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The elephant in the room for seroconverting with hbeag negative
Chronic hepatitis B: Virology, natural history, current management and a glimpse at future opportunities
http://www.sciencedirect.com/science/article/pii/S0166354215001394
8.3 HBeAg(−) chronic hepatitis B
Because HBeAg seroconversion is not possible in HBeAg(−) patients, and HBsAg seroconversion is rare, the objectives of therapy are ALT normalization and achievement of undetectable HBV DNA. Unlike in HBeAg(+) patients, there are no clear pre-treatment IFN responsiveness predictors. NUC treatment yields undetectable HBV DNA in a larger percentage of HBeAg(−) patients, compared to those who are HBeAg(+), in large part because of their 1–2 log10 lower average baseline HBV DNA levels. Given the high risk of relapse with therapy discontinuation (90–97%), even in patients who have achieved sustained ALT normalization and undetectable HBV DNA, lifelong therapy is generally recommended (Santantonio et al., 2000, Hadziyannis et al., 2003, Lai et al., 2006, Lai et al., 2007, Marcellin et al., 2008a and Shouval et al., 2009). Unfortunately, HBsAg clearance is quite rare in HBeAg(−) patients during NUC therapy and is less than 17% with IFN. When quantitative HBsAg changes are used as predictors of response or nonresponse on therapy, providers can guide treatment continuation or discontinuation with moderate to high level of quality.
Highlights from the article:
-hbsag seroconversion is rare
-Unlike in HBeAg(+) patients, there are no clear pre-treatment IFN responsiveness predictors
-Given the high risk of relapse with therapy discontinuation (90–97%), even in patients who have achieved sustained ALT normalization and undetectable HBV DNA, lifelong therapy is generally recommended
-Unfortunately, HBsAg clearance is quite rare in HBeAg(−) patients during NUC therapy and is less than 17% with IFN.
Not sure what is the big hype about getting on nucs and IFN to "seroconvert" just like the myth that maximizing vit d can help somehow, just another fantasy of the forum.
Not sure about you, but I think no sane doctor would put you on treatment against the guidelines based on this data. Probably better to hope for better drugs in the future than gambling with your health. Just my two cents.
http://www.sciencedirect.com/science/article/pii/S0166354215001394
8.3 HBeAg(−) chronic hepatitis B
Because HBeAg seroconversion is not possible in HBeAg(−) patients, and HBsAg seroconversion is rare, the objectives of therapy are ALT normalization and achievement of undetectable HBV DNA. Unlike in HBeAg(+) patients, there are no clear pre-treatment IFN responsiveness predictors. NUC treatment yields undetectable HBV DNA in a larger percentage of HBeAg(−) patients, compared to those who are HBeAg(+), in large part because of their 1–2 log10 lower average baseline HBV DNA levels. Given the high risk of relapse with therapy discontinuation (90–97%), even in patients who have achieved sustained ALT normalization and undetectable HBV DNA, lifelong therapy is generally recommended (Santantonio et al., 2000, Hadziyannis et al., 2003, Lai et al., 2006, Lai et al., 2007, Marcellin et al., 2008a and Shouval et al., 2009). Unfortunately, HBsAg clearance is quite rare in HBeAg(−) patients during NUC therapy and is less than 17% with IFN. When quantitative HBsAg changes are used as predictors of response or nonresponse on therapy, providers can guide treatment continuation or discontinuation with moderate to high level of quality.
Highlights from the article:
-hbsag seroconversion is rare
-Unlike in HBeAg(+) patients, there are no clear pre-treatment IFN responsiveness predictors
-Given the high risk of relapse with therapy discontinuation (90–97%), even in patients who have achieved sustained ALT normalization and undetectable HBV DNA, lifelong therapy is generally recommended
-Unfortunately, HBsAg clearance is quite rare in HBeAg(−) patients during NUC therapy and is less than 17% with IFN.
Not sure what is the big hype about getting on nucs and IFN to "seroconvert" just like the myth that maximizing vit d can help somehow, just another fantasy of the forum.
Not sure about you, but I think no sane doctor would put you on treatment against the guidelines based on this data. Probably better to hope for better drugs in the future than gambling with your health. Just my two cents.
HBV is such an individual disease since it has to do with our own immune system. Then, there are more differences within all of us, such as genotype, subgenotype, mutations, etc. There are many more differences that are very hard to understand, such as host integration factors, why one gets cirrhosis or HCC and the next does not, why one may seroconvert HbsAg and other may not, etc. There are many studies out there with lower and higher seroconversion rates, and the success rate differences may have to do with many of the factors above and not being able to compare apples:apples. Unfortunately, just because one person seroconverts with similar factors does not necessarily mean others will have the same positive outcome.
With that said, while we all here would love to be 'cured', most doctors where we live will not prescribe interferon and most in the US do not even know or can track their HbsAg quant, so what is the point in treating with Interferon? This leaves us oral antivirals, which are very easy to come by. I feel 'the big hype' of getting on NUC's at this point for me is to reduce my chances of possibly getting HCC or cirrhosis as I age, since I know my chances of seroconverting on NUC's alone are very slim. Most and many studies out there that are very positive when it comes to NUC's, from a standpoint of reducing HCC, cirrhosis, or even regressing cirrhosis. The way I look at it and my doctors do, is that treating with NUC's are like treating someone will diabetes, high blood pressure, etc. NUC's very well may not functionally cure us, but they have shown to reduce fibrosis, cirrhosis, and HCC risk, which is a great reason for many to treat.
