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Liver Fibrosis Develops Early, Progresses Quickly After HCV Seroconversion
From Medscape:
Liver Fibrosis Develops Early, Progresses Quickly After Hepatitis C Virus Seroconversion
By Will Boggs MD, December 14, 2014
Liver fibrosis develops early after hepatitis C virus (HCV) seroconversion and progresses quickly to cirrhosis in many patients, according to new findings.
"Within 10 years of HCV infection, about 18% have developed cirrhosis, and this is 3 times higher than controls," Dr. Adeel A. Butt from University of Pittsburgh School of Medicine in Pennsylvania told Reuters Health by email. "Most of this occurs within the first 5 years after infection."
Dr. Butt and colleagues used the Electronically Retrieved Cohort of HCV Infected Veterans (ERCHIVES) to identify 1,840 patients who seroconverted to HCV antibody and then to determine their rate of liver fibrosis progression, compared with 1,840 matched controls who remained HCV antibody-negative.
They plotted the FIB-4 score, which provides an estimation of the degree of liver fibrosis based on routinely obtained blood tests, over time. A FIB-4 score greater than 3.5 indicates cirrhosis.
FIB-4 score progression started early after seroconversion, was most pronounced within the first five years, and continued over a period of 11 years. Progression was consistently higher among HCV-positive patients than among HCV-negative patients, the researchers report in JAMA Internal Medicine, online December 8.
In the HCV-positive group, 18.4% of patients went on to develop cirrhosis, compared with only 6.1% in the HCV-negative group, and the HCV-positive patients had a significantly shorter time to development of liver cirrhosis.
By five years, more than 15% of HCV-positive patients had a diagnosis of cirrhosis, compared with less than 5% of HCV-negative controls.
Only 3.1% of patients in the HCV-positive group developed hepatic decompensation (compared with 1.4% of HCV-negative patients), but their time to first hepatic decompensation was significantly shorter than it was for HCV-negative patients. More than half of the hepatic decompensation events occurred within the first two years of diagnosis of cirrhosis.
Factors associated with a higher risk of cirrhosis among HCV-positive patients included increasing age, white race, hypertension, history of alcohol abuse or dependence, and anemia. Diabetes, hypertension, and anemia were associated with a higher risk of developing hepatic decompensation.
"Future studies should look at a risk prediction model to determine which characteristics most accurately predict future cirrhosis in a given individual," Dr. Butt said. "Contrary to popular thought, a significant proportion of hepatic decompensation occurs without prior diagnosis of cirrhosis. Hence careful follow-up and evaluation for hepatic decompensation should be carried out in all HCV-infected persons regardless of duration of infection and prior diagnosis of cirrhosis."
"If newer treatments demonstrate slowing or reversal of fibrosis progression and delaying development of cirrhosis, our data would suggest treating early in the course of infection," the authors conclude. "On the other hand, if the cirrhosis has already set in, treatment may be helpful in preventing hepatic decompensation in only a small number of those with cirrhosis, since the number who go on to develop this complication is small."
Dr. Marc G. Ghany from the National Institute of Diabetes and Digestive and Kidney Diseases in Bethesda, Maryland, addressed the ongoing debate of whom to treat for chronic HCV in a related editorial.
"All patients with chronic HCV infection should be considered candidates for therapy, and mild liver disease is not a reason to deny a patient therapy who otherwise qualifies for treatment," he told Reuters Health by email.
But treatment is expensive, with costs ranging from $66,000 for 12 weeks of treatment with simeprevir to $84,000 for 12 weeks of treatment with sofosbuvir.
"The hope is that with the approval of other regimens, competition will drive down costs," Dr. Ghany said. "It remains to be seen how much cheaper the drugs will become, but it is unlikely in the near future that costs will decrease to the point where we will be able to treat everyone who is infected with hepatitis C virus."
"We still have to identify the large number of people who are unaware of their diagnosis and get them into care, including counseling on measures to prevent transmission, disease progression, and treatment," he concluded.
"This kind of study should remind physicians about the importance of non-viral, modifiable factors of accelerated liver fibrosis progression," Dr. Francesco Negro from Geneva University Hospital in Switzerland, who has published extensively on HCV infection, told Reuters Health. "One may think that treating HCV with antivirals may be the end of the story, thus forgetting about the formidable impact of alcohol drinking, cannabis smoking, and the metabolic syndrome. The VA population is particularly vulnerable in this respect."
"That their progression seemed to slow down once the diagnosis of cirrhosis was made suggests (although other explanations may be possible) that these persons became aware of the severity of their liver disease and tried to adopt a healthier lifestyle," said Dr. Negro, who was not involved in the research. "If this is true, our job should be to avoid reaching the cirrhotic stage, a stage when the risk of developing liver cancer may be hard to eliminate completely."
"We still have a lot of things to learn regarding the pathophysiology of hepatitis C," he said.
