I acquired hep c in 1984. Had just one biopsy done in 2000 and it showed Grade 2/Stage 2. Drs believe I am cirrhotic now due to Splenomegaly and liver hypertension. I did drink, but not very much. Rarely eat red meat.
52baddog said
Aug 12, 2012
Hi Uval:
I thought you had a biopsy done, isn't biopsy more accurate than fibroscan. They don't have firbroscan in Texas.
So, most doctors recommend biopsy, which is more accurate.
hrsetrdr said
Aug 12, 2012
mallani wrote:
There is no set time frame. It will be quicker if you drink alcohol. In my case I went from Stage 0-1 in 1990 to Stage 3-4 in 1998. By Fibroscan I was cirrhotic (Stage 4) by 2007. So that's about 17 years. The fatty liver in obese patients also accelerates the progression.
So, don't drink, keep your weight normal and eat a healthy diet. Cheers.
So true Malcolm, that's actually great advice for people without liver diseases,as well. My remaining challange is to shed my excess weight and keep it off, as I am trying to dodge the bullet(statistically) and avoid:
1.fatty liver(and all that entails)
2.heart disease
3. vascular disease
4. stroke
5.premature death
6. ? I'm sure that there's something I've missed.
Maggie C said
Aug 12, 2012
My first biopsy was 25 years with the virus. I was then at stage 1. Now, 10 years later, I am diagnosed as stage 3 fibrosis moving into stage 4 cirrhosis after 35 years with the virus. I am about to begin treatment. I am genotype 1. The doctors said it would probably progress from the 25 year marker and they were apparently correct. Best of luck to you.
Uval951 said
Aug 12, 2012
mallani wrote:
A lot depends on the interpreting histopathologist.
Thank you Malcolm, we also transfered the slides to another hospital and are waiting for second opinion and more detail report. Original report of local hospital just provided the score without interpretations. The prof. of Columbia Univ. promised to investigate the slides in details and on this base to suggest the Tx optimal duration - 36 or 48 weeks. We will see him in October.
Uval951 said
Aug 12, 2012
mallani wrote:
There is no set time frame. It will be quicker if you drink alcohol. In my case I went from Stage 0-1 in 1990 to Stage 3-4 in 1998. By Fibroscan I was cirrhotic (Stage 4) by 2007. So that's about 17 years.
Malcolm, you have counted 17 years from F0 to cirrhotic F4. How did you designate Biopsy F3-F4 in 1998? Not cirrhotic?
mallani said
Aug 12, 2012
Hi Uval, Cirrhosis by definition, is Fibrosis Stage 4 (F4). My biopsy in 1998, showed some bridging fibrosis but not enough distortion of the liver architecture. A lot depends on the interpreting histopathologist. My initial report after biopsy was F2-3, but when I transferred to another Hospital, the slides were reviewed by an eminent histopathologist. I have seen the slides, and agree with his opinion.
-- Edited by mallani on Sunday 12th of August 2012 02:11:23 PM
52baddog said
Aug 12, 2012
Thanks for all the information. I guess biopsy is the best way to find out about the liver damage. I am at stage 1 and want to wait for the all oral treatment. My doctor suggested blood test every 6 months and biopsy every year. I am terrified of interferon. My liver enzymes are all normal and my viral load has gone from 207000 to 99600...
People with chronic hepatitis C who have persistently elevated levels of alanine aminotransferase (ALT) and the pro-fibrogenic chemokine monocyte chemotactic protein-1 (MCP-1, also known as CCL-2) during the early stages of infection are significantly more likely to develop advanced liver fibrosis or cirrhosis, according to a small study reported in the July 24, 2012, Proceedings of the National Academy of Sciences.
Only a minority of people with chronic hepatitis C virus (HCV) infection go on to develop advanced disease, but it is not easy to determine in advance who they will be. A better method of predicting progression to severe disease could help guide decisions about when to start treatment. This study was able to show different patterns of cytokines (immune system signaling chemicals) in people with slow and rapid liver disease progression.
Below is an edited excerpt from a NIH press release describing the study and its findings.
NIH Scientists Identify Likely Predictors of Hepatitis C Severity
Viral evolution and host protein levels predict rapid disease progression
Scientists at the National Institutes of Health have identified several factors in people infected with the hepatitis C virus that may predict whether the unusually rapid progression of disease from initial infection to severe liver conditions, such as cirrhosis, will occur. Knowing whether a patient's condition is likely to deteriorate quickly could help physicians decide on the best course of treatment.
