Aa
Autoimmune problems from Interferon
Greetings everyone, I'm new to the board. I was searching the net for info on a HCV CPPD Arthritic connection and came across the post here by Rhon. But since the latest replies to that post are over 5 years old, I thought I'd start a new one. .
I have had HCV 1a for at least 30 years. Liver is still good, but I believe I have had worse problems with Extrahepatic complications all along. I did Tx 6 years ago with Combo because I was feeling sick all the time. I came close, but no SVR. During Tx I developed a bad back problem with sciatica due to arthritic type changes that affected the sciatic nerve. I had other similar type changes since then, some of which would affect the male gender only (yep I'm a guy). I am now looking at trying the Tx with Telapravir, but I am very concerned that it may have been the Interferon that exacerbated some time of autoimmunity causing those arthritic/gouty/plaque type problems to accelerate. Of course I don't know about this for sure. It may have been arthritic changed about to happen anyhow. And of course i don't know that even if this were true that it wouldn't be more advantageous to treat the HCV anyhow because it may be more the problem. I am geared up to with treatment in early September, but would really appreciate some input on this issue to help me decide about doing treatment. Thanks everyone
wishing everyone the best embarking on the new treatment
I have had HCV 1a for at least 30 years. Liver is still good, but I believe I have had worse problems with Extrahepatic complications all along. I did Tx 6 years ago with Combo because I was feeling sick all the time. I came close, but no SVR. During Tx I developed a bad back problem with sciatica due to arthritic type changes that affected the sciatic nerve. I had other similar type changes since then, some of which would affect the male gender only (yep I'm a guy). I am now looking at trying the Tx with Telapravir, but I am very concerned that it may have been the Interferon that exacerbated some time of autoimmunity causing those arthritic/gouty/plaque type problems to accelerate. Of course I don't know about this for sure. It may have been arthritic changed about to happen anyhow. And of course i don't know that even if this were true that it wouldn't be more advantageous to treat the HCV anyhow because it may be more the problem. I am geared up to with treatment in early September, but would really appreciate some input on this issue to help me decide about doing treatment. Thanks everyone
wishing everyone the best embarking on the new treatment
I agree it's not likely that IFN would by itself "cause" autoimmune disease...but it sure could trigger a predisposition, or exacerbate one already developing. I would fit into both of those possibilities, neither of which can be determined with absolute certainty (yet), but are very highly likely based on family history, current symptoms, and a firm diagnosis of having a different type of immune system disorder.
I know about simple autoimmune markers like the ANA, RF, Sed Rate, etc....but answering whether or not my current "arthritic symptoms" (even if they are autoimmune), can be diagnosed with those simple tests is questionable. It's also impossible to ascertain with certainty how much the IFN had to do with it.
I intend to get some lab work done, but I suspect my best information in this regard has to come from networking. Eventually, if the problem progresses, I may get a Rheumy referral. So far, I don't have enough autoimmune disease presentation to get the referral.
Thanks everyone
I know about simple autoimmune markers like the ANA, RF, Sed Rate, etc....but answering whether or not my current "arthritic symptoms" (even if they are autoimmune), can be diagnosed with those simple tests is questionable. It's also impossible to ascertain with certainty how much the IFN had to do with it.
I intend to get some lab work done, but I suspect my best information in this regard has to come from networking. Eventually, if the problem progresses, I may get a Rheumy referral. So far, I don't have enough autoimmune disease presentation to get the referral.
Thanks everyone
IT IS NOT VIRTUALLY IMPOSSIBLE to diagnose Autoimmune Disorders.
I'm sending you an email.
christina
cheesenrice - your post is incorrect!
I'm sending you an email.
christina
cheesenrice - your post is incorrect!
its more than hard to tell - its virtually impossible - if one tests positive for autoimmune factors before treating this could mean several things - the main causes are genetics and chronic viral infections - the immune system is key - underactive immune response is just as likely the culprit as an overactive response - if one tests positive for autoimmune factors during or after tx the "cause" is unknown moot and speculative at best - yes interferon may exaggerate these conditions but theres no proof that it causes them - interferon is essential to a healthy immune response - its also produced naturally in our body - people with chronic hep c have impaired immune systems and NEED help fighting the infection - if the cause is genetic theres not much that can be done at present - if the cause is a chronic viral infection like hep c theres only one thing that can be done
Thanks everyone,
I don't have any diagnosed autoimmune problems, I'm just suspecting that I do. My questions in this regard to all my docs gives me very little confidence one way or the other because the response is typically that it's hard to tell if my problems are autoimmune, and if they are being caused by the hcv, or past tx with ifn. Also having a complex immune system disorder, makes it difficult to determine. So basically, it's on me to figure this out. And it is for this reason that I appreciate the feedback. I think IFN is poison for me. The question remains...how poisonous?
