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Inactive Carrier - Reactivation
I recently had my ALT done and it was at 50 and last year 47 , 1 - 46 normal level. Born hep b carrier, Chinese decent. Always have been inactive carrier at DNA PCR undetectable, but last test result PCR 224 iu/ml , 5.82 per iu / ml copy. This puts me at 1200 or so copies. Do you think I have a reactivation. Never tested for HBeag. I am hbsag positive and hbabc positive. Non reactive to antibody. I am in the USA no hbsag iu/ml quant testing.
Chronic HbeAg negative hepatitis (Immune escape/re-active) develops overtime and not instanteous, it may seem that way if hbdna and ALT are not monitored regularly. In my opinion, the Genotype and precore/BCP mutations tests are not necessary at this stage. 220 iu/ml is still below 2,000 iu/ml and ALT is not 2 x ULN, so guideline will suggest wait and see. However, a Fibroscan score is always useful, for baseline information and a safety insurance. qHbsAg is not available in the US, you may do one when you are in China.
Stephen,
I do not see my liver doc until the 24th of June, but my gen doc ran DNA HBV and at 220 iu/ml and ALT at 50. Last year ALT was at 47 but I did not run a DNA so not sure. Does immune escape come gradually or is it instantaneously? My ALT has always been in the 23 - 35 range ever since 2004. Since I see my doc on the 24th , I want to verify the test I should run. Since I am in US I can not get hbsag quant. Are these the right test to ask for?
hbeag pos or neg?
genotype test
mutant or non mutant strain
DNA quant?
What other test should I ask them to run? Thanks for your help !
I do not see my liver doc until the 24th of June, but my gen doc ran DNA HBV and at 220 iu/ml and ALT at 50. Last year ALT was at 47 but I did not run a DNA so not sure. Does immune escape come gradually or is it instantaneously? My ALT has always been in the 23 - 35 range ever since 2004. Since I see my doc on the 24th , I want to verify the test I should run. Since I am in US I can not get hbsag quant. Are these the right test to ask for?
hbeag pos or neg?
genotype test
mutant or non mutant strain
DNA quant?
What other test should I ask them to run? Thanks for your help !
Hi,
Let me describe what I understand from reading the scientific literature.
For those of us infected with HBV at birth, we all start off with HBeAg positive; sooner or later, we will all seroconvert to HBeAg negative, most by the age of 40. Some will e-seroconvert naturally, others will do so whilst on treatment. After e-seroconversion, our hbvdna should be low, generally less than 2000 iu/ml and our ALT is normal. Scientists call this the Inactive or Immune Control Phase, because during this phase, our immune system seems to be able to control the virus, although not completely eliminating it.
For some,they will stay in this phase for a very long time, without needing treatment and without progression of the liver disease. Some may even lose their HBsAg as they age.
For others, the virus will mutate and they will become active again, even though their HBeAg remains negative. This new phase is called re-active or Immune Escape phase. Hbvdna will increas to > 20,000 iu/ml and ALT will also be elevated. Patients now require medication, else disease will progress and fibrosis increases. It is called Immune Escape phase, because scientists believe the virus develops precore/basal core promoter mutations to escape the pressure exerted by Immune Control.
The question is then asked - do patients in the Immune Escape phase have to take medication forever? Here the guidelines differ. All guidelines will say that those with cirrhosis should take medication forever, or until their cirrhosis regressed sufficiently or they lose their HBsAg. For those with no cirrhosis or compensated cirrhosis, the Asian guideline says they may try to stop under doctor's guidance, European guidelines say no - because after stopping, most will experience an ALT flare that can lead to decompensation, not worth the risk.
Finally, to answer your question. Genotype C is observed to be more likely to develop precore/BCP mutations than genotype B, so it is possible that you too will develop these mutations. But so will some Genotype B patients. The trick is of course to monitor your conditions at least half-yearly and start treatment as soon as hbvdna and ALT increase persistently.
Our experiences with antivirals such as Entecavir and Tenofovir are not that long. It is now accepted that after several years of hbvdna suppression, our T-cell immunity is partially restored. Added to the fact that infected liver cells do die during liver cells turn-over, the loss of cccDNA may exceed replenishment of cccDNA by re-infection.
Finally, a cure or treatment with higher rate of cure should be coming soon.
Let me describe what I understand from reading the scientific literature.
For those of us infected with HBV at birth, we all start off with HBeAg positive; sooner or later, we will all seroconvert to HBeAg negative, most by the age of 40. Some will e-seroconvert naturally, others will do so whilst on treatment. After e-seroconversion, our hbvdna should be low, generally less than 2000 iu/ml and our ALT is normal. Scientists call this the Inactive or Immune Control Phase, because during this phase, our immune system seems to be able to control the virus, although not completely eliminating it.
For some,they will stay in this phase for a very long time, without needing treatment and without progression of the liver disease. Some may even lose their HBsAg as they age.