The study was conducted by an international team of researchers led by Patrizia Farci, MD, chief of the Hepatic Pathogenesis Section in the Laboratory of Infectious Diseases at the National Institute of Allergy and Infectious Diseases (NIAID), part of NIH; and Harvey Alter, MD, chief of clinical studies and associate director of research in the Department of Transfusion Medicine at the NIH Clinical Center. Their findings appeared online July 23 in the Proceedings of the National Academy of Sciences.
"Treatment for hepatitis C is often expensive and poorly tolerated," said NIAID Director Anthony S. Fauci, MD. "Tools that would enable physicians to better predict the course of disease progression in hepatitis C patients would help guide treatment decisions. This small study is a potentially important step in developing such tools."
Symptoms of acute infection with the hepatitis C virus, one of five viruses that cause acute and chronic hepatitis, include fatigue, jaundice, and loss of appetite. Between 70 and 80 percent of people infected with the hepatitis C virus develop chronic infection, which over a patient's lifetime may result in severe liver diseases, such as liver cancer and cirrhosis. The World Health Organization estimates that 130 million to 170 million people live with chronic hepatitis C. Approximately 2.7 million to 3.9 million of those people live in the United States, according to the Centers for Disease Control and Prevention.
After a person is infected with hepatitis C, the virus evolves and circulates in the body in the form of several closely related strains, which allows it to adapt to drug treatments and avoid elimination. Some genetic differences between these strains result in changes to the proteins they encode, while others do not.
"A major mystery in the study of hepatitis C is that the disease course can be highly variable," explained lead researcher Dr. Farci. "Some patients show no symptoms for decades and eventually die of other causes. Other patients rapidly develop cirrhosis and liver cancer, leading to liver-related death in less than ten years."
Studies have found that having a weakened immune system -- for example, as the result of HIV infection or organ transplantation -- can exacerbate hepatitis C-related disease. But this does not fully explain which hepatitis C patients will ultimately experience a more rapid health decline. At present, there is no way to predict how the disease will progress in any given patient.
The new study involved samples collected from six patients who were infected with hepatitis C via contaminated blood transfusions in the 1970s, before the virus was identified. Blood donations have been routinely tested for hepatitis C since 1990. The patients symptoms and clinical outcomes were closely followed from the day they received the transfusion for up to 30 years, and ranged from mild and stable chronic hepatitis C to rapid disease progression and death.
Dr. Alter and his Clinical Center colleagues periodically collected blood serum samples from each of the six patients. Dr. Farci and her NIAID colleagues used up to 17 of these archived samples per patient to obtain and analyze a total of 1,876 genetic sequences of the hepatitis C virus. The researchers used the genetic sequences to reconstruct the evolution of two particular hepatitis C genes, E1 and E2, and the research team analyzed the types of genetic changes that took place in order to understand their relationship with disease progression. They also studied the levels of 39 blood serum proteins during the acute and chronic phases of disease.
"We thoroughly characterized the biological changes that occurred in these patients, and we discovered that patients who developed rapidly progressive disease had specific changes in their blood that were detectable since the early acute phase of infection," said Dr. Farci. Patients with rapid disease progression had significantly higher levels of a protein known as MCP-1, which is believed to play a major role in the development of liver fibrosis, and, eventually, cirrhosis. Moreover, in these patients, the genetic changes in the virus as it evolved over time were less likely to result in changes to the virus proteins.
The researchers say genetic and blood serum markers may one day enable physicians to identify hepatitis C patients at risk for rapid progression and to use this information to adjust their treatment. Additional markers may exist, Dr. Farci explained. The research team is working to increase the sample size by doing similar analyses on the remaining stored samples.
"Now that we know what to look for, we believe it is extremely important to extend our observation to a larger number of patients," Dr. Farci said.
NIAID conducts and supports research -- at NIH, throughout the United States, and worldwide -- to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID website at http://www.niaid.nih.gov.
The NIH Clinical Center (CC) is the clinical research hospital for the National Institutes of Health. Through clinical research, clinician-investigators translate laboratory discoveries into better treatments, therapies and interventions to improve the nation's health. For more information, visit http://clinicalcenter.nih.gov.
8/10/12
Uval951 said
Aug 11, 2012
2005 - F0-F1 - biopsy;
2010 - F4 - fibroscan;
2012 - F3-F4 - biopsy (waiting for second opinion of the same slides)
No alcohol, no red meat, but cirrhotic was developed very fast.
mallani said
Aug 11, 2012
Drank until 1997. Red meat doesn't worry me.
