Aa
Anyone have high ALT and AST after SVR.
I had a general panel done and my AST and ALT were higher now 6 years after SVR than they were when it was achieved. AST (41) 10-35 nrml, ALT 45 9-46 normal. I realize these numbers are not crazy high but I was hoping for a healthier liver than these would indicate. The damage was approximately stage 3. Thanks for any feedback....!
James I think Lynn has given you excellent advice. The test results could have been a fluke however I think you should see a liver specialist. I have been getting blood work and ultrasound every 6 months since I was cured 5 years ago. I need to catch up, I am a little behind this time. Best of luck to you!
2 Comments
Thank you. I’m going to get tested. What test though, I’m so out of the loop AFP, PCR? Also has there been any advances for geno 2 as far as treatment. I appreciate your help.
There are many new treatments. Now available. Have you seen the TV commercials for Harvoni? Harvoni has an excellent cure rate for 1b and several other genotypes.
There are several other new meds available as well.
I would discuss testing with your doctor. If you are concerned about relapse or new infection you would want to have the test for the virus the HCV RNA by PCR
AFP is looking for possible indication of liver cancer HCC but the blood test is imperfect and should be accompanied by abdominal ultrasound.
Because I have cirrhosis I have those tests every six months.
Also those with cirrhosis often will have platelet counts below normal. Min normal at my lab is 150. My platelet count was about 90 before treatment and has risen a little to 110 after treatment. Platelet count is part of a complete blood count test (CBC).
My testing regimen is liver function panel, CBC, AFP and abdominal ultrasound every six months. I was having annual upper endoscopies because I developed esophageal varicies that required banding back in 2012 but since there has been no reoccurrence and I am now cured my doctor has decided I can wait a few years before any additional follow on EGD’s are needed.
There are several other new meds available as well.
I would discuss testing with your doctor. If you are concerned about relapse or new infection you would want to have the test for the virus the HCV RNA by PCR
AFP is looking for possible indication of liver cancer HCC but the blood test is imperfect and should be accompanied by abdominal ultrasound.
Because I have cirrhosis I have those tests every six months.
Also those with cirrhosis often will have platelet counts below normal. Min normal at my lab is 150. My platelet count was about 90 before treatment and has risen a little to 110 after treatment. Platelet count is part of a complete blood count test (CBC).
My testing regimen is liver function panel, CBC, AFP and abdominal ultrasound every six months. I was having annual upper endoscopies because I developed esophageal varicies that required banding back in 2012 but since there has been no reoccurrence and I am now cured my doctor has decided I can wait a few years before any additional follow on EGD’s are needed.
Just to add my personal history I was infected with hep c probably for 37 years before I was cured 2.5 years ago with Harvoni 24 weeks and ribavirin 15 weeks. This was my 5th treatment.
I was having liver biopsies every 5 years after my diagnosis with hep c. On my 4th liver biopsy after likely 30 years of infection I was diagnosed with cirrhosis but had to wait an additional 7 years hoping for a new medicine that could cure me. I was a null responder to my 3 prior treatments with interferon based medicines.
I am a lay person but you could say I have been around the block a few times.
I was having liver biopsies every 5 years after my diagnosis with hep c. On my 4th liver biopsy after likely 30 years of infection I was diagnosed with cirrhosis but had to wait an additional 7 years hoping for a new medicine that could cure me. I was a null responder to my 3 prior treatments with interferon based medicines.
I am a lay person but you could say I have been around the block a few times.
2 Comments
Wow, HCV patients are amazingly strong to endure all of that. I was geno 2 so I only had 24 weeks of Inf and Ribo. Sounds like nothing compared to type 1s, and in your case 3 times. I can only imagine, that stuff took a toll on me in 24 weeks. You are a true HCV warrior! Thanks for your help. I’m going make an appointment tomorrow and try to figure this out. Thanks again.
Good luck!
This is from the AASLD ( American Association for the study liver disease) guidelines
“SVR typically aborts progression of liver injury with regression of liver fibrosis in most, but not all, treated patients (Morisco, 2013); (Morgan, 2010); (George, 2009); (Morgan, 2013); (Singal, 2010). Because of lack of progression, patients without advanced liver fibrosis (ie, Metavir stage F0, F1, or F2) who achieve SVR should receive standard medical care that is recommended for patients who were never infected with HCV.