Liver Fibrosis Develops Early, Progresses Quickly After Hepatitis C Virus Seroconversion
By Will Boggs MD, December 14, 2014
Liver fibrosis develops early after hepatitis C virus (HCV) seroconversion and progresses quickly to cirrhosis in many patients, according to new findings.
"Within 10 years of HCV infection, about 18% have developed cirrhosis, and this is 3 times higher than controls," Dr. Adeel A. Butt from University of Pittsburgh School of Medicine in Pennsylvania told Reuters Health by email. "Most of this occurs within the first 5 years after infection."
Dr. Butt and colleagues used the Electronically Retrieved Cohort of HCV Infected Veterans (ERCHIVES) to identify 1,840 patients who seroconverted to HCV antibody and then to determine their rate of liver fibrosis progression, compared with 1,840 matched controls who remained HCV antibody-negative.
They plotted the FIB-4 score, which provides an estimation of the degree of liver fibrosis based on routinely obtained blood tests, over time. A FIB-4 score greater than 3.5 indicates cirrhosis.
FIB-4 score progression started early after seroconversion, was most pronounced within the first five years, and continued over a period of 11 years. Progression was consistently higher among HCV-positive patients than among HCV-negative patients, the researchers report in JAMA Internal Medicine, online December 8.
In the HCV-positive group, 18.4% of patients went on to develop cirrhosis, compared with only 6.1% in the HCV-negative group, and the HCV-positive patients had a significantly shorter time to development of liver cirrhosis.
By five years, more than 15% of HCV-positive patients had a diagnosis of cirrhosis, compared with less than 5% of HCV-negative controls.
Only 3.1% of patients in the HCV-positive group developed hepatic decompensation (compared with 1.4% of HCV-negative patients), but their time to first hepatic decompensation was significantly shorter than it was for HCV-negative patients. More than half of the hepatic decompensation events occurred within the first two years of diagnosis of cirrhosis.
Factors associated with a higher risk of cirrhosis among HCV-positive patients included increasing age, white race, hypertension, history of alcohol abuse or dependence, and anemia. Diabetes, hypertension, and anemia were associated with a higher risk of developing hepatic decompensation.
"Future studies should look at a risk prediction model to determine which characteristics most accurately predict future cirrhosis in a given individual," Dr. Butt said. "Contrary to popular thought, a significant proportion of hepatic decompensation occurs without prior diagnosis of cirrhosis. Hence careful follow-up and evaluation for hepatic decompensation should be carried out in all HCV-infected persons regardless of duration of infection and prior diagnosis of cirrhosis."
"If newer treatments demonstrate slowing or reversal of fibrosis progression and delaying development of cirrhosis, our data would suggest treating early in the course of infection," the authors conclude. "On the other hand, if the cirrhosis has already set in, treatment may be helpful in preventing hepatic decompensation in only a small number of those with cirrhosis, since the number who go on to develop this complication is small."
Dr. Marc G. Ghany from the National Institute of Diabetes and Digestive and Kidney Diseases in Bethesda, Maryland, addressed the ongoing debate of whom to treat for chronic HCV in a related editorial.
"All patients with chronic HCV infection should be considered candidates for therapy, and mild liver disease is not a reason to deny a patient therapy who otherwise qualifies for treatment," he told Reuters Health by email.
But treatment is expensive, with costs ranging from $66,000 for 12 weeks of treatment with simeprevir to $84,000 for 12 weeks of treatment with sofosbuvir.
"The hope is that with the approval of other regimens, competition will drive down costs," Dr. Ghany said. "It remains to be seen how much cheaper the drugs will become, but it is unlikely in the near future that costs will decrease to the point where we will be able to treat everyone who is infected with hepatitis C virus."
"We still have to identify the large number of people who are unaware of their diagnosis and get them into care, including counseling on measures to prevent transmission, disease progression, and treatment," he concluded.
"This kind of study should remind physicians about the importance of non-viral, modifiable factors of accelerated liver fibrosis progression," Dr. Francesco Negro from Geneva University Hospital in Switzerland, who has published extensively on HCV infection, told Reuters Health. "One may think that treating HCV with antivirals may be the end of the story, thus forgetting about the formidable impact of alcohol drinking, cannabis smoking, and the metabolic syndrome. The VA population is particularly vulnerable in this respect."
"That their progression seemed to slow down once the diagnosis of cirrhosis was made suggests (although other explanations may be possible) that these persons became aware of the severity of their liver disease and tried to adopt a healthier lifestyle," said Dr. Negro, who was not involved in the research. "If this is true, our job should be to avoid reaching the cirrhotic stage, a stage when the risk of developing liver cancer may be hard to eliminate completely."
"We still have a lot of things to learn regarding the pathophysiology of hepatitis C," he said.
Best Answer
Goes back to what I said about who did the study, what theyhought they were measuring, what their control group and test group patients and their histories were, etc! etc., etc., There are studies and then studies. Not all all done accurately or taking into account and allowing for all variables.
