Aa
Safe to take prednisone after SVR?
Some old posts say it can reactivate HCV, even after 8 years, which I find hard to believe, but I don't know anything about steroids. I understand they can have some serious side effects and I'm wondering how damaging they are to the liver. I realize that last statement could be made about any drug, and it's best for your liver to not take anything, but sometimes you have to weigh the good against the bad depending on why you need to take it.
Any info would be appreciated.
Thanks
Any info would be appreciated.
Thanks
Thanks for the great info, Pooh. Very interesting....always something new to learn. :)
Good to know i had vasculitis also in my legs they would swell up and i also had bright red rash like bumps on my legs and they gave me steroids for it 3 different times and it came back they didnt know i had hep c at that time the ER ran every test they could think of but didnt know what was wrong with me so they sent me home with another round of steroids its took a few days for my hep c test to come back i had another bad case with this crazy rash i went back to the ER and the nurse pulled my blood work and found my hep c test was reactive and it was then i went to my hep doc he told me steroids were not good for hep c but was not sure about after im doing so follow up info searching on how to take care of my liver once i am SVR
Thanks Guys again for the info
Thanks Guys again for the info
You will notice that that article talks about reactivation of Hepatitis B. The Hep B virus can be reactivated in some situations because it is a DNA virus. Hepatitis C, on the other hand, is an RNA virus, and it cannot be reactivated.
http://www.epidemic.org/theFacts/viruses/anatomyOfTheVirus/
http://www.epidemic.org/theFacts/viruses/viralReplication/
http://www.epidemic.org/thefacts/viruses/rnaViruses/
http://www.epidemic.org/theFacts/viruses/anatomyOfTheVirus/
http://www.epidemic.org/theFacts/viruses/viralReplication/
http://www.epidemic.org/thefacts/viruses/rnaViruses/
" Hepatotoxicity, Mechanism of Injury
Corticosteroids have multiple adverse side effects, due to their multiplicity of actions affecting virtually all organs. Long-term use has very profound effects on growth and can lead to cataracts, glaucoma, opportunistic infections, thinning of the skin, weight gain and redistribution of fat, insulin resistance and diabetes, hypertension, headache, psychiatric problems, sodium retention and peripheral edema; all of the clinical features of Cushing’s syndrome.
Corticosteroids also have major effects on the liver, particularly when given long-term and in higher than physiologic doses. Glucocorticoid use can result in hepatic enlargement and steatosis and can cause triggering or worsening of nonalcoholic steatohepatitis. Long-term use can also exacerbate chronic viral hepatitis. Importantly, treatment with corticosteroids followed by withdrawal or pulse therapy can cause reactivation of hepatitis B and worsening or de novo induction of autoimmune hepatitis, both of which can be fatal. Finally, high doses of intravenous corticosteroids, largely methylprednisolone, have been associated with acute liver injury which can result in acute liver failure and death. Thus, the hepatic complications of corticosteroids usually represent the worsening or triggering of an underlying liver disease and rarely are the result of drug hepatotoxicity.
Corticosteroid therapy can cause hepatic steatosis and hepatic enlargement, but this is often not clinically apparent, particularly in adults. This effect can occur quite rapidly and is rapidly reversed with discontinuation. High doses and long-term use has been associated with the development or exacerbation of nonalcoholic steatohepatitis with elevations in serum aminotransferase levels and liver histology resembling alcoholic hepatitis with steatosis, chronic inflammation, centrolobular ballooning degeneration and Mallory bodies (Case 1). However, symptomatic or progressive liver injury from corticosteroid-induced steatohepatitis is uncommon. Furthermore, corticosteroids may act to worsen an underlying nonalcoholic fatty liver disease rather than causing the condition de novo. The worsening may be due to direct effects of glucocorticoids on insulin resistance or fatty acid metabolism or may be the result of weight gain which is common with long-term corticosteroid therapy. While simple steatosis induced by corticosteroids is rapidly reversible, steatohepatitis can be slow to resolve upon withdrawal of corticosteroids.
Corticosteroids in high doses can also cause hepatic glycogenosis, in which liver cells exhibit a homogenous appearance and stain strongly for glycogen (using PAS staining with and without diastase). Glycogenosis can also be associated with hepatomegaly (in children) and elevations in serum aminotransferase levels with minimal or no change in alkaline phosphatase or bilirubin levels. Glycogenosis is usually asymptomatic and does not appear to progress to chronic liver injury, cirrhosis or acute liver failure. While glycogenosis has been described largely in patients with poorly controlled type 1 diabetes, it also can occur acutely in patients started on high dose corticosteroids.