Among patients with advanced liver fibrosis (ie, Metavir stage F3 or F4) who achieve SVR, decompensated liver disease (with the exception of HCC) rarely develops during follow-up, and overall survival is prolonged (Morisco, 2013); (Morgan, 2010); (George, 2009); (Morgan, 2013); (Singal, 2010). Liver fibrosis and liver function test results improve in most patients who achieve SVR (Morisco, 2013); (Morgan, 2010); (George, 2009); (Morgan, 2013); (Singal, 2010). Bleeding from esophageal varices is rare after SVR (Morisco, 2013); (Morgan, 2010); (George, 2009); (Morgan, 2013); (Singal, 2010). Patients with cirrhosis should receive routine surveillance endoscopy for detection of esophageal varices if not previously done; if varices are found, they should be treated or followed as indicated (Garcia-Tsao, 2007).
The risk of developing HCC among cirrhotic patients who receive DAA treatment is debated. Multiple studies of cirrhotic patients who achieved SVR with peginterferon/ribavirin reported a significant reduction in the risk of developing HCC (Morisco, 2013); (Morgan, 2010); (George, 2009); (Morgan, 2013); (Singal, 2010). A recent report suggested a higher than expected frequency of HCC in patients with HCV-related cirrhosis treated successfully with DAAs (Reig, 2016). However, a meta-analysis evaluating the incidence of HCC among persons achieving SVR with DAAs found that the risk of HCC did not exceed that seen in patients who experienced SVR with interferon-based treatment after adjustment for baseline risk factors for HCC (Waziry, 2017).
Patients with cirrhosis who achieve SVR remain at risk for HCC. Thus, they should continue to undergo regular surveillance for HCC despite the lowered risk that results after viral eradication (Bruix, 2011). The risk of HCC among patients with advanced fibrosis prior to treatment but who have regression to minimal fibrosis after treatment is not known. In the absence of data to the contrary, such patients remain at some risk for HCC and should be monitored at regular intervals for HCC. Alpha-fetoprotein (AFP) alone is considered an inadequate screening test for HCC (Bruix, 2011).
Patients in whom SVR is achieved but who have another potential cause of liver disease (eg, excessive alcohol use, metabolic syndrome with or without proven fatty liver disease, or iron overload) remain at risk for fibrosis progression. It is recommended that such patients be educated about the risk of liver disease and monitored for liver disease progression with periodic physical examination, blood tests, and potentially, tests for liver fibrosis by a liver disease specialist.
Patients who achieve SVR can be reinfected with HCV if they are re-exposed to the virus. Annual testing for HCV reinfection among patients with ongoing risk for HCV infection (eg, injection drug use or high-risk sexual exposure) is recommended. A flare in liver enzyme levels should prompt immediate evaluation for HCV reinfection“
“SVR typically aborts progression of liver injury with regression of liver fibrosis in most, but not all, treated patients (Morisco, 2013); (Morgan, 2010); (George, 2009); (Morgan, 2013); (Singal, 2010). Because of lack of progression, patients without advanced liver fibrosis (ie, Metavir stage F0, F1, or F2) who achieve SVR should receive standard medical care that is recommended for patients who were never infected with HCV.
Among patients with advanced liver fibrosis (ie, Metavir stage F3 or F4) who achieve SVR, decompensated liver disease (with the exception of HCC) rarely develops during follow-up, and overall survival is prolonged (Morisco, 2013); (Morgan, 2010); (George, 2009); (Morgan, 2013); (Singal, 2010). Liver fibrosis and liver function test results improve in most patients who achieve SVR (Morisco, 2013); (Morgan, 2010); (George, 2009); (Morgan, 2013); (Singal, 2010). Bleeding from esophageal varices is rare after SVR (Morisco, 2013); (Morgan, 2010); (George, 2009); (Morgan, 2013); (Singal, 2010). Patients with cirrhosis should receive routine surveillance endoscopy for detection of esophageal varices if not previously done; if varices are found, they should be treated or followed as indicated (Garcia-Tsao, 2007).
