Hi Bob,
I think this test-tube study may not necessarily reflect what is happening in a person and I don’t have access to the article to see if the amount of change they are observing would have any reasonable effect in people (particularly compared to other drivers of oxidative rate change like eating a meal). Moreover, there’s no evidence that taking that supplement would help anything in people (as mentioned in the article). I would take both with a grain of salt.
TT
That’s terrible that one would be prescribed hiv med for hep b. Maybe it’s the same. I don’t know if hep b meds that are first line of prescription are also used for HIV patients as their first line.
The tenofovir in the HIV medications are sufficient to suppress HBV replication and is the same as the first line HBV treatment.
Got me wondering of the 3 main medication treatments for hep b, what other medication are in there. To treat something else
Yes, this is definitely a good point and it hasn’t escaped scientists’ notice. Many groups have tried drug library screens for hepatitis B using the entirety of FDA-approved drugs to see if there are other compounds already in clinical use that would help with hepatitis B. This is more of @john.tavis’ wheelhouse and he could probably provide more information on it, but I’m not sure this has been particularly productive.
My understanding is that the models of Hepatitis B are not set up in a way such that accurately screening thousands of samples can be done in a practical or economical manner. New approaches (e.g., easy and scalable manners of measuring how different parts of the virus life-cycle are affected) are the main avenues of research, so that this might yield better results.
TT
Hi all,
The collections of approved drugs and those that have been tested in people and proven safe but were not approved for some reason have been extensively tested against HBV by many industrial and academic labs, with no really promising results. We did this against the RNaseH, and the only interesting results were about 4 that substantially increased replication (most definitely NOT what we were looking for!).
The big problem with these “repurposing” studies is that drugs are carefully designed to be specific for their intended target to avoid off-target causes of toxicity. Consequently, it is rare for this to work well. The best examples of successful repurposing are actually entecavir and tenofovir. They were designed against HIV and it is a happy accident that they work against HBV. That is due to the enzymatic similarities between the HIV and HBV reverse transcriptases.
It is possible to do high throughput screening against HBV, but that is remarkably slow and expensive.
Hope this helps.
John
Quick question, I know you are in Australia. I m in the USA. When you state FDA, is that your country or my country’s FDA?
When I talk about the FDA, that refers to the US FDA. The Australian equivalent is the therapeutic goods administration (TGA). My understanding is that the TGA and FDA have recognised each other as having similar standards, and will more readily accept approvals if already approved by the other party.
Thomas
Hello!
My name is Mihai Paraschivescu, a 36 years old Romanian male, living in Romania.
Unfortunately, in March 2023, after a random and unusual abdominal severe pain, I did an abdominal ultrasound, where it was found that I have the HB infection. Since it was just discovered, they’ve said that the rule is that I have to wait for 6 months for the acute phase to end, without any medication, to see if the body is able to get rid of the HB virus itself. Things were however strange already, because the ALT and the other transaminases were at normal levels, not suggesting an acute phase. Please find below the blood results from April 2023:
ALT 34 U/L
GGT 60 U/L
AST 25 U/L
Total bilirubin 1.03 mg/dl
Alkaline phosphatase (ALP) 83 U/L
HBsAg 2716.40 S/CO
Anti-HBsAg 0.12 mUI/mL
HBeAg 0.373 S/CO
Anti-HBeAg 0.01 S/CO
HBV-DNA 3132 UI/mL
After that, they said that I need to do a Fibroscan (transient elastography), where the result was a stiffness of 3.9 kPa (indicating a F0 fibrosis stage). CAP 182 dB/m.
Then I just waited for the 6 months to pass, and redid the blood tests in September. Sadly, it was confirmed not only that I have Chronic HB, but also that the virus load and HBsAg are increasing, as you can see in the results from last month:
ALT 30 U/L
GGT 62 U/L
AST 26 U/L
Total bilirubin 0.84 mg/dl
Alkaline phosphatase (ALP) 112 U/L
HBsAg 3005.74 S/CO
Anti-HBsAg 0 mUI/mL
HBeAg 0.395 S/CO
Anti-HBeAg 0.01 S/CO
HBV-DNA 15652 UI/mL
I also redid the Fibroscan test (transient elastography), which gave a result of 4.7 kPa (considered by the medic stationary stiffness and again indicating a F0 fibrosis stage). CAP 232 dB/m.
