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jangle

Wish They Tested Their Cfs Patients For Pots.

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http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0026358

With 2/3 of their CFS patients responding to Rituximab, it seems highly likely that some of those responders had preexisting POTS. If they had POTS, it would have been interesting to see if the POTS also resolved with Rituximab. Interesting to note is that the study population had a very low frequency of detectable autoantibody, most were ANA negative even.

I emailed the authors asking if they tested their patients for POTS, but I doubt they did. It just seems like they should have, they might have been able to help us POTSIES out.

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I thought most were tested for pots / orthostatic intolerance. I have a cfs diagnosis and have had

poor man's tilt table tests since 1990. I don't see how knowing this has made any difference in

how cfs or pots would be or has been treated at least by traditional medicine. From what I've seen,

They only know the bandaid approach. Integrative or functional doctors look at cfs or pots or any

chronic illness as

a by product of a non functional immune system. Fixing the immune system is where things can

get complicated but imho, they're getting better at this. Tc .. D

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Jangle I think in the Netherlands they do (that's where I live). I've heard people who were tested for CFS and got a POTS diagnoses as well. We have several CFS clinics here which diagnose both CFS and POTS (or perhaps other forms of Dys like OI). In treating they mostly treat the CFS. I've been wondering what CFS treatment would do for me too but, of course :) forgot to ask when I saw my Neuro lately.

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I was diagnosed with ME in 1990. I was not tested for POTS. I believe the NICE guidelines (which the NHS in the UK must follow) states that tilt table tests should NOT be routinely performed. Go figure!

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I was originally diagnosed with CFS (much to my surprise). This was years before I was truly 'struck down' by illness. I knew something wasn't right back then though, and over time though I continued doing everything I had always done, it became harder and harder to the point were to was pretty harrowing. Then suddenly my internal organs and glands swelled up, had a couple high fevers, liver count low... Then thyroid suddenly very over active. Following that, diagnosed with severe POTS. Never been the same since. I had POTS when I was diagnosed with CFS - in fact I am pretty sure I had it all my life, but to a lesser degree before. Does that mean the CFS diagnosis was incorrect, I sometimes wonder( If it is a diagnosis made by excluding anything else that could account for symptoms).

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This is an issue I can't resolve in my mind. OI is recognized as a CFS symptom and so many CFS symptoms are also POTS symptoms, so how do you differentiate the two? I don't think I have CFS and POTS - I think it's all one illness (for me anyway). The American definition doesn't really match up, but if you look at the Canadian definition of CFS, it might as well be POTS. See below. I think they should routinely add TTT as part of a CFS work-up.

http://www.cfids-cab.org/MESA/ccpc.html

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Jangle I think in the Netherlands they do (that's where I live). I've heard people who were tested for CFS and got a POTS diagnoses as well. We have several CFS clinics here which diagnose both CFS and POTS (or perhaps other forms of Dys like OI). In treating they mostly treat the CFS. I've been wondering what CFS treatment would do for me too but, of course :) forgot to ask when I saw my Neuro lately.

Oh sorry what I meant was I wish the researchers in that specific study tested their patients for POTS prior to giving them rituximab. This is because it has been shown that a lot of patients with CFS also have POTS, and if the responders (roughly 2/3 of their patient population) had their POTS reduced or taken away, then that would show efficacy for rituximab in POTS and implicate autoimmune etiology for POTS.

It's almost as if one doesn't even need them to have done it. It's a pretty safe assumption a large portion of them did have POTS, in other studies it's well in excess that CFS patients have POTS and there's no way 30 randomly selected CFS patients, not one of them had POTS. But it needs to be "official" we need measurements and objective signs, not just speculation.

Estimates are 25%+ of CFS patients have POTS, and lots more of them have exaggerated tachycardia upon standing suggestive of the same mechanism of POTS.

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I'm assuming you want to know this med would treat "pots". If you look at dr hain's info on this site,

he gives a list of possible causes for pots. If we use this as a guide, then there can be multiple possible

treatments. Imho, Pots is a wastebasket diagnosis like cfs or ibs.

I'm a wee bit over my head here but my definition of cfs, the old cfids,

means pwcs have an upregulated immune system. I tested positive on what was called the cfs panel in

the early 90's and again in 2006. This showed I had an abundance of antibodies to several viruses.

Maybe if they had stuck with this test as a diagnostic tool for cfs, there would be a lot less confusion.

