Immunoadsorption to remove ß2 adrenergic receptor antibodies in Chronic Fatigue Syndrome CFS/ME (2018) Scheibenbogen et al

[Pibee]

I didn't necessary think level of autoantibodies correlate with symptoms, very clearly and obviously they dont , but could indicate more chance that tthe person has autoimmune problem in general, by some other, not yet discovered antibodies..
well.. this is how I imagine it, but could be way off.

but as @Jonathan Edwards is saying the difference with healthy controls is way too small to indicate these antibodies are pathological in a way like anti-TPO is in Hashimoto and like diseases, but again, there is clearly statistical difference, confirmed in other trials too (esp for other comorbid diseases like POTS), which still says something.
It's not by chance finding. We can not say it's causing symptoms, but dismissing it as irrelevant is also not scientific, because the relevance is confirmed with significance.
I dont know anything about immunology to guess why would some antibodies be significantly elevated in ME/CFS patients, and in top 10% scores in 30% of patients, if they're not relevant for the disease or causing it.

 

[Gingergrrl]

I didn't necessary think level of autoantibodies correlate with symptoms, very clearly and obviously they dont , but could indicate more chance that tthe person has autoimmune problem in general, by some other, not yet discovered antibodies.. well.. this is how I imagine it, but could be way off.

I wanted to clarify that I didn't think that you personally were saying this vs. it that three Neuros told me in 2016 when we discovered I had the calcium channel autoantibody. I had (wrongly) assumed that the higher the autoantibody titer, the worse the symptoms, but they told me this was not the case. It was my ME/CFS and MCAS doctors who felt the autoantibodies were significant (including the Cell Trend Abs) and it was the IVIG & Ritux that have put me almost into what I would call remission (if it were not for remaining POTS and autonomic symptoms). This has to mean something and I wish I knew more about the science to piece it all together.

but as @Jonathan Edwards is saying the difference with healthy controls is way too small to indicate these antibodies are pathological in a way like anti-TPO is in Hashimoto and like diseases

I am just guessing but there must have been a time in science when we did not know about anti-TPO in Hashimoto's and they could have been dismissed just like the beta-adrenergic and anti-muscarinic autoantibodies are being dismissed now (in general, not by you personally)! We now know the calcium channel autoantibodies are linked to small cell lung cancer and LEMS (sometimes, not always) but I am sure there was a point in science that we did not know this either.

but again, there is clearly statistical difference, confirmed in other trials too (esp for other comorbid diseases like POTS), which still says something.

I totally agree with you.

It's not by chance finding. We can not say it's causing symptoms, but dismissing it as irrelevant is also not scientific, because the relevance is confirmed with significance.

I agree.

 

[Jonathan Edwards]

Wish there is somewhere I could read about T cells autoimmunity, as this is so rarely used and discussed.

Some interesting comments, @Pibee. I tend to agree.

It is doubtful whether T cell autoimmunity actually exists, except in the rare genetic AIRE syndrome where there is a defect in thymic selection. A lot of immunologists assume that T cell autoimmunity underlies B cell autoimmunity but in fact whenever you look for it it is not there.

What we do know about are diseases where T cell behaviour is abnormal, but probably not directed at self. These include psoriasis, Crohn's disease and Reiter's syndrome. Some of these conditions are linked to cytokine receptor genes specifically involved in T cell activation. some are linked to innate immune abnormalities. Analysis of blood T cells does not tend to show anything obvious however.

 

[Luther Blissett]

I view it as either ME/CFS will have an autoimmune subgroup, and if so, then these studies are very important in identifying it and leading to additional research. Or the alternative that ME/CFS does NOT have an autoimmune subgroup and in that case, we need to identify the responders to autoimmune treatments (like high dose IVIG, IA or PP, Rituximab, etc) and realize that they are a misdiagnosed group, possibly with a completely different illness, and then pull them out of the ME/CFS research so it does not confound it, which benefits everyone IMO.

You're missing (I think) that

• there could be an autoimmune subgroup
• this study not useful for finding them
• there could be people who respond to autoimmune treatments because of a co-morbid condition with ME

 

[Jonathan Edwards]

You're missing (I think) that

• there could be an autoimmune subgroup
• this study not useful for finding them
• there could be people who respond to autoimmune treatments because of a co-morbid condition with ME

Maybe you meant it but there could be NO autoimmune subgroup.