Now the discussion the medics from my country have, based on the blood results above and on the lack of any fibrosis, is if I should start the treatment with Entecavir or not. They’re especially questioning it because of the normal transaminases levels, which the books say that need to be above limits before starting with a treatment.
What I’m looking for is a specialized second opinion on this, i.e. if the antiviral treatment should be started or not at this point and also which medication is best in 2023, if I need to start the treatment (for example I still don’t understand which is better between Entecavir and Tenofovir for me, or if there is an even better medication).
Thank you for you time and answers!
Hi @Mihai_P,
Sorry to hear that what you had hoped was only an acute HBV infection concluded to be chronic. One of the experts will have a response for you as soon as they can. Until then, I just wanted to welcome you to the community. You have found a good place for understanding and support. Feel free to take a look around the forums and you can do some searches with the magnifying glass on the top right of the mainpage.
-Paul
Dear @Mihai_P,
Welcome to the community and thank you for sharing your story. With HBeAg positive status and moderate HBV DNA levels, your condition doesn’t necessarily fit into a textbook “phase” of chronic HBV infection. My understanding is that people over 30 such as yourself can consider treatment, but there is no outright recommendation to treat. This is because we essentially don’t know if treating you now will cause any different clinical outcomes compared to not treating you.
If you were to begin treatment, then the 2 first-line treatments (tenofovir or entecavir) are both highly potent drugs with minimal side-effects.
Hope this helps,
Thomas
Hello @ThomasTu and thanks for your reply!
I understand, but I just need to make one clarification:
In the results I got from the clinic, both in March and in September, the HBeAg 0.395 S/CO is considered negative (Nonreactiv: < 1.00 S/CO, Reactiv: >= 1.00 S/CO). While Anti-HBeAc 0.01 S/CO is considered positive (Nonreactive: >1.00 S/CO, Reactive: =< 1.00 S/CO).
So HBeAg being negative changes what you said in any way, regarding the start of treatment?
Thanks so much!
@PuallyHBV thank you for your kind words!
Ah, thanks for the clarification @Mihai_P, it is a bit confusing!
My understanding is that if there is no evidence of liver inflammation (and you do not have a family history of liver cancer) then current guidelines would not recommend treatment in HBeAg-neg phase (but you can consider it).
This is based on current EASL guidelines, but these are being updated over time given more research in the field.
Thomas
Thank you @ThomasTu. I went to another medic for a second opinion l, and she suggested that I should do a FibroMax blood tests to decide if medication should be started. I’ll do it on Monday and then it will take 4-6 days for the results to come.
Btw, regarding medication: here in Romania where I live they prescribe Entecavir by default, no alternatives. But from what I’m reading on the internet, in other countries Tenofovir is more common. And it seems that for Tenofovir there are two variations. My question is, which is the best antiviral out there?
Thank you!
Great to hear, @Mihai_P.
In answer to your question, essentially tenofovir and entecavir are equivalent in antiviral effect. I’ll refer you to some responses to a similar post:
Cheers,
Thomas
Hi again @ThomasTu @john.tavis @availlant and other experts from the forum.
I repeated the tests yesterday, after one and a half months, and although I didn’t get yet the result for HB-DNA, I did get the other values, and the HBsAg one scares me honestly. Below you can see what I got so far:
| Fosfataza alcalina | 98 U/L | 40 - 150 U/L |
| Gama GT | 60 U/L | 12-64 U/L |
| TGO/AST | 28 U/L | 5- 34 U/L |
| TGP/ALT | 41 U/L | < 55 U/L |
| HBsAc | 0.22 mUI/mL | Nonreactiv: <10.0 mUI/ml / Reactiv: >=10.0 mUI/ml |
The problem is this one:
| HBsAg cantitativ High Reactiv 35496.17 IU/mL |
Last time when I did it, back in September, the value was 3005 S/CO.
