How do we know someone is autoimmune?
Many of us with cfs/me are negative to many types of tests like ANA.
Many of us with cfs/me are negative to many types of tests like ANA.
My Rituximab experience with RA and ME
- Thread starter Nielk
- Start date
Actually high ANA titer does not necessarily means you have an autoimmune illness. One can live with a high titer and never develop one.
ANA was mentioned in one of the abstracts from the IACFSME, on a longitudinal study following adolescent with infectious mononucleosis and ANA was not a predictive factor in developing ME.
ANA was mentioned in one of the abstracts from the IACFSME, on a longitudinal study following adolescent with infectious mononucleosis and ANA was not a predictive factor in developing ME.
What type of labs are used to diagnose autoimmune illnesses. I understand ANA is used as a guide, im guessing theres other tests and criteria's??
I think most of the tests for autoimmunity test for specific antibodies, so if we don't know what the errant antibodies are for a particular autoimmunity, we can't yet test for it. So... I think we could very well be autoimmune, but have no way to test for it. Or we could (mostly) not be autoimmune, but can't be sure because there's no way to test for autoantibodies we don't know exist. Of course, I could have this all wrong. It wouldn't be the first time. 
ETA: Medline -- Autoimmune Disorders
ETA: Medline -- Autoimmune Disorders
I think most of the tests for autoimmunity test for specific antibodies, so if we don't know what the errant antibodies are for a particular autoimmunity, we can't yet test for it. So... I think we could very well be autoimmune, but have no way to test for it. Or we could (mostly) not be autoimmune, but can't be sure because there's no way to test for autoantibodies we don't know exist. Of course, I could have this all wrong. It wouldn't be the first time.
Well, @Jonathan Edwards would be in a better position than me to answer, however rheumatoid arthritis have measures that correlate very well with proof of illness, RA factor and CCP antibodies.
In the case of lupus, double-stranded DNA is one of the marker that is most sensitive to a diagnosis though it is not as clear cut as RA. Lupus is more difficult to diagnose and the case definition resembles the Fukuda criteria: 'at least 3 of the following'.
What is auto-immune and what is not, is not an easy question to answer and I believe one speaker tackled that at the recent IACFSME.
Maybe that is because there are subgroups with different causes/co-factors? Research tends to average results, which blurs the subgroups, so for example a high finding in half the people and a low finding in the other half ends up showing no correlation/effect.
(Some) antivirals have immune modulatory effects as well, so when they help it may not always be due to killing viruses.
Rheumatoid Arthritis
On the NHS (and in America) you tend to follow a process towards diagnosis once symptoms become apparant and a tentative diagnosis is made. As happened for Gabby (and also myself back in May).
http://www.nhs.uk/Conditions/Rheumatoid-arthritis/Pages/Diagnosis.aspx
If the inflammatory markers are not seen as being present from the blood tests, and the x-ray of your hands doesn't reveal inflammation - despite the swelling (apparently x-rays are not always the best at spotting this either - at least so I have been informed) - and other things cannot be ruled in like e.g. anemia, then you may be tested using anti-ccp which I understand is more sensitive and disease specific (also more expensive):
https://www.rheumatology.org/publications/hotline/1003anticcp.asp
Anti-ccp is also used by the NHS as well as in the US. My GP informed me that it is expensive and they (as GPs) are no longer able to order it. The request must come from a Rheumatologist.
As for differences in treatment. Well I haven't even started on anything yet. And I must say that as typing on a keyboard is now very painful at times and for beyond short durations - and when it all flared I have never felt so ill before - treatment (if I am finally diagnosed) can't come soon enough.
Hopefully if treatment is necessary I can find more relief than Gabby did (@Nielk ) from the drugs that precede the need for Rituximab. Then again of course having ME I also wonder - as does Gabby - if treatment for one might not help the other.
But I am not getting my hopes up. I have been not at all well and have been increasingly short of temper - just waiting for the NHS to process me (plus I have had to try and complete my DLA renewal).
I don't blame the NHS. My doctors have been nothing but kind. If I had been able to go private I am sure it would all have moved much more swiftly - but none of this means a diagnosis will lead to treatment for me with Ritux: long way to go yet.
N.b Gabby and I have been speaking in private. I don't want to derail her thread with my woes - but the anti-ccp test is an important one missing from your list above I think.
On the NHS (and in America) you tend to follow a process towards diagnosis once symptoms become apparant and a tentative diagnosis is made. As happened for Gabby (and also myself back in May).
http://www.nhs.uk/Conditions/Rheumatoid-arthritis/Pages/Diagnosis.aspx
If the inflammatory markers are not seen as being present from the blood tests, and the x-ray of your hands doesn't reveal inflammation - despite the swelling (apparently x-rays are not always the best at spotting this either - at least so I have been informed) - and other things cannot be ruled in like e.g. anemia, then you may be tested using anti-ccp which I understand is more sensitive and disease specific (also more expensive):
https://www.rheumatology.org/publications/hotline/1003anticcp.asp
Anti-ccp is also used by the NHS as well as in the US. My GP informed me that it is expensive and they (as GPs) are no longer able to order it. The request must come from a Rheumatologist.
