Aa
Cummulative Damage?
Any guesses on how much cummulative damage is being done to a liver with ALTs in the 22-69 range over 10 years (average about 41)? Very low viral load. E-negative. E-antibody +.
840. Is Liver Biopsy Required for All Patients (pts) with HBeAg-negative (HBeAg-) Chronic HBV Infection and HBV DNA <20,000 IU/mL?
840 seems to say "do liver biopsy and you will know more about your need for treatment." I guess another variable in the patient's confidence in the treatment. If the patient believes the treatment is effective, biopsy makes sense; if the patient thinks the treatment may not help much and brings with its own bag of headachs, then he/she may not benefit from biopsy.
515. Analyzing HBV-DNA in Liver Tissue for Investigation of Unexplained ALT Elevation in HBsAg Positive Patients with Undetectable Serum HBV-DNA
515. seems to be the same in emphasizing "don't delay treatment." My guess above applies here too: If there is a proven effective cure, then even without DNA testing or biopsy most patients will opt for treatment.
What do you think?
840 seems to say "do liver biopsy and you will know more about your need for treatment." I guess another variable in the patient's confidence in the treatment. If the patient believes the treatment is effective, biopsy makes sense; if the patient thinks the treatment may not help much and brings with its own bag of headachs, then he/she may not benefit from biopsy.
515. Analyzing HBV-DNA in Liver Tissue for Investigation of Unexplained ALT Elevation in HBsAg Positive Patients with Undetectable Serum HBV-DNA
515. seems to be the same in emphasizing "don't delay treatment." My guess above applies here too: If there is a proven effective cure, then even without DNA testing or biopsy most patients will opt for treatment.
What do you think?
concerned,
Could you start a new thread with your question, please. Thanks. More people will see it that way and it will prevent this thread from getting confusing.
Could you start a new thread with your question, please. Thanks. More people will see it that way and it will prevent this thread from getting confusing.
I am interested in finding out what is the average life expectancy of people having HBV?
I acquired the infection at an age of 29 years.....I am now 31 years old.....I am Hbeag -ve, Hbsag +ve, Anti Hbeag +ve, HBV load 3400 copies/ml
how bad does this look?
I acquired the infection at an age of 29 years.....I am now 31 years old.....I am Hbeag -ve, Hbsag +ve, Anti Hbeag +ve, HBV load 3400 copies/ml
how bad does this look?
Actually there were 2 who dealt with elevated ALT...one with elevated ALT w/UND viral load.
840. Is Liver Biopsy Required for All Patients (pts) with HBeAg-negative (HBeAg-) Chronic HBV Infection and HBV DNA <20,000 IU/mL?
and
515. Analyzing HBV-DNA in Liver Tissue for Investigation of Unexplained ALT Elevation in HBsAg Positive Patients with Undetectable Serum HBV-DNA
840. Is Liver Biopsy Required for All Patients (pts) with HBeAg-negative (HBeAg-) Chronic HBV Infection and HBV DNA <20,000 IU/mL?
and
515. Analyzing HBV-DNA in Liver Tissue for Investigation of Unexplained ALT Elevation in HBsAg Positive Patients with Undetectable Serum HBV-DNA
838. Histological Findings Of HBeAg-negative Chronic HBV -Infected Patients With Persistently Normal Serum Alanine Aminotransferase Levels
and
847. Future Hepatitis Activation and Hepatocarcinogenesis in HBeAg-Negative HBV Carriers with Persistently Normal Alanine Aminotransferase, a Prospective Cohort Study
Both suggest HBeAg（-）patients with normal ALT are not enough to be monitored only. On the other hand, there are many more HBeAg（-）patients with normal ALT (inactive carriers), 75%, who go through life normally. My thought is: if the treatment is known to be effective and has an end point, yes. Otherwise, not sure.
and
847. Future Hepatitis Activation and Hepatocarcinogenesis in HBeAg-Negative HBV Carriers with Persistently Normal Alanine Aminotransferase, a Prospective Cohort Study
Both suggest HBeAg（-）patients with normal ALT are not enough to be monitored only. On the other hand, there are many more HBeAg（-）patients with normal ALT (inactive carriers), 75%, who go through life normally. My thought is: if the treatment is known to be effective and has an end point, yes. Otherwise, not sure.