thanks
I don't have any diagnosed autoimmune problems, I'm just suspecting that I do. My questions in this regard to all my docs gives me very little confidence one way or the other because the response is typically that it's hard to tell if my problems are autoimmune, and if they are being caused by the hcv, or past tx with ifn. Also having a complex immune system disorder, makes it difficult to determine. So basically, it's on me to figure this out. And it is for this reason that I appreciate the feedback. I think IFN is poison for me. The question remains...how poisonous?
thanks
I have autoimmune hepatitis and hepititis c. I tried peginterferon/riba in 2008. They took me off treatment at 8 weeks. I ended up with more autoimmune disorders, more damage to my liver and no cure.
So, I hope to get into one of the DAA trials. No more INF for me.
christina
So, I hope to get into one of the DAA trials. No more INF for me.
christina
I guess for me at least 2, preferably 3 DAA's would be what I need and IF I had to take IFN for a short period like a month I might do that to hit it hard and fast, knowing I would have to immediately go on prednisone afterwards for a time.
Stefan Zeuzem, MD:
Although peginterferon lambda, a type III interferon, targets the same signal transduction pathways and the same interferon-sensitive genes inside the cell as type I interferons, the signal is transmitted into the cell through different receptors with a distinct distribution. Unlike interferon alfa receptors that exhibit a wide distribution across cell types, interferon lambda receptors are more restricted to hepatocytes, with much lower abundance on other cell types. The hope is that peginterferon lambda will act as a liver-targeted interferon, providing the advantages of similar antiviral activity to peginterferon alfa but fewer adverse effects related to nonliver targets.
At the 2011 EASL meeting, my colleagues and I[39] presented the results of a Week 12 interim analysis of the EMERGE study, a randomized phase IIb trial evaluating the safety and efficacy of peginterferon lambda/ribavirin vs peginterferon alfa-2a/ribavirin in 526 treatment-naive patients infected with genotypes 1-4 HCV (Capsule Summary). Patients were randomized to 1 of 4 treatment arms:
Peginterferon alfa-2a 180 µg/week plus ribavirin
Peginterferon lambda 120 µg/week plus ribavirin
Peginterferon lambda 180 µg/week plus ribavirin
Peginterferon lambda 240 µg/week plus ribavirin
Ribavirin was dosed at 800 mg/day in patients with genotype 2/3 HCV and 1000-1200 mg/day in patients with genotype 1/4 HCV. Patients with genotype 2/3 infection will receive a total of 24 weeks of treatment, whereas patients with genotype 1/4 infection will receive 48 weeks of therapy. The primary endpoint is complete early virologic response (cEVR) defined as undetectable HCV RNA at Week 12 of treatment.
Rates of RVR were significantly higher with the 2 highest peginterferon lambda doses for all HCV genotypes (14.7% to 16.5% for genotype 1/4; 66.7% to 75.9% for genotype 2/3) vs peginterferon alfa-2a (5.8% for genotype 1/4; 31.0% for genotype 2/3) (P < .05 for each comparison). Among patients with genotype 1/4 infection, cEVR rates were significantly higher at all peginterferon lambda doses (55.0% to 56.3%) relative to peginterferon alfa-2a (37.9%; P < .05 for each comparison); however, cEVR rates were similar with peginterferon lambda (83.3% to 96.6%) vs peginterferon alfa-2a (86.2%) among patients with genotype 2/3 infection, likely owing to the high sensitivity of genotype 2/3 HCV to peginterferon alfa. It will be very interesting to determine if the slight advantage with regard to early antiviral activity translates into improved SVR rates as this trial progresses.
