oops i mean Tenofovir alafenamide
hopefully when truvada comes out it will be easier on the kidneys and better chance for peg add on.
etv has nothing close to an hbsag decline to less than 1000iu/ml by 5 years if not a very very small percentage of patients.your parents should check hbsg but it is not 10 years of etv, they used adv without response for years which is like no therapy for hbsag decline
Since my mom and uncles are going on ETV close to 10 years are they able to gain hbsab +. Will the T cells learn how to gain immunity. I read somewhere that some say tenofovir is a certain amount of years and etv takes a certain amount of years. I wonder how reliable this is.
you also have to consider the food, the deficiencies like vit d deficiency
if not eating organic you can easily get liver cancer from chemicals and pesticides in food
Stephen i'm just commenting on the information that hepbcure posted that his uncle was on entecavir since 2005 so you are correct 9 years on entecavir and then he developed hcc in 2014
Entecavir was only approved by FDA in 2005 (10 years ago), so it would be available in China for less than 10 years.
You don't need to have Hepatitis B or cirrhosis to develop HCC.
Stef you might need to comment on his uncle who get hcc without cirrhosis although he was on entecavir for 15 years. That is interesting
I think the answer to all the questions is one because we have only one way control the infection and try to clear it
entecavir as soon as possible is the first thing, try to get hbsag quant if possible before starting or right after
check vitamin d and intact pth, vit d must be optimized because it can prevent more than 50% cases of hcc and other cancers according to many studies
Check oxidative stress and if abnormal use liposmals to correct it
after many years on etv hbsag may lower, in case it gets less than 1000-1500iu pegintf add on is the only way we have now to go to very low levels of hbsag or clear
Very interesting i will write you also my little story result
Thats good that you are on top of it. I had a US that showed mild imhomogeneous liver and enlarged at 12.4 cm with a a kidney stone. I went to a urologist and he ordered a abdominal CT scan. The abdominal CT scan showed no enlarged liver and normal w/o fatty liver and no longer a kidney stone. I was wondering what the heck is going on. I usually drink 3 liters of water a day, so i was very shock when there was a kidney stone in US. My mother and grandfather had a kidney stone, so I was started drinking a lot of water before. Anyways now I have contradicting results on liver from CT scan and US. My hep doc thinks its fatty liver because I am overweight with a bmi of 28. Working on that currently.
Ya i went to my physical doctor to order ultrasound and same result as last year and 2011 mild coarsened liver. Fibroscan looks ok at 4.8 kpa when it was a year before at 7.6 kpa my viral load fluctuate between 15000 iu and 300 iu monthly so go figure
US is a must every 6 months. If my uncle never had US he would be dead. I think Genotype and mutations are important also, if you are bcp mutation wouldn't you want to US every 6 months. When I walked into my docs office my first test was hbeag , hbv dna, genotype (since i had viral load) and mutation and US. Your doctor being who she is puzzles me. The story that is always sad was about Dr. Mark Lim. No testing and ignorant doctors on hep b. He was a inactive carrier and passed at 32 with HCC. If he had US early maybe he would of had a chance.
Ya she doesnt even run ultrasound as she thinks im still young although my last ultrasound say mild coarsened liver but it isnt concerning her. Also im genotype D and when i asked her for mutation test she said no medical need for it
the overall goal is to get antibodies, but if that is not achievable we would like to avoid hcc. studies have shown bcp mutations, male , genotype c / d , 1st degree relatives make hcc risk high. i currently have 3/4 and the 4th one I have a 2nd degree relative. Do you know your genotype and mutations? I recall reading your post that dr anna lok was your hep doc, so you are in good hands.
Thanks for all the good info unfortunately i can't tell in my situation as im the only lucky one to carry hbv since birth
Grandmother was never treated for hep b, we were unaware at the time until she passed.
My grandmother passed at the age or 73. She had portal hypertension aneurism. She was exercising by her house and suddenly the aneurism erupted. When we found her and sent her to the hospital she had already passed. Up to that point she showed no signs of jaundice. the only thing was her skin was itchy few weeks before she passed.
Sorry, I read the article again...it's 6 families total.
Very good information you gave us all, since many of us do not have that family history of HBV like you do. How old was your grandma when she passed? It doesn't sound like she was ever monitored or treated for her HBV, or am I wrong?
Since you have the family history you may find this article interesting (even though it's dated), as it tracked 5 HBV families, 4 families treated with antivirals and one that was not.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2374938/
Here is a little family history and as much that I can gather from them when I speak to them and my mom. We are chinese decent and sometimes chinese people like to downplay there sickness , they dont want people to look down on them.
1998 - Grandmother passed away from portal hypertension aneurism. Doctor told us that had hep b and cirrhosis
1999 - family members tested for hepatitis b, 3 / 4 children from grandmother were hep bsag +. One of the children were very lucky had antibodies.
2000 - 2002 - not exactly sure the time line but 2 uncles started nucs i think 1 was even on lam not 100% sure though, but I know both were on hespera. I asked them about hbeag + or neg when started but they dont know. Only thing they know was DNA tested and extremely high. I would have to say my uncles based on there age 48 and 46 more than likely hbeag - and reactivation. The one with cirrhosis I would have to guess maybe never seroconv to hbeag - thus the heavy damage from cirrhosis at 48.
2003 - my mother started on hespera and she could not clear und dna with it. uncle with cirrhosis told me he was resistant to hesp and dna never got under 10000 to 12000.
2005 - I know my mom switched to entec and so did my uncles. Everything was pretty quiet until 2014. Uncle with cirrhosis had pretty bad cirrhosis, they said about 40% of liver or more has hardened.
2014 - younger uncle discovered mass on liver via ultrasound then mri revealed mass doubled in size from 7m m to 1.5mm. Chemoebolization done, my mother said it has been close to 1 year and no return.
2015 - my mother has multiple liver cyst as ultrasound report. So far no mass mri shows the liver cyst has not grown. She is monitoring every 6 moths mri now.
In 2009 I was an inactive carrier dna under not detectable by pcr and ast and alt normal. In 2012 my alt raised to 46 but it was confirmed I have fatty liver. I havent been really keeping up until this year, but this year I ran my dna and it was 220iu/ml in may. It jumped to 5190 iu/ml 1 month later. I ran a genotype test and mutation test. I am genotype C and have bcp / pc mutation. My liver specialist said that I need treatment right away becuase of 2nd degree relative with hcc. He told me bcp mutation and genotype c have highter chance of hcc. We were talking about if muts were transferable he said I had a high chance of getting bcp from genetics. Thus my uncle hcc without cirrhosis. My hep doc is well known, UCLA liver director and many studies on his behalf. Myron Tong. He wanted me on tenofovir but with bad kidneys he wanted me to start entec right away only because of the hcc 2nd degree relative.
Chances of hcc without cirrhosis supposed to be low. Im interested tonknow his eag status and viral load as he was on entecavir for almost 15 years. When was he diagnosed with hcc? As you can see i'm statistical person and try to analyze all the data. Im 38 years old just like you but im in no medication
also uncle with hcc had chemoebolization and so far so good. liver is soft and no cirrhosis. chance of hcc and no cirrhosis is very scary to think about. he also told me his afp only went to 90. scary thought. his hcc went from 7mm to 1.5cm in 6 months.
I also know my mother and uncle with hcc had hespera resistance. that is why they switched to entecavir. my mother told me and my uncle told me hespera could not get the dna to und