Thanks for all of the great comments so far. Any thoughts on these new studies:
http://www.hbvadvocate.org/news/reports/HBV_AASLD_2008/Abstracts/Nov2%20Disease%20Progression.htm#Nov2a840
http://www.hbvadvocate.org/news/reports/HBV_AASLD_2008/Abstracts/AASLD%20HBV%20Nov%201.htm#HB515
http://www.hbvadvocate.org/news/reports/HBV_AASLD_2008/Abstracts/Nov2%20Disease%20Progression.htm#Nov2a840
http://www.hbvadvocate.org/news/reports/HBV_AASLD_2008/Abstracts/AASLD%20HBV%20Nov%201.htm#HB515
What is the evidence that the following population characteristics or clinical features associated with hepatitis B are predictive of hepatocellular carcinoma, liver failure, cirrhosis, liverrelated death, and all-cause mortality?
Chronic carriers of HBsAg had substantially higher rates of hepatocellular carcinoma, cirrhosis, and death than people who have never been chronically HBsAg-positive. The annual incidence of hepatocellular carcinoma (HCC) was only 0.1 percent in asymptomatic HBsAg individuals, 1 percent in patients with CHB, but increased to 3-10 percent in patients with cirrhosis. Patients with CHB developed cirrhosis at a rate of 2 percent per year. Reports have shown large differences in clinical event rates across diagnostic groups such as inactive HBsAg carriers, CHB without cirrhosis, and CHB with cirrhosis. A U.S. cohort study followed 400 HBsAg patients (70 percent born in Asia) for over 7 years. Among 110 inactive carriers, none developed HCC or died of a liver-related disease, and only one died of any cause. Among patients with CHB but no cirrhosis, 6 percent developed HCC and died from it, while another 2 percent died from nonliver related causes. Among those with CHB and cirrhosis, 16 percent were diagnosed with HCC and 42 percent died during followup (all from liver-related causes).
Cirrhosis is a strong predictor of HCC and death. Increased HBV deoxyribonucleic acid (DNA) viral load was strongly associated with increased HCC and liver-related mortality after accounting for baseline cirrhosis, HBeAg status, and ALT levels. There was no evidence regarding whether reduction in HBV DNA viral load was associated with better outcomes. HBV genotypes may be associated with differing risk of clinical outcomes. HBsAg loss was associated with a reduction in risk of cirrhosis, but data were sparse. There was no evidence as to whether HBsAg loss was associated with other improved outcomes. HBeAg-positive status was associated with poorer outcomes independent of other disease factors. Reversion or multiple switches in HBeAg status was associated with increased HCC; however, the mechanism of this is unclear. Basal core promoter mutations (T1762/A1764) and the precore (PC) mutation (A1896) were associated with increased HCC and basal core promoter mutations may be associated with small increases in liver-related death rates. ALT was modestly associated with associated with increased risk of HCC and cirrhosis after accounting for baseline cirrhosis, HBeAg status and HBV viral load.
from "Management of Chronic Hepatitis B"，Number 174，prepared by Minnesota Evidence-based Practice Center, Minneapolis, Minnesota for Agency for Healthcare Research and Quality, U.S. Department of Health and Human Services.
