Determining whether to start medication is a complicated process. I think there are (rightly) moves to simplify how we decide if we should treat people with HBV.
The current recommendations according to European guidelines are this (I hope I do it justice, @PLampertico - happy to be corrected):
If you’re over 30 and have a virus load over 2000 IU/mL, you can consider treatment
If you’re HBeAg-postitive and have raised ALT levels and have a virus load over 2000 IU/mL, you should consider treatment
If you’re HBeAg-negative and have a virus load over 2000 IU/mL, you should consider treatment
If you have liver cirrhosis or cancer, you should definitely be on treatment
If you have family history of liver cirrhosis or cancer, you can consider treatment
So you can see from this, you are correct and HBV DNA is considered a major indicator of whether you should be on treatment or not. There have been large studies showing that high HBV DNA levels are linked to worse liver disease in people who are not treated. But the interpretation of these studies is complicated: this doesn’t usually include people in Immune tolerant phase when virus levels are very high, but disease is very low.
You are correct about HBsAg being used to screen for people who are infected with HBV. But recently scientists have been looking at if HBsAg can be used to predict if you can stop viral treatment. Others have also shown there is some link with liver disease progression, but these studies are still being worked on and have not been generalised to the entire population.
I hope this answers your questions and provides some context.
HBsAg (also called HBs and the S antigen) is used as a primary screening tool because the assay for it is quick, easy (just takes a small amount of blood), and relatively inexpensive. These are practical issues that are important when physicians are starting their diagnostic assessment.
HBsAg is the best available marker for a functional cure both becaus studies have indicated that loss of HBsAg is the best readily measured indicator that we have of loss or permanent inactivation of the HBV cccDNA. The cccDNA is a nuclear form of the HBV DNA that is the root cause of HBV persistence. HBsAg is not a perfect marker for a functional cure, but it is the best currently available.
In my case, my hbssg quntative became low( single digits) and then from dec 20 onwards i have done two six monthly labs, it has become non-reactive i. e less than 0.9, should i consider myself functionally cured? My doc has increased the half yearly testing regime (alt, afp, ultrasound, hbv dna) to yearly now.
I’m glad for your results, but I have a question: were you taking medication?
And if so, what medication are you taking?
Has the doctor stopped you from mediation?
And finally, have you created hbsab?
I was never on medication as the labs were always within range in last 8 years after i was diagnosed, regarding hbsab, last year it was around 6.8, after that i didn’t got this done, as doctor didn’t advised to do this.
Glad you won the fight against this devil. Just few question. Where are you from. Did you followed any specific diet. Were you taking any supplement during these years. What were your base line result [DNA load, HbsAg count, e antigen status ].
Glad you won the fight against this devil. Just few question. Where are you from. Did you followed any specific diet.
Were you taking any supplement during these years.
What were your base line result [DNA load, HbsAg count, e antigen status ].
DNA load never went beyond 500 copies, lately they became less than 100
Hbsag count at detection time were in thousands, if i remember it was 8k’s, but lately they were coming into single digits before it became non-reactive i.e less than 0.9,
I was hbeag negative at the time of detection, 8 yrs ago.
Phase 1 corresponds to the previously known Immunotolerant phase, phase 2 is the Hbeag pos CH, phase 3 the Hbeag neg chronic infection, phase 4 tge hbeagbeg CH, see EASL 2017 hbv Guidelines for details