Autoantibodies are commonplace in normal healthy people. Autoimmunity as an aspect of disease implies more than that and at present we do not have strong evidence for autoimmunity as such in ME.

 

[Pibee]

@Jonathan Edwards, arent there also autoreactive T cells in MS?

Also, I dont get why is nobody much excited about CycloME being successful.

 

[Trish]

Also, I dont get why is nobody much excited about CycloME being successful.

I assume you mean Cyclophosphamide. As I understand it, this is, or was, being tested on patients who did not respond to Rituximab by Fluge and Mella, and they found some responded.

I don't know what the status of that research is now that Rituximab has been found not to be effective in the Stage 3 trial.

Can anyone enlighten us?

 

[Jonathan Edwards]

@Jonathan Edwards, arent there also autoreactive T cells in MS?

Also, I dont get why is nobody much excited about CycloME being successful.

The problem with looking at T cell 'auto reactivity' is that you have to look at cell responses to peptides in a dish. And all T cells in a dish respond a bit to anything so you have to decide how much response you consider positive. If there are 1000 brain proteins then there might be 100,000 peptides to look at. How do you decide what is abnormal reactivity? Well, presumably you need to compare with normal T cells and show that there is a consistent overactivity of T cells in MS to certain proteins, like myelin basic protein.

Although people have talked about T cell responses like this for thirty years I am not aware that it is generally accepted that we have good evidence for reliable reactivity. After, if there was it would be another useful diagnostic test option and we should have masses of papers discussing whether T cell responses or oligoclonal bands are more specific. Oligoclonal bands need a lumbar puncture so T cell responses from ordinary good would be a good test to have. I am not aware of any such test and that makes me pretty sure that nobody has actually shown consistent T cell auto reactivity in MS.

The situation is confused by the fact that you probably do get auto reactive T cells in mice that have been deliberately artificially made to react to brain proteins using huge doses of adjuvant. But that is because they have been deliberately made to have T cell reactivities. It does not in any way tell us that human MS is like that.

I may be out of date but things didn't change for the thirty years I followed this while working in the lab.


The problems with cycloME are firstly that it is not blinded so suffers the same problems as PACE in that respect, secondly that cyclophosphamide is very toxic, with long term risk of bladder cancer, and thirdly because cycle hits lots of types of cell any positive result does not help much with understanding the mechanism. Rituximab would have been good because it only hits B cells.

 

[Pibee]

The problem with looking at T cell 'auto reactivity' is that you have to look at cell responses to peptides in a dish. And all T cells in a dish respond a bit to anything so you have to decide how much response you consider positive. If there are 1000 brain proteins then there might be 100,000 peptides to look at. How do you decide what is abnormal reactivity? Well, presumably you need to compare with normal T cells and show that there is a consistent overactivity of T cells in MS to certain proteins, like myelin basic protein.

Although people have talked about T cell responses like this for thirty years I am not aware that it is generally accepted that we have good evidence for reliable reactivity. After, if there was it would be another useful diagnostic test option and we should have masses of papers discussing whether T cell responses or oligoclonal bands are more specific. Oligoclonal bands need a lumbar puncture so T cell responses from ordinary good would be a good test to have. I am not aware of any such test and that makes me pretty sure that nobody has actually shown consistent T cell auto reactivity in MS.

The situation is confused by the fact that you probably do get auto reactive T cells in mice that have been deliberately artificially made to react to brain proteins using huge doses of adjuvant. But that is because they have been deliberately made to have T cell reactivities. It does not in any way tell us that human MS is like that.

I may be out of date but things didn't change for the thirty years I followed this while working in the lab.


The problems with cycloME are firstly that it is not blinded so suffers the same problems as PACE in that respect, secondly that cyclophosphamide is very toxic, with long term risk of bladder cancer, and thirdly because cycle hits lots of types of cell any positive result does not help much with understanding the mechanism. Rituximab would have been good because it only hits B cells.

I see, thanks for explaining. So researching T cells autoreactivity is much more complicated than B cells. Ah..

aboout CycloME, I know it wasnt blinded, but if they said the results are very good, better than Rituximab results, this should be exciting.
Toxic or not, maybe we can get some break for a few years at least :/ I mean, there must be a reason why they did a study at the first place

Btw, I dont understand then about Mark Davis T cell clonal expansion findings, and he compared them to MS and acute Lyme. What would this indicate? This is actually a research on T cells autoimmunity right?
I think he mentioned he has a suspect protein (pathogen?) they react to but still nothing published.

