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POTLUCK

Question About Jaha Autoimmunity Study

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It seemed like a bad idea to steal the other thread on this. My computer will not let me post a link to the article so if someone else can that would be great.

" Autoimmune basis for Postural Orthostatic Tachycardia Syndrome"

The questions are:

1. It appears all 14 POTS patients and none of the controls had autoantibodies to Adrenergic Receptors AND varying effects. (agonist/antagonist, B1, B2 etc.)

A. How sure are they that the POTS patients had autoantibodies, and the controls did not. (i.e. It seems common sense wise that if ALL POTS and no controls have something it is not chance, but is there an element of chance in the results for the study subject?) In other words are they showing up with slightly darker staining for these antibodies than controls and what is the chance this is error?

B. How sure are they of the effect of these antibodies?

Can anyone that knows much about recent research etc. (and some people on this site are incredibly well educated on POTS) comment on how sure this study and the other study on OI and autoantibodies make it that the etiology for a large number of POTS patients illness is autoimmune?????

The question I am asking is not, does everyone with POTS have this, but how sure are they that for a large percentage of POTS patients there is an autoimmune etiology????

The study discussion does not really go into much detail about potential pitfalls in the research methodology etc. and it is really too complex for most people to understand but it, but it seems that many places are doing research on POTS and must have more insight from discussion with each other researchers/doctors specializing in this field about the significance of this.

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For insight into the thought process behind the question it seems there are so many individual interacting factors, effects of epinephrine and norepinephrine, and complex interactions of the body that it is like trying to understand why a huge machine does not run right, and the thing that is necessary is to understand the primary malfunction or in some cases malfunctions if more than one thing is broken. Knowing if POTS is due to an autoimmune problem seems like an enormous step towards this. Some on this website have found the primary etiology, something other than autoimmune such as a mast cell disorder, carcinoid syndrome etc. etc.

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All I know is the research body that did this study(Oklahoma(?) and Vanderbilt) is in the process of having funds raised so that they can do this testing on a widespread basis, so that they have a large group to test this theory on. I am really excited about what they find out, and this is the FIRST thing in POTS research I have been really excited about since following various research organizations for the last 8 years.

I don't know if I have these autoantibodies, but this does make sense with how I presented with the disease 8 years ago, and how my symptoms have progressed.

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Potluck- When I was talking to my POTS neuro about this, he was saying that at Mayo when they found the antibodies that they found which are associated with POTS, they found them in 14% of the patients and that was thought to be a HIGH frequency of occurance. Sounds like a lot of the neurologists aren't taking this new study too seriously at this point for the reason you mentioned- the fact that they found the antibodies in 100% of the patients.

I'm hoping the bigger study will shed more light on the issue either way.

For some reason, I seem to remember reading somewhere that they think about 50% of POTS patients have an autoimmune cause? (How's that for sufficiently vague sources? :rolleyes: ) I know my POTS doc says that just because I haven't shown up with the antibodies that Mayo tests for it doesn't mean my situation isn't autoimmune based. He still thinks it likely is, even with the MCAS component involved apparently.

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Yea, that Mayo study done under Dr. Vernino was for the AAG, and one of their findings was that people that were found to have those antibodies had orthostatic hypOtension. I think the new research of the alpha-1 receptor autoantibodies is showing up as orthostatic hypERtension. It seems we all seem to fall into a few different presenting categories under the POTS umbrella.

The people under Vernino, from what I understand, have the option of IVIG or plasmapheresis treatment. That's what I'm waiting for, for this study to get to that point so there is an actual option of treatment instead of symptom management(which hasn't worked for me anyway).

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I don't know for sure about the antibody results but I know for one all of my health problems started with the Epstein Barr Virus. I have no doubt that was the trigger with me and many other people whether it led to ME or POTS/Auto Dys.

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I think the only true answer to your question is only go to be answered by research. Until then we are just going to have to keep digging for our underlycauses. This is frustrating to say the least. When Tyler was first diagnosied with POTS, my husband and I really thought it was much more than POTS becuase of an article that we read on POTS. Wish I could find it but it stated that if your POTS responded to the medications and exercise, then you would be more likely to recover more quickly. This makes sense but some of us on this forum have some really complicated cases with POTS. I really think that doctors will figure this out but it's going to be a really slow process towards healing for many of us.

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Thank you for the replies.

Chaos- Do you know what antibodies they were testing for at Mayo in regard to the 14%, and is this a test that is available to a patient who wants it?

The JAHA study is very hard to understand both medically and statistically.