An important complication of corticosteroid therapy is the worsening of an underlying chronic viral hepatitis. In chronic hepatitis B, corticosteroids can induce increases in viral replication and serum hepatitis B virus (HBV) DNA levels while decreasing serum aminotransferase levels. Eventually, however, the increase in viral replication can worsen the underlying liver disease. Exacerbation of hepatitis becomes particularly evident when corticosteroids are withdrawn or lowered to physiological levels. As the immune system recovers, hepatitis worsens and serum aminotransferase levels can rise to greater than 10- to 20-fold elevated usually accompanied by a prompt decrease in HBV DNA levels. This flare of disease following withdrawal of corticosteroids can be severe and result in acute liver failure or significant worsening of chronic hepatitis and development of cirrhosis (Case 2). Indeed, even patients with the “inactive carrier states” (as shown by the presence of HBsAg in serum without HBeAg or detectable HBV DNA or any elevation in serum aminotransferase levels) can suffer severe reactivation of disease and acute liver failure as a result of a short course of high dose corticosteroids as occurs with cancer chemotherapy or with treatment of severe autoimmune conditions or even asthma, hay fever or allergic dermatitis. Reactivation of hepatitis B can be prevented by prophylactic use of antiviral therapy during the period of immunosuppression, but even this may not prevent some degree of liver injury.
Corticosteroids also appear to worsen the course of chronic hepatitis C, although in a less dramatic fashion than in chronic hepatitis B. Corticosteroid therapy leads to a rise in hepatitis C virus (HCV) RNA levels which may eventually cause worsening of the underlying liver disease. Chronic hepatitis C appears to be more severe and is particularly difficult to manage in patients receiving chemotherapy or immunosuppression and corticosteroids are believed to be a major factor in this effect. Thus, corticosteroids should be avoided if possible in patients with underlying chronic viral hepatitis.
Corticosteroids are used in the therapy of autoimmune hepatitis and, therefore, are likely to be beneficial rather than harmful in patients with this disease. The difficulty arises when corticosteroids are stopped, which can cause a rebound exacerbation of the autoimmune hepatitis that is often severe and can be fatal. Importantly, there have been multiple reported instances of de novo appearance of severe autoimmune hepatitis in patients who received a short course or pulse of corticosteroids for another, unrelated condition (such as asthma or allergic reactions). In these situations, a mild and subclinical autoimmune hepatitis was likely present before corticosteroids were started, and the suppression of the disease followed by immune rebound caused the clinical presentation of the condition. These patients generally respond to restarting corticosteroids, but may require long-term if not life-long immunosuppressive treatment thereafter."
http://livertox.nlm.nih.gov/Corticosteroids.htm
Corticosteroids have multiple adverse side effects, due to their multiplicity of actions affecting virtually all organs. Long-term use has very profound effects on growth and can lead to cataracts, glaucoma, opportunistic infections, thinning of the skin, weight gain and redistribution of fat, insulin resistance and diabetes, hypertension, headache, psychiatric problems, sodium retention and peripheral edema; all of the clinical features of Cushing’s syndrome.
Corticosteroids also have major effects on the liver, particularly when given long-term and in higher than physiologic doses. Glucocorticoid use can result in hepatic enlargement and steatosis and can cause triggering or worsening of nonalcoholic steatohepatitis. Long-term use can also exacerbate chronic viral hepatitis. Importantly, treatment with corticosteroids followed by withdrawal or pulse therapy can cause reactivation of hepatitis B and worsening or de novo induction of autoimmune hepatitis, both of which can be fatal. Finally, high doses of intravenous corticosteroids, largely methylprednisolone, have been associated with acute liver injury which can result in acute liver failure and death. Thus, the hepatic complications of corticosteroids usually represent the worsening or triggering of an underlying liver disease and rarely are the result of drug hepatotoxicity.
Corticosteroid therapy can cause hepatic steatosis and hepatic enlargement, but this is often not clinically apparent, particularly in adults. This effect can occur quite rapidly and is rapidly reversed with discontinuation. High doses and long-term use has been associated with the development or exacerbation of nonalcoholic steatohepatitis with elevations in serum aminotransferase levels and liver histology resembling alcoholic hepatitis with steatosis, chronic inflammation, centrolobular ballooning degeneration and Mallory bodies (Case 1). However, symptomatic or progressive liver injury from corticosteroid-induced steatohepatitis is uncommon. Furthermore, corticosteroids may act to worsen an underlying nonalcoholic fatty liver disease rather than causing the condition de novo. The worsening may be due to direct effects of glucocorticoids on insulin resistance or fatty acid metabolism or may be the result of weight gain which is common with long-term corticosteroid therapy. While simple steatosis induced by corticosteroids is rapidly reversible, steatohepatitis can be slow to resolve upon withdrawal of corticosteroids.