As for differences in treatment. Well I haven't even started on anything yet. And I must say that as typing on a keyboard is now very painful at times and for beyond short durations - and when it all flared I have never felt so ill before - treatment (if I am finally diagnosed) can't come soon enough.
Hopefully if treatment is necessary I can find more relief than Gabby did (@Nielk ) from the drugs that precede the need for Rituximab. Then again of course having ME I also wonder - as does Gabby - if treatment for one might not help the other.
But I am not getting my hopes up. I have been not at all well and have been increasingly short of temper - just waiting for the NHS to process me (plus I have had to try and complete my DLA renewal).
I don't blame the NHS. My doctors have been nothing but kind. If I had been able to go private I am sure it would all have moved much more swiftly - but none of this means a diagnosis will lead to treatment for me with Ritux: long way to go yet.
N.b Gabby and I have been speaking in private. I don't want to derail her thread with my woes - but the anti-ccp test is an important one missing from your list above I think.
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Back to the question autoimmunity or not.
Of course we all have our personal theories and stories (and sometimes successes with certain treatments), but anecdotal evidence is only able to give us a hint, nothing more. Sometimes it even fools us. That is why we desperately need as many randomised, placebo-controlled studies as possible, made by the top scientists and doctors.
The only study I know with truly remarkable results is the Retuximab study from Norway. If you read it, you ll see that some patients had incredible improvements and even some went into complete remission. And the disease followed a pattern very similar to other autoimmune diseases. The lagging response (dying Plasma cells and the depletion of antibodies) and the slow return of symptoms, if the treatment stops.
Of course it only worked with 60-70% of the patients. But this is nevertheless a fantastic result! A 100% cure in medicine is very rare. In RA, MS and Lupus, you often have patients, who are resistant to the standard treatment and nobody knows why. So you try other immunosupressive drugs and at the end you are able to help 90%.
The Valgangaciclovir study from Stanford was a bit disappointing. There were some improvements, but it was not overwhelming. I think, Dr. Montoya himself stated somewhere, that he now thinks some antivirals work, because of immune modulation, and not because they kill viruses. And he now uses Colchicine, which is also used in other autoimmune diseases.
The Ampligen study had some mixed results, but some people improved. The mechanism of action is not completely clear. But it certainly has an effect on the immune system.
When I had the course about autoimmune diseases in med school, they told us nearly one hundred times, that we don't know the cause of them. There are some theories, but no certainty.
Wikipedia about MS:
"The cause of MS is unknown; however, it is believed to occur as a result of some combination of environmental factors such as infectious agents and genetics. Theories try to combine the data into likely explanations, but none has proved definitive. (...) Decreased sunlight exposure resulting in decreased vitamin D production has also been put forward as an explanation. (...) Modern genetics have discovered at least twelve other genes outside the HLA locus that modestly increase the probability of MS. (...) Human herpes viruses are a candidate group of viruses. Individuals having never been infected by the Epstein-Barr virus are at a reduced risk of getting MS, whereas those infected as young adults are at a greater risk than those having had it at a younger age."
All this sounds very, very, very familiar.
As others pointed out, if we don't know the autoantibodies, driving our symptoms, we cannot test them. Even MS is mostly diagnosed through symptoms and brain scanning and not blood tests.
I don't want to say, that ME/CFS is definitely an autoimmune disease. But the studies from Norway are a very strong hint into this direction. There are probably some subtypes (as in MS, RA and Lupus as well). I think the cause and the trigger are not the most important to find, but working treatment and further insights into the pathophysiology. If the scientist can point the system, which is broken (certain nerves, the endothelium e.g.), we would have a diagnostic tool and probably a better control of symptoms.
Of course we all have our personal theories and stories (and sometimes successes with certain treatments), but anecdotal evidence is only able to give us a hint, nothing more. Sometimes it even fools us. That is why we desperately need as many randomised, placebo-controlled studies as possible, made by the top scientists and doctors.
The only study I know with truly remarkable results is the Retuximab study from Norway. If you read it, you ll see that some patients had incredible improvements and even some went into complete remission. And the disease followed a pattern very similar to other autoimmune diseases. The lagging response (dying Plasma cells and the depletion of antibodies) and the slow return of symptoms, if the treatment stops.
Of course it only worked with 60-70% of the patients. But this is nevertheless a fantastic result! A 100% cure in medicine is very rare. In RA, MS and Lupus, you often have patients, who are resistant to the standard treatment and nobody knows why. So you try other immunosupressive drugs and at the end you are able to help 90%.
The Valgangaciclovir study from Stanford was a bit disappointing. There were some improvements, but it was not overwhelming. I think, Dr. Montoya himself stated somewhere, that he now thinks some antivirals work, because of immune modulation, and not because they kill viruses. And he now uses Colchicine, which is also used in other autoimmune diseases.
The Ampligen study had some mixed results, but some people improved. The mechanism of action is not completely clear. But it certainly has an effect on the immune system.