Chronic carriers of HBsAg had substantially higher rates of hepatocellular carcinoma, cirrhosis, and death than people who have never been chronically HBsAg-positive. The annual incidence of hepatocellular carcinoma (HCC) was only 0.1 percent in asymptomatic HBsAg individuals, 1 percent in patients with CHB, but increased to 3-10 percent in patients with cirrhosis. Patients with CHB developed cirrhosis at a rate of 2 percent per year. Reports have shown large differences in clinical event rates across diagnostic groups such as inactive HBsAg carriers, CHB without cirrhosis, and CHB with cirrhosis. A U.S. cohort study followed 400 HBsAg patients (70 percent born in Asia) for over 7 years. Among 110 inactive carriers, none developed HCC or died of a liver-related disease, and only one died of any cause. Among patients with CHB but no cirrhosis, 6 percent developed HCC and died from it, while another 2 percent died from nonliver related causes. Among those with CHB and cirrhosis, 16 percent were diagnosed with HCC and 42 percent died during followup (all from liver-related causes).
Cirrhosis is a strong predictor of HCC and death. Increased HBV deoxyribonucleic acid (DNA) viral load was strongly associated with increased HCC and liver-related mortality after accounting for baseline cirrhosis, HBeAg status, and ALT levels. There was no evidence regarding whether reduction in HBV DNA viral load was associated with better outcomes. HBV genotypes may be associated with differing risk of clinical outcomes. HBsAg loss was associated with a reduction in risk of cirrhosis, but data were sparse. There was no evidence as to whether HBsAg loss was associated with other improved outcomes. HBeAg-positive status was associated with poorer outcomes independent of other disease factors. Reversion or multiple switches in HBeAg status was associated with increased HCC; however, the mechanism of this is unclear. Basal core promoter mutations (T1762/A1764) and the precore (PC) mutation (A1896) were associated with increased HCC and basal core promoter mutations may be associated with small increases in liver-related death rates. ALT was modestly associated with associated with increased risk of HCC and cirrhosis after accounting for baseline cirrhosis, HBeAg status and HBV viral load.
from "Management of Chronic Hepatitis B"，Number 174，prepared by Minnesota Evidence-based Practice Center, Minneapolis, Minnesota for Agency for Healthcare Research and Quality, U.S. Department of Health and Human Services.
Your comments were quite fine, so don't blame your wife and enjoy your tennis.
You are quite right that the liver is accomadating and regenerating. As long as we do not overstretch it, it does not even need to use its full capacity to give us a full life.
You are quite right that the liver is accomadating and regenerating. As long as we do not overstretch it, it does not even need to use its full capacity to give us a full life.
I guess “perfectly healthy” is a relative term. While nothing is ever perfect or 100% when dealing with nature, I would say that medically speaking, a biopsy result of stage 0 grade 0 is as close to “perfectly healthy” as you can get.
My guess is that most of the damage done to the liver of someone with HBV occurs in the active stage of the disease. As long the damage was minimal while in the active stage of the disease, the liver should start to heal in the inactive stage and may even return to a level that a biopsy would not show any damage or inflammation.
I would think that liver of anyone who is an inactive carrier and lives a liver friendly lifestyle is no worse off and may even be better off than the liver of the “average” person, especially when you consider how the average person without a chronic disease usually doesn’t pay as much attention to how they treat their bodies as someone with a chronic disease might.
I hope my previous post didn’t make it sound like I was saying that someone with HBV cannot have as healthy of a liver or live the healthy life of someone without HBV……I actually meant that there can be no difference and that if you if you take someone in the inactive carrier state of HBV and the average person who has never had HBV and gave both people a biopsy, the results could easily show the same thing if the inactive carriers liver has had time to regenerate and heal from any damage that may have occurred while in the active state of the disease. The liver is truly an amazing organ in the way that it can start to heal itself if given the chance, and the inactive phase of HBV can provide such a chance.
I was feeling rushed when during my previous post and may not have phrased it very clearly. My wife was giving me that look as if to say, “Hurry up and get of the computer so we can go play tennis”. Can’t really blame her….it is a beautiful day here and I needed the exercise.
My guess is that most of the damage done to the liver of someone with HBV occurs in the active stage of the disease. As long the damage was minimal while in the active stage of the disease, the liver should start to heal in the inactive stage and may even return to a level that a biopsy would not show any damage or inflammation.