My question is actually: to what kind of therapy his findings actually lead to? Things like Cyclo that kill T cells?

 

[Jonathan Edwards]

Btw, I dont understand then about Mark Davis T cell clonal expansion findings, and he compared them to MS and acute Lyme. What would this indicate? This is actually a research on T cells autoimmunity right?
I think he mentioned he has a suspect protein (pathogen?) they react to but still nothing published.

My question is actually: to what kind of therapy his findings actually lead to? Things like Cyclo that kill T cells?

T cell clonal expansion does not mean T cell auto reactivity. In Lyme the T cells will be anti-Lyme. In MS I think the T cell expansion is in the brain. That is a quite different matter because once T cells get to a tissue they will expand clones either in response to antigen or innate signals. They cannot be compared with blood T cells, which puzzled me with the Davis news briefing. There may be clinical expansion in blood too but that does not mean the T cells are recognising self. After all in 'flu' we feel terrible because T cells are expanding very usefully in response to 'flu' virus.

I don't think Mark Davis's findings lead to anything very specific so far. If T cells are involved we need to know in what way. You might want more of them or less of them. Cycle kills T cells but not very usefully unless you use huge doses with severe long term risks.

 

[Gingergrrl]

You're missing (I think) that

• there could be an autoimmune subgroup
• this study not useful for finding them
• there could be people who respond to autoimmune treatments because of a co-morbid condition with ME

I think I didn't explain it well but I think we are saying the same thing. In your scenario #1, there turns out to be an autoimmune sub-group within ME/CFS which is one of the options I was referring to. I did not state your scenario #2, but I agree with you, that this particular study may not be the study that finds it. But I also think this study is a good first step for future research and should not be discarded so quickly IMO. I also mentioned your scenario #3, which is that ME/CFS is NOT an autoimmune condition and the responders have either a co-morbid, or completely different diagnosis and this is why they responded. If we could identify these individuals, they could be studied separately, which does not confound the research and benefits everyone IMO.

Autoantibodies are commonplace in normal healthy people.

But what about in very sick people like myself? I was going to mention those in the Ritux and Immunoadsorption studies who had high autoantibody levels AND were very sick. But even if we discount them for some reason, I will use myself as an example.

I got sick in Jan 2013 and by 2015, I could not breathe, stand, or walk without a wheelchair and could not eat food without anaphylaxis and ended up in hospital. I would consider someone who could not breathe, walk, or eat food to be very sick. By early 2016, we started to identify that I had all of these autoantibodies (except for the two Hashimoto Abs which we'd discovered in 2013). In my case, I have all of these autoantibodies AND I am not a "normal, healthy person". So the example does not relate to me, even though it might to others if they have autoantibodies but are in good health. But those people would not be participants in these studies!

 

[Jonathan Edwards]

But what about in very sick people like myself? I was going to mention those in the Ritux and Immunoadsorption studies who had high autoantibody levels AND were very sick. But even if we discount them for some reason, I will use myself as an example.

I got sick in Jan 2013 and by 2015, I could not breathe, stand, or walk without a wheelchair and could not eat food without anaphylaxis and ended up in hospital. In my case, I have all of these autoantibodies AND I am not a "normal, healthy person". So the example does not relate to me, even though it might to others if they have autoantibodies but are in good health. But those people would not be participants in these studies!

I very fair question @Gingergrrl, but here is my answer.

Autoantibodies are only taken as likely to be important in an illness if they are the sort of antibodies that correlate with that particular illness. That statistical correlation is the way of having confidence that they are not just there by chance. For some illnesses the correlation is strong enough to make things easy because the number of healthy people with the autoantibody is small (for instance for anti-DNA antibodies). For other illnesses like hypothyroidism the correlation is more blurred - about 25-30% of normal people may have thyroid antibodies. But if the antibody does not fit the illness it is ignored because there is no correlation to the wrong sort of illness.

It can also help if levels are very high because often very high levels are rare in normal people. For the antibodies Dr Scheibenbogen has been studying, if I remember rightly the highest levels were actually in normal people - or at least there was no obvious difference between top levels in normals and ME. And these are antibodies that do not seem to correlate tightly with any particular illness - they are blurry ones. They seemed to be slightly more common in ME but there have been reports of them being slightly more common in other things and not much has come of it.

