I finished treatment during the middle of last year and post treatment assessment ended in December. So the last follow up test I did was from that month which was part of the trial. I’m back to being monitored under the health system so the next follow is in about 3 months time.
I think you are quite right with what you said about vir 3434. Fingers crossed my hbsag remains low. I guess try to live healthy and look out for treatment options that help with the chances
Thank you, I’m glad to be participating in this forum. This illness can have an isolating effect, so Im more than happy to share my experience :).
I will definitely talk to the doctor about the options. It did cross my mind whether to undergo interferon treatment again. If I did do it again I would know what to expect so I suppose that’s a positive. Hopefully my hbsag remains low. You are quite right, low hbsag seems to generate better outcomes.
I thought I provide an update. This is my blood test from last month.
A bit of a surprise. Grateful to see the appearance of hbsab. But there appears to be co-existance of hbsag. I have had a read of a couple of threads on this forum that discussed co-existance, which was helpful.
I have gone back and asked if they have quantifiable data for hbsag and hbeag.
Business as usual. I will continue to take tenovofir and do my six monthly checkups. I guess the job ain’t done until there’s no signs of hbsag and hbeag.
That’s great, congratulations on the anti-HBs antibody coming up! Indeed, you’re right that there is this co-existence of HBsAg, but it’s a good sign that you have such high levels of antibody. Hopefully the HBsAg will continue going down over time.
@ThomasTu Need to discuss on the point whether hbsag is correlated with liver disease progression like HCC or cancer? As you said ghat hbsag doesnt correlate with liver disease but Mr. Andrew suggested it the exact opposite way in one of his old post.
Mr Andrew Vaillant @availlant mentioned in his post that HCC is directly related with Integrated HBV DNA. And as per him most of the hbsag(>99.99%) come from integrated HBV DNA. So it means high values of hbsag is equal to highly active integrated HBV DNA so that higher chances of HCC or liver disease progression??
The above needs to be taken with some understanding of subtleties - low HBsAg levels (less than 100 IU/mL for example) are correlated with better outcomes like HBsAg loss and lower risk of disease progression. In some studies, higher HBsAg levels (more vs less than 200 IU/mL) can predict risk of liver cancer recurrence after surgery.
However, there are also patients with very high levels of HBsAg level who have healthy looking livers (e.g. patients in immune tolerance phase) and those who have low HBsAg levels with bad liver disease progression (e.g. cirrhotic patients in HBeAg-negative phase).
As such, HBsAg levels alone cannot provide information about your risk of liver disease.
Regarding to the question about high value of HBsAg is correlated with liver disease progression?
Currently, HBV DNA level is the most importantly risk and etiologic factor in HCC development. REVEAL HBV study (Clin Liv Dis 2007 ) found that there was linear correlation between HBV DNA level and HCC occurrence. This may be due to the fact that having a high HBV DNA causes the body immune system to fight the infection leading to necroinflammatory processes and liver tissue healing resulting in fibrosis and cirrhosis meanwhile integrated HBV DNA with hepatocytes clonal expansion leading to genome instability resulting in HCC development. However, HBsAg levels may be risk factor that correlates with HCC occurrence but not causation.High HBsAg levels indicate that HBsAg production comes from transcriptional activity of cccDNA and integrated HBV DNA especially in HBeAg -ve CHB patients. So , this may reflect that the higher HBsAg levels the more increase in transcriptional activity and amount of integrated HBV DNA in hepatocytes. Cohort studies (Data from GSK 2025) about distribution of HBsAg in CHB patients with both treatment- naive or treatment -experienced and showed that approximately half of these patients had HBsAg levels > 1,000 IU/ ml and about one third > 3,000 IU/ml .
One study (Lim J H . Medicine 2021 )found that reduction in qHBsAg level could be used as predictive factor of HCC development in CHB patients treated with TDF or ETV . Another study (Vo T T .et al Asian Pac J Cancer Prevention 2019) found that HBsAg > 100 IU/ml and > 1,000 IU/ml are associated with increased risk of HCC. Most populations in this study were treatment-naive CHB patients.
qHBsAg level can accurately reflect disease activity and viral replication and could help to indicate inactive HBV infection if qHBsAg < 1,000 IU/ml in untreated HBeAg -ve CHB patients with low viral load.
Antiviral drugs (Tenofovir/Entecavir) can suppress the viral load to the point where it is undetectable but doesn’t affect HBsAg production. Therefore, it is the body immune system that controls the transcriptional activity of cccDNA and integrated HBV DNA . If the immune system is strong, it can control and eliminate infected hepatocytes leading to decreased HBsAg level resulting in reduction of HCC occurrence . These patients need to take care of their health to maintain strong immune system especially their liver health.I hope this may help you.