52baddog said
Aug 11, 2012
Thanks Malcom, I don't drink and have started eating organic since diagnosed with Hep C. Also, I don't eat red meat.
Did you drink alcohol, red meat during the 17 years?
mallani said
Aug 11, 2012
There is no set time frame. It will be quicker if you drink alcohol. In my case I went from Stage 0-1 in 1990 to Stage 3-4 in 1998. By Fibroscan I was cirrhotic (Stage 4) by 2007. So that's about 17 years. The fatty liver in obese patients also accelerates the progression.
So, don't drink, keep your weight normal and eat a healthy diet. Cheers.
52baddog said
Aug 11, 2012
Does anybody know how long it takes to go from stage 1 to stage 2,3, 4....
The doctor says sometimes it takes 20 years, but then he says sometimes it takes 5 years.
I acquired hep c in 1984. Had just one biopsy done in 2000 and it showed Grade 2/Stage 2. Drs believe I am cirrhotic now due to Splenomegaly and liver hypertension. I did drink, but not very much. Rarely eat red meat.
Hi Uval:
I thought you had a biopsy done, isn't biopsy more accurate than fibroscan. They don't have firbroscan in Texas.
So, most doctors recommend biopsy, which is more accurate.
So true Malcolm, that's actually great advice for people without liver diseases,as well. My remaining challange is to shed my excess weight and keep it off, as I am trying to dodge the bullet(statistically) and avoid:
1.fatty liver(and all that entails)
2.heart disease
3. vascular disease
4. stroke
5.premature death
6. ? I'm sure that there's something I've missed.
Malcolm, you have counted 17 years from F0 to cirrhotic F4. How did you designate Biopsy F3-F4 in 1998? Not cirrhotic?
Hi Uval, Cirrhosis by definition, is Fibrosis Stage 4 (F4). My biopsy in 1998, showed some bridging fibrosis but not enough distortion of the liver architecture. A lot depends on the interpreting histopathologist. My initial report after biopsy was F2-3, but when I transferred to another Hospital, the slides were reviewed by an eminent histopathologist. I have seen the slides, and agree with his opinion.
-- Edited by mallani on Sunday 12th of August 2012 02:11:23 PM
Thanks for all the information. I guess biopsy is the best way to find out about the liver damage. I am at stage 1 and want to wait for the all oral treatment. My doctor suggested blood test every 6 months and biopsy every year. I am terrified of interferon. My liver enzymes are all normal and my viral load has gone from 207000 to 99600...
Recieved this today
Early Biomarker Changes Predict Which Hepatitis C Patients Develop Severe Liver Disease
HCVŠ Russell Kightley
People with chronic hepatitis C who have persistently elevated levels of alanine aminotransferase (ALT) and the pro-fibrogenic chemokine monocyte chemotactic protein-1 (MCP-1, also known as CCL-2) during the early stages of infection are significantly more likely to develop advanced liver fibrosis or cirrhosis, according to a small study reported in the July 24, 2012, Proceedings of the National Academy of Sciences.
Only a minority of people with chronic hepatitis C virus (HCV) infection go on to develop advanced disease, but it is not easy to determine in advance who they will be. A better method of predicting progression to severe disease could help guide decisions about when to start treatment. This study was able to show different patterns of cytokines (immune system signaling chemicals) in people with slow and rapid liver disease progression.
Below is an edited excerpt from a NIH press release describing the study and its findings.
NIH Scientists Identify Likely Predictors of Hepatitis C Severity
Viral evolution and host protein levels predict rapid disease progression
Scientists at the National Institutes of Health have identified several factors in people infected with the hepatitis C virus that may predict whether the unusually rapid progression of disease from initial infection to severe liver conditions, such as cirrhosis, will occur. Knowing whether a patient's condition is likely to deteriorate quickly could help physicians decide on the best course of treatment.
The study was conducted by an international team of researchers led by Patrizia Farci, MD, chief of the Hepatic Pathogenesis Section in the Laboratory of Infectious Diseases at the National Institute of Allergy and Infectious Diseases (NIAID), part of NIH; and Harvey Alter, MD, chief of clinical studies and associate director of research in the Department of Transfusion Medicine at the NIH Clinical Center. Their findings appeared online July 23 in the Proceedings of the National Academy of Sciences.
"Treatment for hepatitis C is often expensive and poorly tolerated," said NIAID Director Anthony S. Fauci, MD. "Tools that would enable physicians to better predict the course of disease progression in hepatitis C patients would help guide treatment decisions. This small study is a potentially important step in developing such tools."