This analysis also provided promising safety data demonstrating a more than 2-fold lower incidence of myalgia, pyrexia, arthralgia, chills, and rash with peginterferon lambda/ribavirin vs peginterferon alfa-2a/ribavirin. The most frequent adverse events among patients receiving peginterferon lambda included fatigue, headache, nausea, and insomnia. Hematologic toxicities were less frequent with peginterferon lambda vs peginterferon alfa-2a, including a lower rate of hemoglobin < 10 g/dL (12.9% to 20.5% vs 43.9%, respectively), a lower rate of neutrophil count < 750 cells/mm3 (0% to 0.8% vs 15.2%, respectively), and a lower incidence of platelet count < 25,000 cells/mm3 (0% vs 1.5). For most adverse events, a clear dose relationship was not apparent for peginterferon lambda. However, aminotransferase elevations were more frequent with the highest peginterferon lambda dose (17.4%) relative to lower doses of peginterferon lambda (0.8% to 2.3%) and to peginterferon alfa-2a (7.6%). Direct hyperbilirubinemia was also more frequent with peginterferon lambda vs peginterferon alfa-2a. Indeed, 4 patients discontinued peginterferon lambda as a result of elevated bilirubin vs 0 patients receiving peginterferon alfa-2a. After discontinuing or reducing the dose of peginterferon lambda, bilirubin levels decreased rapidly. This study only enrolled patients without cirrhosis, therefore more safety data will be needed for this drug, particularly in patients who have advanced fibrosis and cirrhosis.
Paul Y. Kwo, MD:
A notable finding from this study was the demonstration of the extent to which peginterferon alfa contributes to anemia when given with ribavirin. The difference in the frequencies of reduced hemoglobin levels with peginterferon lambda vs peginterferon alfa-2a was substantial.
Graham R. Foster, FRCP, PhD:
This dataset is certainly of great interest. However, one unknown is whether peginterferon lambda will have sufficient immunostimulatory activity to impart sustained viral suppression. It certainly demonstrates a high level of activity against HCV in the liver and is, therefore, an effective antiviral agent; however, the SVR data from this trial will be of critical importance.
Paul Y. Kwo, MD:
Resuming our earlier discussion on the potentially diminished role of peginterferon therapy for HCV in the future, I suspect interferon use will not be eliminated for all patients. It is reasonable to hope that most patients will be candidates for combinations of DAA therapies without interferon in the next 5-10 years. However, there likely will be some patients in whom interferon will be required, and if peginterferon lambda persists in development with the same promising results, it may be a very viable choice
Although peginterferon lambda, a type III interferon, targets the same signal transduction pathways and the same interferon-sensitive genes inside the cell as type I interferons, the signal is transmitted into the cell through different receptors with a distinct distribution. Unlike interferon alfa receptors that exhibit a wide distribution across cell types, interferon lambda receptors are more restricted to hepatocytes, with much lower abundance on other cell types. The hope is that peginterferon lambda will act as a liver-targeted interferon, providing the advantages of similar antiviral activity to peginterferon alfa but fewer adverse effects related to nonliver targets.
At the 2011 EASL meeting, my colleagues and I[39] presented the results of a Week 12 interim analysis of the EMERGE study, a randomized phase IIb trial evaluating the safety and efficacy of peginterferon lambda/ribavirin vs peginterferon alfa-2a/ribavirin in 526 treatment-naive patients infected with genotypes 1-4 HCV (Capsule Summary). Patients were randomized to 1 of 4 treatment arms:
Peginterferon alfa-2a 180 µg/week plus ribavirin
Peginterferon lambda 120 µg/week plus ribavirin
Peginterferon lambda 180 µg/week plus ribavirin
Peginterferon lambda 240 µg/week plus ribavirin
Ribavirin was dosed at 800 mg/day in patients with genotype 2/3 HCV and 1000-1200 mg/day in patients with genotype 1/4 HCV. Patients with genotype 2/3 infection will receive a total of 24 weeks of treatment, whereas patients with genotype 1/4 infection will receive 48 weeks of therapy. The primary endpoint is complete early virologic response (cEVR) defined as undetectable HCV RNA at Week 12 of treatment.
Rates of RVR were significantly higher with the 2 highest peginterferon lambda doses for all HCV genotypes (14.7% to 16.5% for genotype 1/4; 66.7% to 75.9% for genotype 2/3) vs peginterferon alfa-2a (5.8% for genotype 1/4; 31.0% for genotype 2/3) (P < .05 for each comparison). Among patients with genotype 1/4 infection, cEVR rates were significantly higher at all peginterferon lambda doses (55.0% to 56.3%) relative to peginterferon alfa-2a (37.9%; P < .05 for each comparison); however, cEVR rates were similar with peginterferon lambda (83.3% to 96.6%) vs peginterferon alfa-2a (86.2%) among patients with genotype 2/3 infection, likely owing to the high sensitivity of genotype 2/3 HCV to peginterferon alfa. It will be very interesting to determine if the slight advantage with regard to early antiviral activity translates into improved SVR rates as this trial progresses.