I have a little insight medically ( I.e. B1 & B2 receptor antibodies acting as both agonists and antagonists and also thus causing reflex actions such as an increase in the persons own Epi/NE response) This makes a lot of sense and could account for many "odd" things in POTS ( such as my more Hyperadrenergic POTS picture, or people's differing clinical pictures all with the common denominator of a change in their adrenergic responses)

Statistically it is very unclear to me. The study does not discuss potential flaws in the methodology and research. What is the chance of error-that people did not have antibodies to the receptors or that some did not? I am sure some researchers in POTS must be more clear on this from reading the study or discussing it with the researchers who completed it. Or the researchers that completed it must have some ideas on the question of potential error.

I have not found much in the way of discussion of this. ( I agree it is an excellent thing to have POTS discussed in JAHA, either way, to draw more attention to it, and I am all in favor of the large study to continue research into this.)

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POTLUCK- I don't know which specific test he was referring to that came back with a 14% prevalence but these are the antibody tests that I had run at Mayo recently. When I was at Cleveland Clinic a few years ago, they ordered some of these same antibody tests and sent them to Mayo so it seems you can have them drawn elsewhere and sent there.

Neuronal (V-G) K+ channel Ab

AGNA,1 Serum

AChR Ganglionic Neuronal Ab S

CRMP-5, Serum

PCA 2, Serum

ANNA-3, Serum

PCA-Tr, Serum

GAD 65 Ab

Striat Muscle Ab

PCA-1, Serum

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The comments about this study on the Dysatonomia international website seem to indicate they are certain the POTS patients had antibodies and the controls did not. As I said the paper itself did not explain potentials for error on this. Maybe they are certain the POTS patients all had antibodies, but if that is so it would seem most of diagnosed POTS patients will have them, as it is too coincidental for 14/14 at two centers.

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it says 14 out of 14. 14/14 isnt 14 percent, its 100%. (Of pots patients tested)

The study is saying antibodies to the alpha 1 adrenergic receptor are causing an interference with veins ability to constrict. They took samples from different universities and had the same result, even when the samples were blinded to the scientists. This is promising and its worth donating.

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Potsticker63- the 14% was referring to a study done on different antibodies at Mayo. It was not in reference to this study at Oklahoma and Vanderbilt.

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Is this the 14%? ....

"In 13.8% of patients, onset was subacute, and ganglionic acetylcholine receptor antibody was detected in 14.6%, suggesting an autoimmune origin in at least 1 in 7 patients" which I believe is this one ---> AChR Ganglionic Neuronal Ab.

http://www.ncbi.nlm.nih.gov/pubmed/17352367

If so, I think Dr. Raj in video from the conference said they aren't finding these in POTS patients anymore.

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I hear they are doing the follow up study in early July at a conference, so maybe there will be more info. available soon.

This topic is very interesting, and may prove to be the cause of POTS in most patients.

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The causal effects of many antibodies can be identified – I wonder what the researchers think is the cause of these (adrenergic receptor) antibodies. Second – what is their recommendation for treatment?

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Will their be any published results from the study done July 2014 with a larger number of people tested than the original 14/14 study.

Also, if not published yet or if this will not be published does anyone know anything about the actual results? How many people in the larger study had the antibodies? Did it show up in different types of patients such as Hyperadrenergic?

It is good news that they have obtained an even larger grant to work on this but it has been 8 months, shouldn't results be available from the July 2014 study?

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I did not understand everything my doctor told me, but what he told me looks like the same as in that study youre talking about. My doctor told me about a treament with immunoglobulins and I may get this new treatment in 6 months. Does anybody get this treatment today?
For 2 years ago doctors understod that norepinephrine is working in some pots-patients, today they know why. Recently they found out more about these antibodies and treatment. It seems to me that there is hope for many of us :-)
I am so grateful, things will change. In future we'll feel better or perhaps be fine!

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I think this is the most current update on where the research stands...sounds like the fundraising was just to get the research started on the larger group but will be a more comprehensive study than just whether or not they found antibodies, so I'm thinking no published paper for a while still.

http://www.dysautonomiainternational.org/page.php?ID=178

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Ugh, I have NO patience waiting for results from this study!!

Dops, I'm curious what your doctor found in you that he says you might get the immunoglobulin in 6 months? Was it based on labs or just your clinical presentation? I so hope I can get a doctor to understand this information and work with me on it.

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Sue1234: I did not understand him really well, but he talked about a few different receptors (alpha 1 adrenergetic and beta1+2-receptors) and that autoimmunity tests indicated a high activity of these receptors. Further he talked about something which "inactivates" my bodies own adrenaline/epinephrine and that is why I have to take noradrenaline/norepinephrine. The information about the receptors is based on my bloodsamples but he could explain my symtoms with the results of the lab. This is stuff I don't understand ;-) People working with it maybe understand and can explain it better :D

I think they are already testing the new treatment in the first patients, but just in bedridden patients. But perhaps he meant that they will start testing in six months.

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