The risk of developing HCC among cirrhotic patients who receive DAA treatment is debated. Multiple studies of cirrhotic patients who achieved SVR with peginterferon/ribavirin reported a significant reduction in the risk of developing HCC (Morisco, 2013); (Morgan, 2010); (George, 2009); (Morgan, 2013); (Singal, 2010). A recent report suggested a higher than expected frequency of HCC in patients with HCV-related cirrhosis treated successfully with DAAs (Reig, 2016). However, a meta-analysis evaluating the incidence of HCC among persons achieving SVR with DAAs found that the risk of HCC did not exceed that seen in patients who experienced SVR with interferon-based treatment after adjustment for baseline risk factors for HCC (Waziry, 2017).
Patients with cirrhosis who achieve SVR remain at risk for HCC. Thus, they should continue to undergo regular surveillance for HCC despite the lowered risk that results after viral eradication (Bruix, 2011). The risk of HCC among patients with advanced fibrosis prior to treatment but who have regression to minimal fibrosis after treatment is not known. In the absence of data to the contrary, such patients remain at some risk for HCC and should be monitored at regular intervals for HCC. Alpha-fetoprotein (AFP) alone is considered an inadequate screening test for HCC (Bruix, 2011).
Patients in whom SVR is achieved but who have another potential cause of liver disease (eg, excessive alcohol use, metabolic syndrome with or without proven fatty liver disease, or iron overload) remain at risk for fibrosis progression. It is recommended that such patients be educated about the risk of liver disease and monitored for liver disease progression with periodic physical examination, blood tests, and potentially, tests for liver fibrosis by a liver disease specialist.
Patients who achieve SVR can be reinfected with HCV if they are re-exposed to the virus. Annual testing for HCV reinfection among patients with ongoing risk for HCV infection (eg, injection drug use or high-risk sexual exposure) is recommended. A flare in liver enzyme levels should prompt immediate evaluation for HCV reinfection“
With F3 fibrosis aka borderline cirrhosis per the AASLD post treatment guidelines for follow up for those with F3 or F4 fibrosis you should be under the continuing care of a hepatologist or at least a gastroenterologist. Are you having liver ultrasounds every six months and AFP blood testing?
How were you diagnosed F3 was it by liver biopsy? Have you had your fibrosis tested since you were cured? Many people are experiencing reduction in fibrosis levels but not all. Even those with F4 cirrhosis have about a 50/50 chance of improvement in liver damage with time. However, even with cure as a patient with F3 you must continue to be careful with your liver. Even if you no longer have hep c to damage your liver without treating your liver kindly you can still progress to F4 cirrhosis. Having cirrhosis is one thing that can cause mild elevation in ALT.
There are many things that can cause liver enzymes to rise slightly.
Have you tested for HCV RNA by PCR to ensure you are still cured? Don’t have an antibody test as you were infected in the past and will always test positive.
Have you discussed this with your liver specialist and what did they think? My suggestion if you have not been seeing a liver specialist and discuss your concerns. There are new tests for liver damage that are non invasive like a liver biopsy. One is a blood test called Fibrosure and the other is a devise similar to a ultrasound that has a kind of thump to measure liver stiffness called a Fibroscan.
I did find this info:
“AST may also be ordered, either by itself or with other tests, for people who are at an increased risk for liver disease since many people with mild liver damage will have no signs or symptoms. Some examples include:
Persons who might have been exposed to hepatitis viruses
Persons who are heavy drinkers
Persons who have a history of liver disease in their family
Persons taking drugs that can damage the liver
Persons who are overweight and/or have diabetes
When AST is used to monitor treatment of persons with liver disease, it may be ordered on a regular basis during the course of treatment to determine whether the therapy is effective.
What does the test result mean?
Low levels of AST in the blood are expected and are normal.
Very high levels of AST (more than 10 times normal) are usually due to acute hepatitis, sometimes due to a viral infection. With acute hepatitis, AST levels usually stay high for about 1-2 months but can take as long as 3-6 months to return to normal. Levels of AST may also be markedly elevated (often over 100 times normal) as a result of exposure to drugs or other substances that are toxic to the liver as well as in conditions that cause decreased blood flow (ischemia) to the liver.
With chronic hepatitis, AST levels are usually not as high, often less than 4 times normal, and are more likely to be normal than are ALT levels. AST often varies between normal and slightly increased with chronic hepatitis, so the test may be ordered frequently to determine the pattern. Such moderate increases may also be seen in other diseases of the liver, especially when the bile ducts are blocked, or with cirrhosis or certain cancers of the liver. AST may also increase after heart attacks and with muscle injury, usually to a much greater degree than ALT.