Tc .. D

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Although there are different causes of POTS like there are for CFS, I don't think there are many different types of mechanisms. What I mean is, there's many different paths you can take to a building, but in the end there is one building.

Now in the case of POTS, there very much likely are different mechanisms, so it's unlikely to be just one mechanism. But where I'm thinking is that the most prevalent mechanism is NET deficiency. I believe this afflicts most POTS patients as well as CFS patients. In addition to NET deficiency, there can be other things going on in addition to the NET deficiency which explains the additional symptoms people experience. Things like Mito, EDS, MCAD, etc. etc.

It's sort of like Lupus, yes there is a diagnosis of Lupus, but some people with Lupus have CNS involvement. Yes there is a diagnosis of POTS, but some POTS patients have mitochondrial disorders or connective tissue disorders in addition to their baseline POTS.

But I don't think there are many different causes of baseline POTS. If there were, then the NET deficiency study would have observed a large standard deviation in their NET study of POTS patients. The fact that it was small, pretty much says that the overwhelming majority of POTS patients have NET deficiency. Since people with CFS also have orthostatic tachycardia in large numbers, I'm assuming they too have NET deficiency.

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I was tested by Vandy for NET deficiency. It was negative. I think they've only found it in one family - if we're talking about the same thing. Isn't this what Linda Smith (the founder of NDRF and she was on Mystery Diagnosis) has?

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I was tested by Vandy for NET deficiency. It was negative. I think they've only found it in one family - if we're talking about the same thing. Isn't this what Linda Smith (the founder of NDRF and she was on Mystery Diagnosis) has?

Naomi are you talking about NET deficiency gene or the actual NET protein levels?

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I don't know - lol. What I had was a genetic test - are you talking about protein levels?

http://atvb.ahajourn...11.244343.short

What this study found was that although people had normal NET genes, there's something going on acting on the normal gene that is repressing its transcription.

In other words, there's something that's inhibiting your gene from producing enough NET proteins.

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In other words, there's something that's inhibiting your gene from producing enough NET proteins.

OK, thank you. That makes total sense. Gonna go read about it....

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My immunologist wants to try me on a drug in this class but wants to get a rheumy to back him up due to insurance purposes (hence me waiting to see if I can get in with a rheumy at Hopkins). He feels that, although my ANA is negative, my elevated C4a, my biopsy indicating suspected immune mediated inflammatory connective tissue disease, and my clinical presentation warrants trying this class of drugs. I don't have a CFS dx, but, it seems that this class of drugs is being found to have good treatment results in more and more types of disease.

Also IVIg is starting to have more and more applications. There was just a news segment I heard this week saying that one study has had positive results using IVIg to slow/stop the progression is Alzheimer's.

I all seems to be coming back to controlling our immune systems...doesn't it?

Edited by corina
enlarged text

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This is an issue I can't resolve in my mind. OI is recognized as a CFS symptom and so many CFS symptoms are also POTS symptoms, so how do you differentiate the two? I don't think I have CFS and POTS - I think it's all one illness (for me anyway). The American definition doesn't really match up, but if you look at the Canadian definition of CFS, it might as well be POTS. See below. I think they should routinely add TTT as part of a CFS work-up.

http://www.cfids-cab.../MESA/ccpc.html

Thanks for posting this, Naomi! I had no idea there was that much overlap between the two syndromes, so I thought it was finally time to learn a little about what all of you know already :) .

I ended up following the links and watched a three hour talk by Dr Cheney about CFS and Diastolic Cardiomyopathy. I felt that there was a ton of really relevant information for Pots patients as well because of all of the overlapping symptoms. Really interesting stuff... he said the cardiac insufficiency theory could account for SOB, arrythmia's, MVP, chest pain that mimics heart attack, dyspnea on exertion, temperature dysregulation, food intolerances, etc, etc. Based on what he saw during my first stress test, my internist thought I had cardiomyopathy. He was soo convinced that he ordered a second echocardiogram (I just had one two weeks before) and was surprised when it came out looking "normal". I had changes in my ecg's as well.

This Cardiac Insufficiency theory potentially offers an explanation as to why exercise might not work for some of us. I have struggled to try to exercise and still can't get beyond six minutes on the recumbant bike without bad effects. I know there are lots of potential mechanisms at play with Pots and this may fit in somewhere for some of us.

