it), but I will do this somewhere in October - November and I will come back with the value and also with the value for hbv dna and we can discuss more on it.  

I point out the document with different levels of hbsAg quant because the big difference betwen hanovra and pisa, but maybe I don't understand the correct meaning of the phases.
What is the relation between inactive carrier or low replictive phase and immune tolerance or immune clearance or chronic hbv ?

[StephenCastlecrag]

The correlations depend on which phase: immune tolerance, immune clearance, inactive, and HBeAg-ve active, you are in. Since there are no easy to use correlations, most doctors do not test for it. However, as Stef2011 will tell you, it can be used to monitor the progress or non-progress of trial medications. Stef2011 will also tell you (he will tell me if I am wrong) that if you have low serum HbsAg, you are on your way to seroconversion.

I personally believe that serum HBsAg quantity is a surrogate marker for amount of transcriptionally active cccDNA in the liver. That sounds impressive, doesn't it?

[4est]

I've see a document regarding hbsag quantitative: http://www.natap.org/2011/APSL/APSL_05.htm and I was surprise about the differences between hanovra and pisa and different phases.
Any ideas on this ?

[4est]

you are wright, the paper is old and I've read some new paper results and unfortunately I observe that in some context correlation was found and in other correlation was not found.
I'm still curios about the hbsag quantitative use in every day practice.

i also read about the case that hbv dna was undetectable and hbsag was relay high (e.g: 35000), so in this case the correlation is hard to found or to be explained.

@stef2011 has seams to have some more info regarding hbsag quantitative but also he still not understand the correlation (or no correlation) between hbsag and hbvdna.  

anyway, I'm curios about the people that had hbsag quantitative - what doctors say about it if some  tratament was started base on this hbsag quantitative.

[StephenCastlecrag]

Your paper is a bit old. There are more recent papers. The correlations are not that simple. Many people on antivirals have 0 hbvdna but various quantities of serum HbsAg.

[4est]

I just try to get some date from the readers of this forum to see if we can notice the correlation.

[stef2011]

that correlation is present without therapy, on therapy:

interferon lowers hbsag
tenofovir, entecavir and other antivirals increase hbsag