This analysis also provided promising safety data demonstrating a more than 2-fold lower incidence of myalgia, pyrexia, arthralgia, chills, and rash with peginterferon lambda/ribavirin vs peginterferon alfa-2a/ribavirin. The most frequent adverse events among patients receiving peginterferon lambda included fatigue, headache, nausea, and insomnia. Hematologic toxicities were less frequent with peginterferon lambda vs peginterferon alfa-2a, including a lower rate of hemoglobin < 10 g/dL (12.9% to 20.5% vs 43.9%, respectively), a lower rate of neutrophil count < 750 cells/mm3 (0% to 0.8% vs 15.2%, respectively), and a lower incidence of platelet count < 25,000 cells/mm3 (0% vs 1.5). For most adverse events, a clear dose relationship was not apparent for peginterferon lambda. However, aminotransferase elevations were more frequent with the highest peginterferon lambda dose (17.4%) relative to lower doses of peginterferon lambda (0.8% to 2.3%) and to peginterferon alfa-2a (7.6%). Direct hyperbilirubinemia was also more frequent with peginterferon lambda vs peginterferon alfa-2a. Indeed, 4 patients discontinued peginterferon lambda as a result of elevated bilirubin vs 0 patients receiving peginterferon alfa-2a. After discontinuing or reducing the dose of peginterferon lambda, bilirubin levels decreased rapidly. This study only enrolled patients without cirrhosis, therefore more safety data will be needed for this drug, particularly in patients who have advanced fibrosis and cirrhosis.
Paul Y. Kwo, MD:
A notable finding from this study was the demonstration of the extent to which peginterferon alfa contributes to anemia when given with ribavirin. The difference in the frequencies of reduced hemoglobin levels with peginterferon lambda vs peginterferon alfa-2a was substantial.
Graham R. Foster, FRCP, PhD:
This dataset is certainly of great interest. However, one unknown is whether peginterferon lambda will have sufficient immunostimulatory activity to impart sustained viral suppression. It certainly demonstrates a high level of activity against HCV in the liver and is, therefore, an effective antiviral agent; however, the SVR data from this trial will be of critical importance.
Paul Y. Kwo, MD:
Resuming our earlier discussion on the potentially diminished role of peginterferon therapy for HCV in the future, I suspect interferon use will not be eliminated for all patients. It is reasonable to hope that most patients will be candidates for combinations of DAA therapies without interferon in the next 5-10 years. However, there likely will be some patients in whom interferon will be required, and if peginterferon lambda persists in development with the same promising results, it may be a very viable choice
Thanks penn, I agree about the waiting. Even though my autoimmune disease status is uncertain, the possibility is high for me. This decision to tx keeps coming back to the biopsy. If over stage 2, waiting 3 years for the DAA's does not seem prudent. Otherwise, sit it out.
Bizzy, after IFN triggered my autoimmune problems, my Hep Dr Donald Jensen of Chicago told me years ago " You can never go on IFN again. You need to wait for a non-IFN treatment" So now I wait....
Bizzy, after IFN triggered my autoimmune problems, my Hep Dr Donald Jensen of Chicago told me years ago " You can never go on IFN again. You need to wait for a non-IFN treatment" So now I wait....
It's been years since I've had the common Autoimmune tests like RA, ANA, etc. They were normal. My immune testing for me/cfs has been far from normal. These tests are not mainstream and involve very complex functions that go well over my head of understanding. I can say that me/cfs is an inflammatory disease with a cytokine panels showing extremely elevated cytokines such IL6&8. Also tested is RNaseL, TNFa, and most significantly the NK cell count and function, which for people with me/cfs is all but non existent. Anyhow, me/cfs is not considered an autoimmune disease entirely. I believe my doc who treats this would be able to spot typical autoimmune problems like RA and Lupus. But I could see some of the more obscure arthritis conditions being missed because they are dealing with much more complex and serious conditions. The last test he had done that to the best of my knowledge that would have anything to do with autoimmunity was the VIP (Vasoactive Intestinal Peptide). Anyhow, you would think that since I have blood being tested by the best immunologist in the country, they would spot autoimmunity....but then again, this is not what they are looking for.
I did have a flare of psoriasis with SOC, but that cleared quickly post Tx. I realize that the arthritic conditions I have that seemed to be exacerbated by past IFN tx, is not RA. I also realize the best way to rule out an autoimmune disease is to see a Rheumy. I saw an Osteo a few days ago and he said...It doesn't sounds like RA, but that I would have to see a Rheumy because they have all kinds of tests for diagnosing other autoimmune conditions, including the ones that show negative on common tests. I'll end up there eventually, but doubt it will be before needing to decide about Tx.