We have talked on the forums for a good few years and my impress is that your illness is not just ME. It certainly sounds as if you have an autoimmune disease. Not being able to breathe is not a feature of ME as far as I know. And my understanding is that you have other autoantibodies that might be more relevant. So I think you have been right to think of yourself as an exception.

 

[Gingergrrl]

very fair question @Gingergrrl, but here is my answer.

Thank you for your detailed answer and I really am trying to understand all of this! I think someone like me could end up in a study like Dr. Scheibenbogen's (in theory, I do not live in Germany!) and could confound the results which would not be helpful for me, for the study, or for anyone.

Autoantibodies are only taken as likely to be important in an illness if they are the sort of antibodies that correlate with that particular illness. That statistical correlation is the way of having confidence that they are not just there by chance.

How would someone figure out the statistical correlation that you mention? My doctors (and these are really solid doctors: an Endo who treats my Hashimoto's, an MCAS specialist who is an immunologist, and an ME/CFS specialist) all feel that my autoantibodies, including the Cell Trend autoantibodies, are extremely relevant in my case. But (other than Hashimoto's) these autoantibodies do not correlate with a specific illness at this point in science. The beta-adrenergic Abs correlate with POTS (which was confirmed for me on TTT at Stanford and every doc I have ever seen agrees that I have POTS). The calcium channel autoantibody correlates with LEMS and small cell lung cancer (but I do not have either disease) and the anti GAD65 Ab correlates with diabetes (which I do not have) and Stiff Person Syndrome (which I do not have). And the anti-muscarinic Abs, I am told, can correlate with ME/CFS (which I believe I do not have) and with muscle weakness (which was profound for me prior to IVIG & Rituximab).

It seems to me (and I'd love to hear your thoughts on this) that autoantibodies exist BEFORE they are officially correlated with a specific disease by scientists. Someone (and it might have been you!) once told me that Dr. Angela Vincent discovers thousands of new autoantibodies every year that do not yet correlate with any specific disease (but they may in the future). So at this point in time, my two Hashi's autoantibodies link to Hashimoto's Disease b/c prior to being put on Armour Thyroid both were VERY high, my TSH was high, my T3 & T4 were off, etc, and I had the symptoms of hypothyroidism (in 2013).

But the other Auto-abs are less clear. I had many symptoms matching with LEMS and SPS (stiff person syndrome) prior to treatment but absolutely did not meet criteria for either disease, just like I do not meet criteria for ME/CFS. Without question I meet full criteria for POTS (but now even my POTS is greatly improved w/my treatments). And my positive ANA (1:160, speckled pattern) is probably a reflection of all of this "Autoimmune chaos" as my doctors call it. So wouldn't it be logical that even though my illness has no official name (besides POTS & MCAS) that it is autoantibody driven and some day science will give it a label? It is maddening not to have a name, and this will sound weird, but there would be some comfort to knowing it is ME/CFS and I can stop searching.

For other illnesses like hypothyroidism the correlation is more blurred - about 25-30% of normal people may have thyroid antibodies.

I agree but in my case, I really do have Hashimoto's per all doctors who've seen me.

But if the antibody does not fit the illness it is ignored because there is no correlation to the wrong sort of illness.

I am not sure what you mean re: "no correlation to the wrong sort of illness" and keep re-reading that sentence! I think I said it all above but I don't understand why autoantibodies would be ignored in someone who is extremely ill and symptomatic like I was (pre-treatment) vs. investigating them further and doing appropriate autoimmune treatments?

For the antibodies Dr Scheibenbogen has been studying, if I remember rightly the highest levels were actually in normal people - or at least there was no obvious difference between top levels in normals and ME. And these are antibodies that do not seem to correlate tightly with any particular illness - they are blurry ones. They seemed to be slightly more common in ME but there have been reports of them being slightly more common in other things and not much has come of it.

I actually do not know the statistics on this so I can't comment. But I think the autoantibodies (at this point in time) that do not correlate tightly with any particular illness and are "blurry" as you say, may still be extremely important. I believe without question they are important in my case, and I believe they may also be important in some cases of ME/CFS if there turns out to be an autoimmune subgroup (which I still think there might be and I think Dr. Scheibenbogen does, too).