I don’t know why they’ve changed the measure unit this time from S/CO to IU/mL and also I don’t know if we 're looking at the same values where only the unit of measurement differs. But I highly doubt that’s the case.
I’m still waiting for the HB-DNA result which I will get on Tuesday/Wednesday next week, but I’m already scared by such a high HBsAg value. Am I right in being scared or isn’t it something to concern me that much?
By the way, as I was telling you last time, I also did a FibroMax which came with F0, A0, S0-S1, N0 and H0. Also the Fibroscan gave a value of 4.7 kPa and since my ALTs values were always normal, they’ve said that probably I don’t need to start with the antiviral treatment.
Until today when I got the new HBsAg value, and they don’t know what to do with me anymore.
I also did a MRI abdominal check and beside a 2.5x2.5 hemangioma, there’s nothing wrong with my liver so far.
I’m grateful for any feedback or insight I might get from you!
Thank you so much!
– Mihai
Dear @Mihai_P,
Your first HBsAg test result (3005 S/Co) is a from a qualitative test which cannot accurately quantify the level of HBsAg present. However, with this ratio of signal to cutoff S/Co the amount of HBsAg present in this first test result is certainly significant.
There is no point in comparing (numerically) this result to your most recent result (35496.17 IU/mL) which is from a quantitative test. However, I don’t think there has been a meaningful change in the level of HBsAg present. It is important to understand the HBsAg levels like this are not uncommon in chronic HBV infection, even under NUC therapy. Also changes in HBsAg do not predict potential progression in liver disease.
The important thing is that your liver function assessments and fiborscan are normal. Please get back to us with your HBV DNA when you get it.
Best regards,
Thank you for the reply and explanations @availlant (and @ThomasTu on the other thread).
This is pretty much in line with what healthcare providers are saying here in Romania where I live, that is: HB-DNA being the true marker of the disease progression and the one saying if medication should be started or not, while the HBsAg quantitative values can be ignored.
The first thing that troubles me regarding this is the medical studies and articles I’ve read, which make a correlation between the level of HBsAg higher than 2000 IU/mL, HBeAg negative, and the high incidence of HCC later down the road (usually after 10-20 years).
Secondly, only with the previously known HB-DNA of 15000 UI/mL and the value of HBsAg of 35496 IU/mL, one healthcare professional I’ve been going to is already recommending starting the Entecavir treatment. While other two healthcare professionals are saying that HBsAg value does not matter, HB-DNA is relatively low and will probably fluctuate between 3000 and 15000 IU/mL, and overall the disease has been there for decades and pretty much is inactive, so treatment is not required, unless I personally decide to start it.
So with these two “sets” of information and decisions, I’m really confused and torn, to say the least. I would really appreciate if you could give me your perspective on these two points from above.
Thank you again!
– Mihai
Dear @Mihai_P,
You are not alone in your confusion. Guidelines in different parts of the world take different approaches:
Liver cancer is caused at least in part by the buildup of insertions of viral DNA in cells of the liver which accumulates over the lifetime of infection. You are right that the risk of liver cancer is elevated in individuals with chronic HBV infection - which is why the approach in (1) makes sense. There is also data to suggest that early initiation of suppressive therapy (ETV / TDF / TAF) lowers the risk of liver cancer.
This is important debate currently in the field.
You may want to consider starting therapy even though you do not have liver disease as the long term safety profile of these medications is excellent. I encourage you to discuss with with your doctor.
Best regards,
Thank you again for your reply @availlant, I really appreciate it.
I’ll definitely discuss this further with my healthcare providers and also come back here with my HB-DNA result when I’ll get it in the coming days.
However, one thing that confuses me is this (based on my limited knowledge and understanding):
HBsAg is a marker of how many of the hepatocytes are infected by the virus, while HB-DNA says how much of the virus is in the blood.
Also, antiviral medicine as Entecavir and Tenofovir are capable of taking down the viral load to low or even undetectable levels.
But antiviral medicine does not (normally) decrease the values of HBsAg.
So if high levels of HBsAg can be a risk of HCC development in the future, how can antivirals be of any help if they can’t take down also the HBsAg values?
I’m sure I’m missing something in my reasoning
Thank you,
– Mihai