My Hep doc said that IFN can cause these kinds of progressive arthritic conditions, but HCV can as well....it's hard to tease out which it is. For me, I think it's both, and that's one hell of a catch 22....unless, I wait for tx that doesn't include IFN.
My me/cfs doc says the Tx will not exacerbate my me/cfs, but even though he knows these complex immune disorders, and even uses Ampligen (Cousin of IFN) for some tx's, he's not very familiar with treating HCV.
I've made tremendous progress with my me/cfs. This is rare. Very few get to recover. ME/CFS obviously has an infectious pathogenesis and HCV, at least for me, has some role in this. I have put all diagnosed infections down and have only the HCV left. Will SVR take me across the finish line of getting my life back fully? I suspect it will ultimately. Will the IFN cause exacerbated health problems defeating the purpose of Tx? It's possible as well. Can I wait for tripple DAA's without IFN, 3 years down the road and therefore avoid this threat? I very reluctantly have to say that a biopsy may be the final factor answering that question.
I really appreciate everyone taking the time to help me sort this out. Thank you.
I did have a flare of psoriasis with SOC, but that cleared quickly post Tx. I realize that the arthritic conditions I have that seemed to be exacerbated by past IFN tx, is not RA. I also realize the best way to rule out an autoimmune disease is to see a Rheumy. I saw an Osteo a few days ago and he said...It doesn't sounds like RA, but that I would have to see a Rheumy because they have all kinds of tests for diagnosing other autoimmune conditions, including the ones that show negative on common tests. I'll end up there eventually, but doubt it will be before needing to decide about Tx.
My Hep doc said that IFN can cause these kinds of progressive arthritic conditions, but HCV can as well....it's hard to tease out which it is. For me, I think it's both, and that's one hell of a catch 22....unless, I wait for tx that doesn't include IFN.
My me/cfs doc says the Tx will not exacerbate my me/cfs, but even though he knows these complex immune disorders, and even uses Ampligen (Cousin of IFN) for some tx's, he's not very familiar with treating HCV.
I've made tremendous progress with my me/cfs. This is rare. Very few get to recover. ME/CFS obviously has an infectious pathogenesis and HCV, at least for me, has some role in this. I have put all diagnosed infections down and have only the HCV left. Will SVR take me across the finish line of getting my life back fully? I suspect it will ultimately. Will the IFN cause exacerbated health problems defeating the purpose of Tx? It's possible as well. Can I wait for tripple DAA's without IFN, 3 years down the road and therefore avoid this threat? I very reluctantly have to say that a biopsy may be the final factor answering that question.
I really appreciate everyone taking the time to help me sort this out. Thank you.
Rheumatoid arthritis is an autoimmune condition and different from arthritis in general. There are tests that can determine if what you have is rheumatoid arthritis and it has it's own treatment approach, as I understand it. As well, you can be tested for the presence of thyroid antibodies prior to treatment - if you don't have thyroid issues already - to determine if you're more or less likely to develop thyroid issues while on treatment, if the interferon will be more or less likely to trigger them. I developed thyroid issues while on treatment and arthritis shortly after stopping treatment. I was tested for rheumatoid arthritis as one autoimmune condition can lead to another so my docs thought it was reasonable to test. It came back negative. I mention that to say that not all arthritis is a result of autoimmune conditions, mine isn't. I'd echo Susie's advice and pursue it with a rheumatologist or your Hepatologist. Good luck with all this, I know you're sifting through quite a bit.
Trish
Trish
As far as re-treating goes... As you would already know your chances of success have increased with the availability of the new meds...possibly tempered somewhat by your previous unsuccesful attempt.
Having had as you mentioned ..the virus now for a least 30 years.and with progression of damage known to speed up for most when past 50 years old the benefits of re-treating may outweigh the risks.
Always a personal decision tho..made with a knowledgeable doctor.
Good luck..
Will
I am wondering about this new study drug peg-interferon lambda which seems to be showing good results with reduced sides.
Thanks Susie, Weighing potential benefit against potential hazard is precisely what I'm doing. I am talking with numerous health professionals on this issue, but that alone is not enough. Networking with others in the same situation, and who have "already been there" is often a more powerful tool when asking these kinds of questions. I am looking everywhere possible for these answers. Thanks for your input.
This is really a discussion to have with your rheumatologist and possibly your hep doc. We do know that autoimmune issues can be made worse by interferon. So, to me, it would be a risk vs benefit discussion. Good luck with your decision making.
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