For others, the virus will mutate and they will become active again, even though their HBeAg remains negative. This new phase is called re-active or Immune Escape phase. Hbvdna will increas to > 20,000 iu/ml and ALT will also be elevated. Patients now require medication, else disease will progress and fibrosis increases. It is called Immune Escape phase, because scientists believe the virus develops precore/basal core promoter mutations to escape the pressure exerted by Immune Control.
The question is then asked - do patients in the Immune Escape phase have to take medication forever? Here the guidelines differ. All guidelines will say that those with cirrhosis should take medication forever, or until their cirrhosis regressed sufficiently or they lose their HBsAg. For those with no cirrhosis or compensated cirrhosis, the Asian guideline says they may try to stop under doctor's guidance, European guidelines say no - because after stopping, most will experience an ALT flare that can lead to decompensation, not worth the risk.
Finally, to answer your question. Genotype C is observed to be more likely to develop precore/BCP mutations than genotype B, so it is possible that you too will develop these mutations. But so will some Genotype B patients. The trick is of course to monitor your conditions at least half-yearly and start treatment as soon as hbvdna and ALT increase persistently.
Our experiences with antivirals such as Entecavir and Tenofovir are not that long. It is now accepted that after several years of hbvdna suppression, our T-cell immunity is partially restored. Added to the fact that infected liver cells do die during liver cells turn-over, the loss of cccDNA may exceed replenishment of cccDNA by re-infection.
Finally, a cure or treatment with higher rate of cure should be coming soon.
Stephen
Just talked to my mother and my uncles and they say they always have to take virals. I think they are hbeag - with mutation and once off virals hbv DNa starts to replicate fast. She told me after many test the doctor told her she could never be off virals. They are all on entcevir. One of my uncle has cirrhosis and was told he has 2 years max, about 5 years ago. He seems fine but i could see the yellow in his eyes. If they are became hbeag - and mutation and we are on the same strain / genotype does that put me at a higher risk for hbeag - with precor or be mutation?
Just talked to my mother and my uncles and they say they always have to take virals. I think they are hbeag - with mutation and once off virals hbv DNa starts to replicate fast. She told me after many test the doctor told her she could never be off virals. They are all on entcevir. One of my uncle has cirrhosis and was told he has 2 years max, about 5 years ago. He seems fine but i could see the yellow in his eyes. If they are became hbeag - and mutation and we are on the same strain / genotype does that put me at a higher risk for hbeag - with precor or be mutation?
Yes, you would be passed on the same genotype of HBV from your mother, most probably genotype B or C. All HBV infections, regardless of genotypes, would go through various phases, the most significant being from HBeAg positive to HBeAg negative, for example, most hbvers infected at birth, would be HBeAg negative by the age of 40. For some, they will transition from HBeAg-negative inactive to HBeAg-negative active. Whether you would follow your family's footstep and become HBeAg-negative active that requires treatment is not certain, as it is very much the result of interaction between the virus and your own host factors.
It is rather unusual for your mother and relatives to be on antiviral for over 10 years, for a small percentage of patients can be cured after long term treatment.
I agree, for HBV, the stigma is often worst than the disease itself.
It is rather unusual for your mother and relatives to be on antiviral for over 10 years, for a small percentage of patients can be cured after long term treatment.
I agree, for HBV, the stigma is often worst than the disease itself.
Stephen,
Thanks for responding. I hate this disease, my grandmother died from it my mother and my 2 uncles have it. They are all on long term virals since age 50 now 65, 63 and 61. If they are hbeag negative and on virals long term would I have the same mutation since we come from the same strain of hep b. I asked my mom if she knew anything about her hep b, but she says all she knows is that she has to take meds everyday. Since they are on long term meds and never seroconverted I must assume it is hbeag negative. Is my chance greater to follow there footsteps, treatment wise. The one thing I can proudly say about this disease that it stops here with me. My son got immunizied and I never wish this on anyone. I am lucky I am local Los Angeles and fibro scan is a 30 min drive. I do not see my doctor until the 24 of June, but he told me when I was 30 that by age 40 I might need to take meds, and at 37 here I am. We'll see.
Thanks for responding. I hate this disease, my grandmother died from it my mother and my 2 uncles have it. They are all on long term virals since age 50 now 65, 63 and 61. If they are hbeag negative and on virals long term would I have the same mutation since we come from the same strain of hep b. I asked my mom if she knew anything about her hep b, but she says all she knows is that she has to take meds everyday. Since they are on long term meds and never seroconverted I must assume it is hbeag negative. Is my chance greater to follow there footsteps, treatment wise. The one thing I can proudly say about this disease that it stops here with me. My son got immunizied and I never wish this on anyone. I am lucky I am local Los Angeles and fibro scan is a 30 min drive. I do not see my doctor until the 24 of June, but he told me when I was 30 that by age 40 I might need to take meds, and at 37 here I am. We'll see.
Hard to tell, I think it is too early to tell based on one increase. There are many reasons for slightly elevated ALT.. I think you should check your ALT and viral load again in a few months time. If you have an opportunity, you should have a Fibroscan, just as a baseline. I think you are HBeAg negative.
Just my opinion.
Just my opinion.
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