We have talked on the forums for a good few years and my impress is that your illness is not just ME. It certainly sounds as if you have an autoimmune disease.

I wasn't sure what you thought and for some reason, it is a relief to hear you say that I have an autoimmune disease. I'm assuming this is b/c I have 11 autoantibodies (possibly more) regardless if they fully match w/a known illness (like lupus or LEMS). And I assume also b/c I have done so incredibly well w/two autoimmune treatments: high dose IVIG & Rituximab. Right now I am taking care of my dog who just had back surgery (I post about this on the other board and won't get off track here) but aside from how incredibly difficult this is physically and emotionally, I am currently the healthiest I've been since 2013, and without question since 2015 where I was near death from anaphylaxis in hospital.

I was on a steady decline for 4+ years (my illness was never relapsing-remitting) until I did these treatments. I don't know what happens when I stop the treatments but I know at present, I can breathe, I can walk without wheelchair (short distances only), and my MCAS/allergic reactions remain in remission. So I am happy when you validate I have an autoimmune disease but I wish I knew which one (besides Hashimoto's). I have been given the label "Autoimmune POTS" by several docs which I agree is accurate. But no doctor can explain the level of muscle weakness and breathing weakness (pre-treatment) that is now gone, b/c it exceeds any definition of POTS alone. The only explanation is that it is due to some of the autoantibodies (anti-muscarinic, calcium channel, and anti GAD65). Does this make sense? I find it so hard to believe there are not others in my situation and I can't be the only person on earth with this particular version of an illness!

Not being able to breathe is not a feature of ME as far as I know.

I agree and it was one of the main reasons that I never felt I matched with ME (besides that I have no cognitive/mental fatigue, brain fog, or PEM). But I had extreme muscle fatigue and weakness pre-treatment and my daily life was that of an invalid who could not open a water bottle, turn on a shower faucet, or open their own front door.

And my understanding is that you have other autoantibodies that might be more relevant.

Which ones do you think are relevant in my case? My feeling was that you completely discount the autoantibodies that Dr. Scheibenbogen is studying (Cell Trend) but I am positive for 7 of 9 of them and I think they are very relevant and important (even if she ultimately cannot make a connection to ME/CFS and she discovers a new illness). I hate to see them discounted and many doctors believe in them. Dr. Jill Schofield (who is not my doctor but I had several e-mails w/her and watched her present about this topic for Dysautonomia International) also feels these autoantibodies are very relevant to the emerging field of "Autoimmune Dysautonomia". She practices in Colorado and uses treatments similar to mine for autoimmune dysautonomia (which matches my experience exactly).

 

[Jonathan Edwards]

Dear @Gingergrrl,
These are all very reasonable questions but they do have answers!
The maths of correlations between tests and illnesses is quite subtle and complicated. As non-mathematical ordinary people we are actually quite good at picking out what signifies what. We can work out that if there is a mark on the kitchen floor of a sort we have never seen before it may well be something to do with the new shopping trolley we bought last week. Correlations can be got from large numbers of things that match or from very unusual things that occur together when nothing else matches. If someone has a unique type of illness and has a unique pattern of autoantibodies that is quite likely to be relevant.

Also I spent thirty years looking at antibody correlations with disease and I got to know which ones pan out as relevant and which ones tend not to. So did Angela Vincent. We have very much the same opinion on all the antibodies I know about - which ones are definitely relevant and which ones maybe not. Antibodies to muscarinic and adrenergic receptors are hard to interpret. Thyroid autoantibodies are easy - they cause disease. But they are still blurry on the correlation. That does not matter because we have come to understand that they often 'hitch-hike' on to other autoimmune diseases and are rather common anyway. It is all very complex but you will find that most immunologists who have actually worked on finding new antibodies themselves have a similar opinion of them.

 

[Gingergrrl]

These are all very reasonable questions but they do have answers!

Thank you and I appreciate you saying that. I don't want to take this thread off track but I think this is all okay since it is about autoantibodies (including the beta-adrenergic and anti-muscarinic in the study) and my feeling that these autoantibodies are very important and that I want doctors like Dr. Scheibenbogen to continue her line of research.

If someone has a unique type of illness and has a unique pattern of autoantibodies that is quite likely to be relevant.