Example, Many many years ago when I was taking a statistics class, we read a study that flatly stated that Entry level Women wore much higher heels than upper management women. Well, duh!, No ajdustments for age, education, job requirements, etc. Any woman , and most men could have told them that and saved the cost of the study.
Example, Many many years ago when I was taking a statistics class, we read a study that flatly stated that Entry level Women wore much higher heels than upper management women. Well, duh!, No ajdustments for age, education, job requirements, etc. Any woman , and most men could have told them that and saved the cost of the study.
There's something here I'm not getting at all. The control group does not have the virus right? Or did they have it and achieve SVR? But then they would still have the antibodies and it says the control group is HCV antibody negative.
Why would any of the control group develop fibrosis/cirrhosis at all? Are there drinkers in the group? If so how come this is not mentioned? They talk about alcohol abuse in the HCV positive group, but not the control group. Also how do they know the exact time of seroconversion of the study group? Did they inoculate them or something? (I of course realize this is not the case)
It doesn't take a rocket scientist to figure that everyone with the virus should be treated and the sooner is better than later when irreversible damage has set in. This whole thing about only treating the sickest patients is just plain wrong, both scientifically and morally.
Why would any of the control group develop fibrosis/cirrhosis at all? Are there drinkers in the group? If so how come this is not mentioned? They talk about alcohol abuse in the HCV positive group, but not the control group. Also how do they know the exact time of seroconversion of the study group? Did they inoculate them or something? (I of course realize this is not the case)
It doesn't take a rocket scientist to figure that everyone with the virus should be treated and the sooner is better than later when irreversible damage has set in. This whole thing about only treating the sickest patients is just plain wrong, both scientifically and morally.
I don't buy it at all. First, how do they know when seroconversion occurs for each person in the group. Second, they are using a lesser accurate (blood test) to determine cirrhosis progress. Third, it seems like the VA is involved for God's sake.
"Fibrosis
"If left untreated, the inflamed liver will start to scar. As excess scar tissue grows, it replaces healthy liver tissue. This process is called fibrosis. (Scar tissue is a kind of fibrous tissue.)
Scar tissue cannot do the work that healthy liver tissue can. Moreover, scar tissue can keep blood from flowing through your liver. As more scar tissue builds up, your liver may not work as well as it once did. Or, the healthy part of your liver has to work harder to make up for the scarred part.
If your liver disease is diagnosed and treated successfully at this stage, there’s still a chance that your liver can heal itself over time."
There is a difference.
----------------------------------------
Worriedmom
" She went from late stage 3 to stage 0-1 in 5 years of successful treatment."
Late stage 3 would be what's called borderline or "early" so no surprise there was healing.
"If left untreated, the inflamed liver will start to scar. As excess scar tissue grows, it replaces healthy liver tissue. This process is called fibrosis. (Scar tissue is a kind of fibrous tissue.)
Scar tissue cannot do the work that healthy liver tissue can. Moreover, scar tissue can keep blood from flowing through your liver. As more scar tissue builds up, your liver may not work as well as it once did. Or, the healthy part of your liver has to work harder to make up for the scarred part.
If your liver disease is diagnosed and treated successfully at this stage, there’s still a chance that your liver can heal itself over time."
There is a difference.
----------------------------------------
Worriedmom
" She went from late stage 3 to stage 0-1 in 5 years of successful treatment."
Late stage 3 would be what's called borderline or "early" so no surprise there was healing.
I agree I think one should treat as soon as possible, with the new drugs. The only reason I think I had it for 30 years was because I was given an injection of a blood product back in 77, gama globulin. I was exposed to Hepatitis and the doctor thought it would help my immune system :)
Is there anyway to tell exactly how long someone has had hepatitis C? Because it my understanding is for the most part people don't know. Except maybe if from a documented blood transfusion where infection was proven.
Or a documented accident where the hepatitis C factor was known.
This watchful waiting after you find out you have hepatitis C seems like a gamble. There are so many variables in how fast hepatitis C can advance once your infected. Lifestyle, general health, your own chemistry could change how fast hepatitis C advances over the years. So a study of any kind is going to be difficult to show accurate results.
Do I think you should treat your hepatitis C as soon as you find out at any stage. Yes! The sooner the better.
Or a documented accident where the hepatitis C factor was known.
This watchful waiting after you find out you have hepatitis C seems like a gamble. There are so many variables in how fast hepatitis C can advance once your infected. Lifestyle, general health, your own chemistry could change how fast hepatitis C advances over the years. So a study of any kind is going to be difficult to show accurate results.
Do I think you should treat your hepatitis C as soon as you find out at any stage. Yes! The sooner the better.
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Being cirrhotic this really jumped out at me.
"On the other hand, if the cirrhosis has already set in, treatment may be helpful in preventing hepatic decompensation in only a small number of those with cirrhosis, since the number who go on to develop this complication is small."
Not only is he saying its still possible to go on to decompensation but not a damn word on reversing cirrhosis. Which I already knew.