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This article was not published till June 21, 2012. At least you are staying on top of things Jangle! I do not think I can read the full article. It looks like maybe I can access it for 1 day for $20. I do not know if I could print it if I can access it.

Did the POTS patients in the study show expression of the NET gene that overlapped with the normals and how much difference? This is very interesting, as it actually shows something wrong, or not functioning in all POTS patients that results in the postural tachycardia etc. Even if the thing that is wrong is a result of more than one etiology. Epigenic Modification of the NET gene could even be a normal healthy body response that has gone wrong, as is the case in most illnesses. In my own case being on the Propranolol LA 80 BID for over 20 years ( for tremor/ blood pressure ) might cause the body to try to correct what the body sees as incorrect by epigenic modification.

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This article was not published till June 21, 2012. At least you are staying on top of things Jangle! I do not think I can read the full article. It looks like maybe I can access it for 1 day for $20. I do not know if I could print it if I can access it.

Did the POTS patients in the study show expression of the NET gene that overlapped with the normals and how much difference? This is very interesting, as it actually shows something wrong, or not functioning in all POTS patients that results in the postural tachycardia etc. Even if the thing that is wrong is a result of more than one etiology. Epigenic Modification of the NET gene could even be a normal healthy body response that has gone wrong, as is the case in most illnesses. In my own case being on the Propranolol LA 80 BID for over 20 years ( for tremor/ blood pressure ) might cause the body to try to correct what the body sees as incorrect by epigenic modification.

POTLUCK, I don't see the individual numbers of NET levels of the POTS patients. However, it was a low average with a very low standard deviation suggesting that pretty much all the POTS patients had reduced NET.

EDIT: they might have posted it in the online data supplement, I don't have access.

Yes it is exciting to know what likely is causing the POTS, however there isn't a well defined treatment available to go with that thought. I believe by suppressing the cytokines with immune drugs it could boost NET levels by the Hand2 pathway, but that is something that would need to be experimentally verified.

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Some people have both and there is an overlap in symptoms between POTS and CFS. I don't know as much about CFS bc I don't have it. But it involves not just being chronically tired (which everyone with POTS is), but things like low grade fever, swollen glands, etc. Some POTS patients have these type of symptoms, but I am inclined to think that most do not. And I am not sure how much CFS patients' problems are positional in nature. Frankly I am glad I have POTS and not CFS - it seems like CFS would be worse than the form of POTS I have.

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This article was not published till June 21, 2012. At least you are staying on top of things Jangle! I do not think I can read the full article. It looks like maybe I can access it for 1 day for $20. I do not know if I could print it if I can access it.

Did the POTS patients in the study show expression of the NET gene that overlapped with the normals and how much difference? This is very interesting, as it actually shows something wrong, or not functioning in all POTS patients that results in the postural tachycardia etc. Even if the thing that is wrong is a result of more than one etiology. Epigenic Modification of the NET gene could even be a normal healthy body response that has gone wrong, as is the case in most illnesses. In my own case being on the Propranolol LA 80 BID for over 20 years ( for tremor/ blood pressure ) might cause the body to try to correct what the body sees as incorrect by epigenic modification.

POTLUCK, I don't see the individual numbers of NET levels of the POTS patients. However, it was a low average with a very low standard deviation suggesting that pretty much all the POTS patients had reduced NET.

EDIT: they might have posted it in the online data supplement, I don't have access.

Yes it is exciting to know what likely is causing the POTS, however there isn't a well defined treatment available to go with that thought. I believe by suppressing the cytokines with immune drugs it could boost NET levels by the Hand2 pathway, but that is something that would need to be experimentally verified.

I do not know much about this. I tried googling Hand2 and NET to learn a little more and found this article. It looks like the gene is something the body uses in development, that is maybe accidentally being turned on by injury. ( As they mention this in abstract. ) It looks like a while before the immune drugs will be tested, especially with cost being a huge factor.

http://www.ncbi.nlm.nih.gov/pubmed/21241805

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There are natural things that can be done to suppress cytokines. I'm working to lower my TNF and B cells with tumeric and ginger also astragalus. Since, having autoantibodies coming back positive recently - I figured I might as well do what I can to maybe help things - while waiting for more testing. If the test come back with better numbers, in the mean-time, then I will know this is working and would rather suppress things this way than with traditional meds - with all their side effects. So far, so good.. I'm also increasing blood flow with things like alpha lipoic acid and vit C. So, we will see what time does with these things.