This is extremely validating to hear and it is my feeling and the feeling of my two doctors. I do not see any other explanation for my bizarre constellation of symptoms outside of these autoantibodies and I believe they are behind everything that I have experienced (except possibly my MCAS was triggered by toxic mold exposure).

Also I spent thirty years looking at antibody correlations with disease and I got to know which ones pan out as relevant and which ones tend not to. So did Angela Vincent. We have very much the same opinion on all the antibodies I know about - which ones are definitely relevant and which ones maybe not.

I assumed that you both had similar experience and opinions re: autoantibodies and I tried contacting Dr. Vincent in the past via the e-mail on her website but never got a reply. I figured she either did not receive it or I was just too random contacting her from the US (and she had better things to do with her time LOL which I totally understand). Dr. Schofield (who I mentioned in a prior post) did return my e-mail and she felt that I was on the right track with high dose IVIG and Rituximab which was validating (but of course she cannot give medical advise as I am not her patient).

Antibodies to muscarinic and adrenergic receptors are hard to interpret.

I do not disagree that they are hard to interpret but these autoantibodies exist (outside of what someone thinks of Cell Trend) and they must mean something! If someone has "Significant POTS" which is how Stanford described my TTT test AND I also have high levels of beta-adrenergic autoantibodies, there must be a correlation. And a good percentage of PWME also have POTS (but have not been tested for these auto-antibodies, although anyone can if they send their blood sample to Cell Trend in Germany like I did).

So if Dr. Scheibenbogen can identify a sub-group with Autoimmune POTS and finds a treatment for this, it would benefit people with POTS, both who have ME and who do not. IMO eliminating Autoimmune POTS would be very significant. Heck, even if just providing proof to the majority of doctors that POTS even exists, let alone Autoimmune POTS exists, would benefit so many patients worldwide.

Thyroid autoantibodies are easy - they cause disease. But they are still blurry on the correlation. That does not matter because we have come to understand that they often 'hitch-hike' on to other autoimmune diseases and are rather common anyway.

When I was first diagnosed with Hashimoto's, I had several doctors describe it as the "gateway" to other autoimmune diseases and that they would be very surprised if I did not go on to develop other autoimmune diseases. I had hoped they were wrong (and already had POTS and was sick at that time). But I assumed they meant well-known autoimmune diseases vs. these random unique autoantibodies that do not fit with a specific disease.

The average doctor (in the US) has never heard of, let alone treated, anyone like me. I am extremely lucky to have two very solid doctors who are very interested in my case and open to trying treatments that turned out to be life-changing. But it took several years to find them and no one can explain how high dose IVIG works in autoimmunity or what happens to me once I stop my treatments. (I do understand how Rituximab works but we also do not know what happens when I stop it).

I was also curious, to go back to your original point, why do the Hashimoto's autoantibodies "hitch-hike" onto other autoimmune diseases (to use your term)? Everything started out viral to me and there was a time period (ten months post Mono/EBV) in early 2013 that my symptoms were a fairly good match with ME/CFS and then all the viral stuff shifted into auto-immunity (I assume from the EBV virus).

It is all very complex but you will find that most immunologists who have actually worked on finding new antibodies themselves have a similar opinion of them.

But how do you find an immunologist who has worked on this stuff? My MCAS doctor is an immunologist and he has saved my life and found treatments that eliminated my anaphylaxis and is the prescriber of my current regime. But autoantibodies like mine are not his specialty. No one claims the paraneoplastic autoantibodies (not even oncology) let alone the beta-adrenergic or anti-muscarinic! To me they seem very interesting (but not to doctors) so that is why I am so grateful when someone like Dr. Scheibenbogen comes along and wants to study them.

 

[Pibee]

It can also help if levels are very high because often very high levels are rare in normal people. For the antibodies Dr Scheibenbogen has been studying, if I remember rightly the highest levels were actually in normal people - or at least there was no obvious difference between top levels in normals and ME.

Not sure if it changes anything, especially because it wasnt positive in other studies, but this was not the case for M1 antibody in study by Tanaka S et al. (2003). As you can see highest scores for CFS are way above scores from HC and other AI patients. The method is different though, as is explained here.
@Gingergirl , was your M1 exceptionally high? EDIT: I ran into now it was 13. I think mine is 14. But i think cant be compared to this chart bc not the same units.