It is interesting too, if you read old guidelines to treat they use to use DNA 20,000 iu/ml to treat for all with HBV. Now, we know with HbeAg the guidelines suggest treating at much lower DNA. These guidelines are not finite and have the option to change. For example, last week WHO now says anyone diagnosised with HIV should go on treatment, rather than waiting for the CD4 count to drop. Will this be the future of HBV, if they find NUC's greatly reduce fibrosis or HCC long term, especially if treating before fibrosis or cirrhosis sets in? Much of the guidelines come from countries where they pay for treatment, so we may not get to treating all since it would be very expensive. Or, we may if long term it proves treatment reduces costly consequences of HBV, such as HCC. It is interesting and just goes to show how HBV (like HIV) is ever changing. We have come so far but obviously have a long way to go unfortunately.
With that said, while we all here would love to be 'cured', most doctors where we live will not prescribe interferon and most in the US do not even know or can track their HbsAg quant, so what is the point in treating with Interferon? This leaves us oral antivirals, which are very easy to come by. I feel 'the big hype' of getting on NUC's at this point for me is to reduce my chances of possibly getting HCC or cirrhosis as I age, since I know my chances of seroconverting on NUC's alone are very slim. Most and many studies out there that are very positive when it comes to NUC's, from a standpoint of reducing HCC, cirrhosis, or even regressing cirrhosis. The way I look at it and my doctors do, is that treating with NUC's are like treating someone will diabetes, high blood pressure, etc. NUC's very well may not functionally cure us, but they have shown to reduce fibrosis, cirrhosis, and HCC risk, which is a great reason for many to treat.
It is interesting too, if you read old guidelines to treat they use to use DNA 20,000 iu/ml to treat for all with HBV. Now, we know with HbeAg the guidelines suggest treating at much lower DNA. These guidelines are not finite and have the option to change. For example, last week WHO now says anyone diagnosised with HIV should go on treatment, rather than waiting for the CD4 count to drop. Will this be the future of HBV, if they find NUC's greatly reduce fibrosis or HCC long term, especially if treating before fibrosis or cirrhosis sets in? Much of the guidelines come from countries where they pay for treatment, so we may not get to treating all since it would be very expensive. Or, we may if long term it proves treatment reduces costly consequences of HBV, such as HCC. It is interesting and just goes to show how HBV (like HIV) is ever changing. We have come so far but obviously have a long way to go unfortunately.
I just want to clarify for the general readers. There are tow types of HbeAg negative:
1. Immune Control Phase
"A “non-replicative” phase (previously known as “inactive carrier”), characterized by low (or more commonly undetectable) serum HBV DNA, HBeAg(−) status, and normal ALT. Although patients in this phase were once referred to as “healthy carriers” this oxymoronic phrase should be eliminated."
[quote from the same article].
2. HBeAg negative chronic hepatitis.[aka Immune Escape Phase]
In the Immune Control Phase, no treatment is needed but patients must monitor regularly as it can transition to the Immune Escape Phase. In the Immune Control Phase, s-seroconversion (naturally of course), is not uncommon.
In the Immune Escape Phase (HBeAg-ve chronic Hepatitis). A sane doctor will treat. Some doctors think you can also stop after several years of treatment. Many doctors are studying adding PegIFN to the treatment in order to achieve s-seroconversion. All these options should become clearer when results of studies and clinical trials are analyzed.
1. Immune Control Phase
"A “non-replicative” phase (previously known as “inactive carrier”), characterized by low (or more commonly undetectable) serum HBV DNA, HBeAg(−) status, and normal ALT. Although patients in this phase were once referred to as “healthy carriers” this oxymoronic phrase should be eliminated."
[quote from the same article].
2. HBeAg negative chronic hepatitis.[aka Immune Escape Phase]
In the Immune Control Phase, no treatment is needed but patients must monitor regularly as it can transition to the Immune Escape Phase. In the Immune Control Phase, s-seroconversion (naturally of course), is not uncommon.
In the Immune Escape Phase (HBeAg-ve chronic Hepatitis). A sane doctor will treat. Some doctors think you can also stop after several years of treatment. Many doctors are studying adding PegIFN to the treatment in order to achieve s-seroconversion. All these options should become clearer when results of studies and clinical trials are analyzed.
Doing vit d may not be a cure for hbv but some way it is helping ppl. It may be a bridge to cure which still is incomplete. Many things are there unproven but that's what we are trying to do ie some safe attempts to prove.
Treatment in hbeag neg can be justified both positively and negatively. It should not b overlooked that fibrosis is more rapid in e ag neg ppl. and is considered more harmful than e ag pos. There are various reasons that justifies treatment initiation in e ags though not all are the appropriate candidates. If only treatment is the option y make us vulnerable to the danger of future risks hoping for a cure which is still unachievable.
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