Issie

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This article was not published till June 21, 2012. At least you are staying on top of things Jangle! I do not think I can read the full article. It looks like maybe I can access it for 1 day for $20. I do not know if I could print it if I can access it.

Did the POTS patients in the study show expression of the NET gene that overlapped with the normals and how much difference? This is very interesting, as it actually shows something wrong, or not functioning in all POTS patients that results in the postural tachycardia etc. Even if the thing that is wrong is a result of more than one etiology. Epigenic Modification of the NET gene could even be a normal healthy body response that has gone wrong, as is the case in most illnesses. In my own case being on the Propranolol LA 80 BID for over 20 years ( for tremor/ blood pressure ) might cause the body to try to correct what the body sees as incorrect by epigenic modification.

POTLUCK, I don't see the individual numbers of NET levels of the POTS patients. However, it was a low average with a very low standard deviation suggesting that pretty much all the POTS patients had reduced NET.

EDIT: they might have posted it in the online data supplement, I don't have access.

Yes it is exciting to know what likely is causing the POTS, however there isn't a well defined treatment available to go with that thought. I believe by suppressing the cytokines with immune drugs it could boost NET levels by the Hand2 pathway, but that is something that would need to be experimentally verified.

Looking at this abstract and another from this group and I was wondering again about the Histone Deacetylase (HDAC) inhibitors

http://www.landesbioscience.com/journals/cc/BaylesCC9-22.pdf

http://en.wikipedia.org/wiki/Histone_deacetylase_inhibitor

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Thanks, Potluck - looks like this might really have some relevance to this. I know you took valproic acid in the past for your epilepsy - do you think that's what helped you before? Did you get off it and then have a relapse with POTS?

Issie

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I don't know a huge amount about POTS yet, I'm still pursuing a correct diagnosis, but from my years of experience with ME, here's what I can tell you.

1. It's rare for people diagnosed with ME or CFS to get tested for POTS. It should be one of the things they test as standard when making a diagnosis, but those are generally relatively cheap and easy things such as blood tests for anaemia. Once you have a CFS/ME diagnosis, it usually becomes very difficult to access healthcare, including tests for other conditions.

2. There's huge symptom overlap, which is not made easier by the various different diagnostic criteria for ME/CFS and the likelihood that there is a high rate of misdiagnosis running both ways. I think it's very likely that there are some people wrongly diagnosed with ME/CFS who have POTS alone, some people wrongly diagnosed with POTS who have ME/CFS alone, and a large number of people who have both. I couldn't even begin to guess at the figures. In about twenty years I think they'll be able to tease this apart properly, but right now they don't have a clue.

3. Someone mentioned low-grade fever and swollen glands as ME/CFS symptoms. They're common, especially in the early stages, but long-term I'm not even sure if they're present in the majority of patients. There was a poll on Phoenix Rising showing that most of us have body temperatures which run a little lower than normal, if anything. I was very fluey in my first year of ME, and since then a fever has been extremely rare (though running hot and cold has increased as a problem, it rarely shows up on the thermometer), and I don't get much in the way of swollen glands either, just some mild tenderness from time to time. I'm not sure how typical I am. I hear those issues being raised a certain amount on PR, but not very much, and nowhere near as much as other symptoms.

4. Prof Julia Newton, who does research into both ME and POTS, has hypothesised that ME patients get increasing autonomic symptoms as the severity of their ME increases. I looked at that statement and thought, "Yep, that's it exactly for me," but other people on PR said it wasn't true of them. Some of them had bad autonomic symptoms from the start, some of them never got the autonomic symptoms even when they were severe. I think this could be down to misdiagnosis rates, ME and/or POTS, subsets and so on. There's a thread about this on PR somewhere.

5. Rituximab was mentioned. I know very little about this except that it's chemotherapy, it's been showing promising results, and it's too early to know much about what happens long-term. I also know that a few people think there are mast cell problems going on with ME (it seems to be a fairly new idea), and I gather that some forms of mastocytosis are treated with chemotherapy.

6. Condition changing with movement - hard to judge, since the primary symptom of ME is exercise intolerance and post-exertional malaise (PEM). I don't have a good feel yet for exactly how this works with POTS, so it's hard for me to compare the two. With ME, the worst of the reaction to exertion very often occurs some time later, typically the next day. However, symptoms will flare up enough at the time that the activity will be curtailed due to them. People with ME usually feel better lying down, and are very bad at standing up.

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