Corticosteroids in high doses can also cause hepatic glycogenosis, in which liver cells exhibit a homogenous appearance and stain strongly for glycogen (using PAS staining with and without diastase). Glycogenosis can also be associated with hepatomegaly (in children) and elevations in serum aminotransferase levels with minimal or no change in alkaline phosphatase or bilirubin levels. Glycogenosis is usually asymptomatic and does not appear to progress to chronic liver injury, cirrhosis or acute liver failure. While glycogenosis has been described largely in patients with poorly controlled type 1 diabetes, it also can occur acutely in patients started on high dose corticosteroids.
An important complication of corticosteroid therapy is the worsening of an underlying chronic viral hepatitis. In chronic hepatitis B, corticosteroids can induce increases in viral replication and serum hepatitis B virus (HBV) DNA levels while decreasing serum aminotransferase levels. Eventually, however, the increase in viral replication can worsen the underlying liver disease. Exacerbation of hepatitis becomes particularly evident when corticosteroids are withdrawn or lowered to physiological levels. As the immune system recovers, hepatitis worsens and serum aminotransferase levels can rise to greater than 10- to 20-fold elevated usually accompanied by a prompt decrease in HBV DNA levels. This flare of disease following withdrawal of corticosteroids can be severe and result in acute liver failure or significant worsening of chronic hepatitis and development of cirrhosis (Case 2). Indeed, even patients with the “inactive carrier states” (as shown by the presence of HBsAg in serum without HBeAg or detectable HBV DNA or any elevation in serum aminotransferase levels) can suffer severe reactivation of disease and acute liver failure as a result of a short course of high dose corticosteroids as occurs with cancer chemotherapy or with treatment of severe autoimmune conditions or even asthma, hay fever or allergic dermatitis. Reactivation of hepatitis B can be prevented by prophylactic use of antiviral therapy during the period of immunosuppression, but even this may not prevent some degree of liver injury.
Corticosteroids also appear to worsen the course of chronic hepatitis C, although in a less dramatic fashion than in chronic hepatitis B. Corticosteroid therapy leads to a rise in hepatitis C virus (HCV) RNA levels which may eventually cause worsening of the underlying liver disease. Chronic hepatitis C appears to be more severe and is particularly difficult to manage in patients receiving chemotherapy or immunosuppression and corticosteroids are believed to be a major factor in this effect. Thus, corticosteroids should be avoided if possible in patients with underlying chronic viral hepatitis.
Corticosteroids are used in the therapy of autoimmune hepatitis and, therefore, are likely to be beneficial rather than harmful in patients with this disease. The difficulty arises when corticosteroids are stopped, which can cause a rebound exacerbation of the autoimmune hepatitis that is often severe and can be fatal. Importantly, there have been multiple reported instances of de novo appearance of severe autoimmune hepatitis in patients who received a short course or pulse of corticosteroids for another, unrelated condition (such as asthma or allergic reactions). In these situations, a mild and subclinical autoimmune hepatitis was likely present before corticosteroids were started, and the suppression of the disease followed by immune rebound caused the clinical presentation of the condition. These patients generally respond to restarting corticosteroids, but may require long-term if not life-long immunosuppressive treatment thereafter."
http://livertox.nlm.nih.gov/Corticosteroids.htm
I developed Systemic Vasculitis in 1993. In retrospect, I now know it was the Hepatitis C that caused it. The Systemic Vasculitis caused Pericarditis, Pericardial Effusion (fluid in the sac around the heart), Pleuritis, Pleural Effusions (fluid in the sacs around the lungs), and Hemolytic Anemia. My hemoglobin was 9. I was very ill, off work for 7 months, and on high dose steroids for a year. I had no choice but to take the steroids. I would have died without them. If the steroids had failed to work, the next drug they would use was Cytoxan. Lucky for me the steroids did work and the Vasculitis eventually disappeared. However, I was never the same as I had been before I had the Systemic Vasculitis. I never regained all of my pep and energy. It just was not the same. Prior to the Vasculitis I was thin, actually underweight. I never had a weight problem. If I did gain weight, it fell off of me in a week. After the Vasculitis my weight kept climbing up, and I had difficulty losing it. In fact, it was next to impossible to lose the weight and it kept creeping up. In addition, my blood sugar was creeping up, slowly, but it was creeping.
Now, I know the Hep C caused the Vasculitis. What I do not know is what effect the steroids had on the viral load. No one knew I had Hep C in 1993 so no one was testing my VL. Of course, the virus was already present, so it was not "reactivated," but it may have increased while I was on steroids (due to the immune suppression). However, I will never know if it did or did not. What I do know is that I have had Hep C for about 37-38 years and that my metabolism changed after I had Systemic Vasculitis. And I know that when I was diagnosed in July 2011, my liver biopsy showed Grade 2, Stage 2.