I would think that liver of anyone who is an inactive carrier and lives a liver friendly lifestyle is no worse off and may even be better off than the liver of the “average” person, especially when you consider how the average person without a chronic disease usually doesn’t pay as much attention to how they treat their bodies as someone with a chronic disease might.
I hope my previous post didn’t make it sound like I was saying that someone with HBV cannot have as healthy of a liver or live the healthy life of someone without HBV……I actually meant that there can be no difference and that if you if you take someone in the inactive carrier state of HBV and the average person who has never had HBV and gave both people a biopsy, the results could easily show the same thing if the inactive carriers liver has had time to regenerate and heal from any damage that may have occurred while in the active state of the disease. The liver is truly an amazing organ in the way that it can start to heal itself if given the chance, and the inactive phase of HBV can provide such a chance.
I was feeling rushed when during my previous post and may not have phrased it very clearly. My wife was giving me that look as if to say, “Hurry up and get of the computer so we can go play tennis”. Can’t really blame her….it is a beautiful day here and I needed the exercise.
Who has a perfectly healthy liver? Does such a liver exist? Even with some and fibrosis, 75% of intactive carrier live a perfectly healthy life like the non-HBV folks:
Some patients who are HBsAg-positive have persistently low or undetectable HBV DNA and no elevation in serum ALT. These patients, referred to as inactive carriers, have little or no active viral replication. They are generally HBeAg-negative and anti-HBe-positive.
After seroconversion, most patients remain negative for HBeAg and positive for anti-HBe antibody. Seroconversion is usually accompanied by stabilization of hepatitis, characterized by normalization of ALT levels and decreases in HBV DNA to low (<1000 copies/mL) or undetectable levels, depending on the assays used. This condition is commonly referred to as the “inactive carrier state.” Histologically, minimal to mild hepatitis may be observed, although the degree of fibrosis may be variable. For example, inactive cirrhosis may be identified in patients who had severe liver injury before seroconversion. Most patients remain in this phase for many years, if not indefinitely.
Some patients who are HBsAg-positive have persistently low or undetectable HBV DNA and no elevation in serum ALT. These patients, referred to as inactive carriers, have little or no active viral replication. They are generally HBeAg-negative and anti-HBe-positive.
After seroconversion, most patients remain negative for HBeAg and positive for anti-HBe antibody. Seroconversion is usually accompanied by stabilization of hepatitis, characterized by normalization of ALT levels and decreases in HBV DNA to low (<1000 copies/mL) or undetectable levels, depending on the assays used. This condition is commonly referred to as the “inactive carrier state.” Histologically, minimal to mild hepatitis may be observed, although the degree of fibrosis may be variable. For example, inactive cirrhosis may be identified in patients who had severe liver injury before seroconversion. Most patients remain in this phase for many years, if not indefinitely.
I’ll offer up a guess and a theory without being absolutely sure.
I would guess that VERY minimal damage would have occurred over that time period with those results.
Since the liver is capable of regeneration, I would suspect that while some damage may have occorred, there is ALSO some healing occurring. I would think that if a biopsy had been done at year 1 and then another biopsy at year 10, there would more than likely be NO change on the stage or grade of the bx.
When I had my bx done, it was Stage 2 and Grade 2. My doctor told me that when I clear HCV and get HBV under control, that my liver condition could improve to Stage1, Grade 1, but would probably never improve all the way back to a perfectly healthy liver status of Stage0 Grade0. But I think that someone with chronic HBV can have a bx result of Stage 0 as long as the Stage never reached past stage 1. I think it may have something to do with stage 2 having some fibrosis that makes it harder for the liver to heal completely. This is my take on it anyway.
I would guess that someone with HBV that has those results and that eats right and avoids alcohol or any unneeded medication, may not have the liver of a person who lives a healthy lifestyle and doesn’t have HBV, but they probably don’t receive much, if any more damage than someone who does not have HBV and eats fast food and drinks alcohol on a fairly regular basis…..if that made any sense.