Symptoms of acute infection with the hepatitis C virus, one of five viruses that cause acute and chronic hepatitis, include fatigue, jaundice, and loss of appetite. Between 70 and 80 percent of people infected with the hepatitis C virus develop chronic infection, which over a patient's lifetime may result in severe liver diseases, such as liver cancer and cirrhosis. The World Health Organization estimates that 130 million to 170 million people live with chronic hepatitis C. Approximately 2.7 million to 3.9 million of those people live in the United States, according to the Centers for Disease Control and Prevention.
After a person is infected with hepatitis C, the virus evolves and circulates in the body in the form of several closely related strains, which allows it to adapt to drug treatments and avoid elimination. Some genetic differences between these strains result in changes to the proteins they encode, while others do not.
"A major mystery in the study of hepatitis C is that the disease course can be highly variable," explained lead researcher Dr. Farci. "Some patients show no symptoms for decades and eventually die of other causes. Other patients rapidly develop cirrhosis and liver cancer, leading to liver-related death in less than ten years."
Studies have found that having a weakened immune system -- for example, as the result of HIV infection or organ transplantation -- can exacerbate hepatitis C-related disease. But this does not fully explain which hepatitis C patients will ultimately experience a more rapid health decline. At present, there is no way to predict how the disease will progress in any given patient.
The new study involved samples collected from six patients who were infected with hepatitis C via contaminated blood transfusions in the 1970s, before the virus was identified. Blood donations have been routinely tested for hepatitis C since 1990. The patients symptoms and clinical outcomes were closely followed from the day they received the transfusion for up to 30 years, and ranged from mild and stable chronic hepatitis C to rapid disease progression and death.
Dr. Alter and his Clinical Center colleagues periodically collected blood serum samples from each of the six patients. Dr. Farci and her NIAID colleagues used up to 17 of these archived samples per patient to obtain and analyze a total of 1,876 genetic sequences of the hepatitis C virus. The researchers used the genetic sequences to reconstruct the evolution of two particular hepatitis C genes, E1 and E2, and the research team analyzed the types of genetic changes that took place in order to understand their relationship with disease progression. They also studied the levels of 39 blood serum proteins during the acute and chronic phases of disease.
"We thoroughly characterized the biological changes that occurred in these patients, and we discovered that patients who developed rapidly progressive disease had specific changes in their blood that were detectable since the early acute phase of infection," said Dr. Farci. Patients with rapid disease progression had significantly higher levels of a protein known as MCP-1, which is believed to play a major role in the development of liver fibrosis, and, eventually, cirrhosis. Moreover, in these patients, the genetic changes in the virus as it evolved over time were less likely to result in changes to the virus proteins.
The researchers say genetic and blood serum markers may one day enable physicians to identify hepatitis C patients at risk for rapid progression and to use this information to adjust their treatment. Additional markers may exist, Dr. Farci explained. The research team is working to increase the sample size by doing similar analyses on the remaining stored samples.
"Now that we know what to look for, we believe it is extremely important to extend our observation to a larger number of patients," Dr. Farci said.
NIAID conducts and supports research -- at NIH, throughout the United States, and worldwide -- to study the causes of infectious and immune-mediated diseases, and to develop better means of preventing, diagnosing and treating these illnesses. News releases, fact sheets and other NIAID-related materials are available on the NIAID website at http://www.niaid.nih.gov.
The NIH Clinical Center (CC) is the clinical research hospital for the National Institutes of Health. Through clinical research, clinician-investigators translate laboratory discoveries into better treatments, therapies and interventions to improve the nation's health. For more information, visit http://clinicalcenter.nih.gov.
8/10/12
2005 - F0-F1 - biopsy;
2010 - F4 - fibroscan;
2012 - F3-F4 - biopsy (waiting for second opinion of the same slides)
No alcohol, no red meat, but cirrhotic was developed very fast.
Drank until 1997. Red meat doesn't worry me.
Thanks Malcom, I don't drink and have started eating organic since diagnosed with Hep C. Also, I don't eat red meat.
Did you drink alcohol, red meat during the 17 years?
There is no set time frame. It will be quicker if you drink alcohol. In my case I went from Stage 0-1 in 1990 to Stage 3-4 in 1998. By Fibroscan I was cirrhotic (Stage 4) by 2007. So that's about 17 years. The fatty liver in obese patients also accelerates the progression.
So, don't drink, keep your weight normal and eat a healthy diet. Cheers.
Does anybody know how long it takes to go from stage 1 to stage 2,3, 4....
The doctor says sometimes it takes 20 years, but then he says sometimes it takes 5 years.
I am confused......