I did find an article which is quite good and I will copy and paste it in the next post.
Now, I know the Hep C caused the Vasculitis. What I do not know is what effect the steroids had on the viral load. No one knew I had Hep C in 1993 so no one was testing my VL. Of course, the virus was already present, so it was not "reactivated," but it may have increased while I was on steroids (due to the immune suppression). However, I will never know if it did or did not. What I do know is that I have had Hep C for about 37-38 years and that my metabolism changed after I had Systemic Vasculitis. And I know that when I was diagnosed in July 2011, my liver biopsy showed Grade 2, Stage 2.
I did find an article which is quite good and I will copy and paste it in the next post.
I guess I should not read some of these old posts. The one I read about reactivating the virus after 8 years was really old and probably back in the day when they didn't believe SVR was a cure. I thought it was a little crazy to think you could reactivate something when it is no longer there.
I will of course check with my dr, but I was just wondering if anyone had any info on the issue. Not that I don't trust my dr, but sometimes people on this site have had experiences that not every doctor has run into yet.
I will of course check with my dr, but I was just wondering if anyone had any info on the issue. Not that I don't trust my dr, but sometimes people on this site have had experiences that not every doctor has run into yet.
"Safe to take prednisone after SVR?" "Some old posts say it can reactivate HCV, even after 8 years,"
-----------------------------------------
If one has attained SVR (defined as UND 24 weeks after end of treatment) one is considered cured of Hep C. Attaining SVR indicates that a person no longer has the virus in the body. It is gone. A virus that is not present cannot be reactivated. Therefore, since it is no longer in the body, it cannot be reactivated.
Concerning the effect that prednisone could potentially have on a person's liver and whether someone should take it, that would depend on the status of a person's liver and should be discussed with ones treating Hepatologist.
-----------------------------------------
If one has attained SVR (defined as UND 24 weeks after end of treatment) one is considered cured of Hep C. Attaining SVR indicates that a person no longer has the virus in the body. It is gone. A virus that is not present cannot be reactivated. Therefore, since it is no longer in the body, it cannot be reactivated.
Concerning the effect that prednisone could potentially have on a person's liver and whether someone should take it, that would depend on the status of a person's liver and should be discussed with ones treating Hepatologist.
Hi FFH...
Been awhile :)
This is from one of my prev. posts.
Hope there is some helpful info in this article for you..
As you mentioned most drugs must be filleted thru the liver and to take nothing is ideal .however not always realistic.
This is a powerful drug but the evidence would support it not being a problem with an SVR, however obviously with consultation from a knowledgeable physician(ideally a hepa)
All the best...
Will
Impact of steroids on hepatitis C virus replication in vivo and in vitro
"In conclusion, despite clinical evidence that the use of steroids aggravates recurrence of HCV, our in vitro study suggests that there is no direct stimulatory effect of steroids on the replication of HCV. As such, the increased viral loads after high-dose steroid treatment are more likely due to a downregulation of the immune response. In such patients, a dampened immune response allows viruses like HCV to replicate free of immune-mediated killing of their host cells. When a change occurs, such as a tapering or an alteration of immunosuppressant drugs, the immune system reinitiates and vigorously attempts to control the virus, resulting in acceleration of liver damage. Therefore, either steroid avoidance or maintaining low levels, coupled with a slow tapering of corticosteroids, may be beneficial to HCV-infected transplantation recipients."
http://www.ncbi.nlm.nih.gov/pubmed/17911459?ordinalpos=11&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Been awhile :)
This is from one of my prev. posts.
Hope there is some helpful info in this article for you..
As you mentioned most drugs must be filleted thru the liver and to take nothing is ideal .however not always realistic.
This is a powerful drug but the evidence would support it not being a problem with an SVR, however obviously with consultation from a knowledgeable physician(ideally a hepa)
All the best...
Will
Impact of steroids on hepatitis C virus replication in vivo and in vitro
"In conclusion, despite clinical evidence that the use of steroids aggravates recurrence of HCV, our in vitro study suggests that there is no direct stimulatory effect of steroids on the replication of HCV. As such, the increased viral loads after high-dose steroid treatment are more likely due to a downregulation of the immune response. In such patients, a dampened immune response allows viruses like HCV to replicate free of immune-mediated killing of their host cells. When a change occurs, such as a tapering or an alteration of immunosuppressant drugs, the immune system reinitiates and vigorously attempts to control the virus, resulting in acceleration of liver damage. Therefore, either steroid avoidance or maintaining low levels, coupled with a slow tapering of corticosteroids, may be beneficial to HCV-infected transplantation recipients."
http://www.ncbi.nlm.nih.gov/pubmed/17911459?ordinalpos=11&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
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