So to sum up my guess:
Very minimal if any permanent damage with those results and time frame and no change on a biopsy if it had been performed and the beginning and end of that time frame.
I would guess that VERY minimal damage would have occurred over that time period with those results.
Since the liver is capable of regeneration, I would suspect that while some damage may have occorred, there is ALSO some healing occurring. I would think that if a biopsy had been done at year 1 and then another biopsy at year 10, there would more than likely be NO change on the stage or grade of the bx.
When I had my bx done, it was Stage 2 and Grade 2. My doctor told me that when I clear HCV and get HBV under control, that my liver condition could improve to Stage1, Grade 1, but would probably never improve all the way back to a perfectly healthy liver status of Stage0 Grade0. But I think that someone with chronic HBV can have a bx result of Stage 0 as long as the Stage never reached past stage 1. I think it may have something to do with stage 2 having some fibrosis that makes it harder for the liver to heal completely. This is my take on it anyway.
I would guess that someone with HBV that has those results and that eats right and avoids alcohol or any unneeded medication, may not have the liver of a person who lives a healthy lifestyle and doesn’t have HBV, but they probably don’t receive much, if any more damage than someone who does not have HBV and eats fast food and drinks alcohol on a fairly regular basis…..if that made any sense.
So to sum up my guess:
Very minimal if any permanent damage with those results and time frame and no change on a biopsy if it had been performed and the beginning and end of that time frame.
A liver biopsy should not be done unless absolutely necessary, certainly not done as a routine. After all, it is an invasive procedure that takes a tiny piece of liver out of you.
i'm almost where Zelly is
doctor plans to do a biopsy in march to be sure.
all signs leads to an inactive state but one never knows
i had an ultra sound done ( for the first time) two months ago and it came back normal.
i think a biopsy will kind of give me a peace of mind.
how often should i get a biopsy done ? anyone ?
doctor plans to do a biopsy in march to be sure.
all signs leads to an inactive state but one never knows
i had an ultra sound done ( for the first time) two months ago and it came back normal.
i think a biopsy will kind of give me a peace of mind.
how often should i get a biopsy done ? anyone ?
I don't think there is any set equation to compute cummulative damage. The only way to know for sure is a biopsy.
But I think chances are that it's not that bad. From my personal experience, dating back to my earliest lab (1999) that I kept records of (before being diagnosed), my labs probably averaged in the low 50's. As a male, it should really be in the low to mid 20's. So that's a good 7 years of cummulative damage before I knew anything. But all sonograms thus far said liver look normal (knock on wood). So I and my doctors think it should be okay, which I know can't be confirmed unless a biopsy is done. But I try to take it one step at a time and not read too much into it. So far so good. I suspect for you as well.
But I think chances are that it's not that bad. From my personal experience, dating back to my earliest lab (1999) that I kept records of (before being diagnosed), my labs probably averaged in the low 50's. As a male, it should really be in the low to mid 20's. So that's a good 7 years of cummulative damage before I knew anything. But all sonograms thus far said liver look normal (knock on wood). So I and my doctors think it should be okay, which I know can't be confirmed unless a biopsy is done. But I try to take it one step at a time and not read too much into it. So far so good. I suspect for you as well.
The word is "cumulative". I know that. I was testing everyone else. ;-)
cajim, will get back after I hold out for a few more thoughts from others.
cajim, will get back after I hold out for a few more thoughts from others.
Could it be that ALTs are results of damage to liver cells by immune system trying to fight HBV? As a result, ALTs do not damage the liver. Further, elevated ALTs sometimes are related to what is eaten rather than the stable status of the liver. 41 for ALT seems to be closer to normal than abnormal. When I read the many lab posts on ****.***, the concerned ALTs are at least above 68, many are in hundreds.
Personally I think the picture presented is more like that of an inactive carrier rather than one that warrants worry. What's your opinion?
Personally I think the picture presented is more like that of an inactive carrier rather than one that warrants worry. What's your opinion?
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