Also in another study also by Tanaka et al with antibodies to M1, on psychiatric patients, the upper results for psychiatric patients were much higher than for HC or AI. I wonder in general if these autoantibodies can cause Autoimmune encephalitis. It would definitely explain my symptoms that dont seem classical ME.

Chart A (top left) is for anti-M1 (CHRM1)

I didnt find Tanaka (2003) CFS study but the difference in findings could be the defintiion that misdiagnosed some psychiatric patients as CFS (?!).

 

[Amw66]

@Gingergrrl . I think it is likely that there are others who will present similar to yourself. The difference may be access to testing and talking to someone who has even a bit if a clue.

Here in the UK it is difficult to even get a full thyroid panel done on NHS, let alone anything more complex.
Our mono testing does not even look at serology.

It is chicken and egg - if looked for there nay be many more, but convincing someone to look wider without a set criteria is harder.

Sadly there seems to be little room for the general " searching" that often offers up insights into completely unexpected things.

 

[Gingergrrl]

@Gingergirl , was your M1 exceptionally high? EDIT: I ran into now it was 13. I think mine is 14. But i think cant be compared to this chart bc not the same units.

@Pibee Sorry I missed your post and didn't get tagged b/c I spell my avatar "gingergrrl" with two R's. I just looked at my Cell Trend results to answer your question and my M1 was 13.0 in the initial test and went up to 15.2 in the 2nd test. Both tests were prior to my treatment and we ran it twice since I was positive for 7/9 autoantibodies and wanted to be sure it was accurate. The lab did not know the 2nd sample was me (b/c I sent the first sample myself from Los Angeles with my name and my doctor sent 2nd one from his office w/a patient ID# but not my name). Both sets of results were incredibly similar although the numbers were not an exact match. The M1 cut-off for Cell Trend that is considered "Negative" is below "9".

I wonder in general if these autoantibodies can cause Autoimmune encephalitis. It would definitely explain my symptoms that dont seem classical ME.

I had not heard of these autoantibodies causing autoimmune encephalitis but I think there is so much that we just do not know yet.

 

[Gingergrrl]

@Gingergrrl I think it is likely that there are others who will present similar to yourself. The difference may be access to testing and talking to someone who has even a bit if a clue.

I know that access to testing is a major issue but even without testing, I haven't found many people on PR or S4ME that match my set of symptoms. I have definitely found many people with POTS and/or MCAS, but the muscle and breathing weakness that I had doesn't seem to match with many people here.

Here in the UK it is difficult to even get a full thyroid panel done on NHS, let alone anything more complex. Our mono testing does not even look at serology.

I am so sorry and a thyroid panel is pretty standard here for both PCP's and Endocrinologists. How do they test for Mono in the UK without serology?

It is chicken and egg - if looked for there nay be many more, but convincing someone to look wider without a set criteria is harder.

I agree. It can be hard here, too, with the average doctor and it takes finding someone exceptional in my experience who is willing to dig deeper. I realize this is not an option in the UK (and I think you are assigned to a specific GP by where you live, although I might be incorrect on this).

Edit: I re-read my post and did NOT mean that there are not exceptional doctors in the UK vs. that you are assigned to a GP and don't have the freedom to get 2nd or 3rd opinions or travel to other doctors and pay privately, etc.

 

[Pibee]

@Pibee Sorry I missed your post and didn't get tagged b/c I spell my avatar "gingergrrl" with two R's. I just looked at my Cell Trend results to answer your question and my M1 was 13.0 in the initial test and went up to 15.2 in the 2nd test. Both tests were prior to my treatment and we ran it twice since I was positive for 7/9 autoantibodies and wanted to be sure it was accurate. The lab did not know the 2nd sample was me (b/c I sent the first sample myself from Los Angeles with my name and my doctor sent 2nd one from his office w/a patient ID# but not my name). Both sets of results were incredibly similar although the numbers were not an exact match. The M1 cut-off for Cell Trend that is considered "Negative" is below "9".

That's what I wanted to do! send with other name! hah, now I know I dont have to. Spare $500. But will try to test new angiotensin II abs.

I had not heard of these autoantibodies causing autoimmune encephalitis but I think there is so much that we just do not know yet.

Well, there are some research o them in schizophrenia and other in neuropsychiatric illness so the autors hypothesis was that it can cause it.