AST is often performed together with the ALT test or as part of a liver panel. For more about AST results in relation to other liver tests, see the Liver Panel article.
In most types of liver disease, the ALT level is higher than AST and the AST/ALT ratio will be low (less than 1). There are a few exceptions; the AST/ALT ratio is usually increased in alcoholic hepatitis, cirrhosis, hepatitis C virus-related chronic liver disease, and in the first day or two of acute hepatitis or injury from bile duct obstruction. With heart or muscle injury, AST is often much higher than ALT (often 3-5 times as high) and levels tend to stay higher than ALT for longer than with liver injury.”
Best of luck to you
How were you diagnosed F3 was it by liver biopsy? Have you had your fibrosis tested since you were cured? Many people are experiencing reduction in fibrosis levels but not all. Even those with F4 cirrhosis have about a 50/50 chance of improvement in liver damage with time. However, even with cure as a patient with F3 you must continue to be careful with your liver. Even if you no longer have hep c to damage your liver without treating your liver kindly you can still progress to F4 cirrhosis. Having cirrhosis is one thing that can cause mild elevation in ALT.
There are many things that can cause liver enzymes to rise slightly.
Have you tested for HCV RNA by PCR to ensure you are still cured? Don’t have an antibody test as you were infected in the past and will always test positive.
Have you discussed this with your liver specialist and what did they think? My suggestion if you have not been seeing a liver specialist and discuss your concerns. There are new tests for liver damage that are non invasive like a liver biopsy. One is a blood test called Fibrosure and the other is a devise similar to a ultrasound that has a kind of thump to measure liver stiffness called a Fibroscan.
I did find this info:
“AST may also be ordered, either by itself or with other tests, for people who are at an increased risk for liver disease since many people with mild liver damage will have no signs or symptoms. Some examples include:
Persons who might have been exposed to hepatitis viruses
Persons who are heavy drinkers
Persons who have a history of liver disease in their family
Persons taking drugs that can damage the liver
Persons who are overweight and/or have diabetes
When AST is used to monitor treatment of persons with liver disease, it may be ordered on a regular basis during the course of treatment to determine whether the therapy is effective.
What does the test result mean?
Low levels of AST in the blood are expected and are normal.
Very high levels of AST (more than 10 times normal) are usually due to acute hepatitis, sometimes due to a viral infection. With acute hepatitis, AST levels usually stay high for about 1-2 months but can take as long as 3-6 months to return to normal. Levels of AST may also be markedly elevated (often over 100 times normal) as a result of exposure to drugs or other substances that are toxic to the liver as well as in conditions that cause decreased blood flow (ischemia) to the liver.
With chronic hepatitis, AST levels are usually not as high, often less than 4 times normal, and are more likely to be normal than are ALT levels. AST often varies between normal and slightly increased with chronic hepatitis, so the test may be ordered frequently to determine the pattern. Such moderate increases may also be seen in other diseases of the liver, especially when the bile ducts are blocked, or with cirrhosis or certain cancers of the liver. AST may also increase after heart attacks and with muscle injury, usually to a much greater degree than ALT.
AST is often performed together with the ALT test or as part of a liver panel. For more about AST results in relation to other liver tests, see the Liver Panel article.
In most types of liver disease, the ALT level is higher than AST and the AST/ALT ratio will be low (less than 1). There are a few exceptions; the AST/ALT ratio is usually increased in alcoholic hepatitis, cirrhosis, hepatitis C virus-related chronic liver disease, and in the first day or two of acute hepatitis or injury from bile duct obstruction. With heart or muscle injury, AST is often much higher than ALT (often 3-5 times as high) and levels tend to stay higher than ALT for longer than with liver injury.”
Best of luck to you
3 Comments
Thanks great suggestion. I did have a biopsy, and have never had any follow up since SVR. I appreciate your reply!
Just checking on advances in treatment for type 2, good to see that new options are available that don’t include Peg, so I’ll get PCR, and a less invasive process than a biopsy, to see where I’m at condition wise
Thanks again!
Thanks again!
Hi I’m a little confused as to what test to ask for as I am now under Medicaid and not my old insurance. Thanks for your help much appreciated.
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