When I had the course about autoimmune diseases in med school, they told us nearly one hundred times, that we don't know the cause of them. There are some theories, but no certainty.
Wikipedia about MS:
"The cause of MS is unknown; however, it is believed to occur as a result of some combination of environmental factors such as infectious agents and genetics. Theories try to combine the data into likely explanations, but none has proved definitive. (...) Decreased sunlight exposure resulting in decreased vitamin D production has also been put forward as an explanation. (...) Modern genetics have discovered at least twelve other genes outside the HLA locus that modestly increase the probability of MS. (...) Human herpes viruses are a candidate group of viruses. Individuals having never been infected by the Epstein-Barr virus are at a reduced risk of getting MS, whereas those infected as young adults are at a greater risk than those having had it at a younger age."
All this sounds very, very, very familiar.
As others pointed out, if we don't know the autoantibodies, driving our symptoms, we cannot test them. Even MS is mostly diagnosed through symptoms and brain scanning and not blood tests.
I don't want to say, that ME/CFS is definitely an autoimmune disease. But the studies from Norway are a very strong hint into this direction. There are probably some subtypes (as in MS, RA and Lupus as well). I think the cause and the trigger are not the most important to find, but working treatment and further insights into the pathophysiology. If the scientist can point the system, which is broken (certain nerves, the endothelium e.g.), we would have a diagnostic tool and probably a better control of symptoms.
Well I go to the Dr. Klimas group (I assume top of line tests) and they keep testing me and say I am not. I just don't know enough of which tests relate to the autoimunity (I remember one like ANA I think or something like that, keep being negative).
Ahhh I see now in the top about ANA and @SOC point. I guess I might not know then if I am autoimune. The funny thing, I am doing great CFS wise, is OI quiking my butt. I have finally raised my NK numbers and functions. HH6V is still an issue, cosaxie is back too. But I don't feel the CFS as bad as the OI now.
Ahhh I see now in the top about ANA and @SOC point. I guess I might not know then if I am autoimune. The funny thing, I am doing great CFS wise, is OI quiking my butt. I have finally raised my NK numbers and functions. HH6V is still an issue, cosaxie is back too. But I don't feel the CFS as bad as the OI now.
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This thread is about Nielk and her ME/RA/Ritux experience. Not really about anything to do with autoimmunity and the theories therein. Interesting though they may be. Could we not start a different thread for them?
Agree, i dont think we can make any conclusions but i find it interesting to try and find similarities between the treatments that have had some success.
I do wish those in Norway ie patients could post on here more about there responses. I think its hard to compare treatment success at this stage as there is alot more who have tried other treatments vs rituximab which has limitation on prescribing due to it being administered iv etc, so the numbers treated with rituximab are alot lower then other treatments. Its also about getting the correct diagnosis as there has been some non responders to rituximab but improved with methotrexate, or a combination of the two.
I would really like to see some numbers on the percentage who have improved 100% from rituximab. The one thing in common amongst all treatments are relapses occurring frequently. I dont think we have to pick one or the other but look into combinations of treatments.
Viral testing and active viral testing is just so behind the times, i think researchers need to be able to more accurately diagnose chronic infections alot more accurately as well as better research into inflammation involved in autoimmune illnesses with cytokines etc to help diagnose autoimmune aspects. Seem like testing autoimmune testing isnt much better then ME.
I do wish those in Norway ie patients could post on here more about there responses. I think its hard to compare treatment success at this stage as there is alot more who have tried other treatments vs rituximab which has limitation on prescribing due to it being administered iv etc, so the numbers treated with rituximab are alot lower then other treatments. Its also about getting the correct diagnosis as there has been some non responders to rituximab but improved with methotrexate, or a combination of the two.
I would really like to see some numbers on the percentage who have improved 100% from rituximab. The one thing in common amongst all treatments are relapses occurring frequently. I dont think we have to pick one or the other but look into combinations of treatments.
Viral testing and active viral testing is just so behind the times, i think researchers need to be able to more accurately diagnose chronic infections alot more accurately as well as better research into inflammation involved in autoimmune illnesses with cytokines etc to help diagnose autoimmune aspects. Seem like testing autoimmune testing isnt much better then ME.
Sorry to hear you're so ill at the mo @Firestormm - it's bad enough having ME without something else horrible on top of it.
Thanks so much for posting in detail about your experience, @Neilk - very interesting for the rest of us! I've got my fingers crossed for you.
Thanks so much for posting in detail about your experience, @Neilk - very interesting for the rest of us! I've got my fingers crossed for you.
@heapsreal this is for you. From the first Rituximab study. I am sure that you have seen this before. http://www.plosone.org/article/info:doi/10.1371/journal.pone.0026358
I'm not sure this autoimmune vs not autoimmune discussion is really appropriate for this thread, given it it is supposed to be about Nielk's experiences.
The only thing I want to read about in this thread is how much better Nielk is doing after treatment.
The only thing I want to read about in this thread is how much better Nielk is doing after treatment.