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.
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.
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?
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 ?
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"
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$.
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.
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.
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.
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.
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.
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