Dr Grubbs team ‘Strongly Suggests’ Autoimmunity in Dysautonomia

Belbyr

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Do you remember about what the cost was and turn around time for results? Mayo won't tell me, they said they have to speak with the doctor to order it.
 

Gingergrrl

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Do you remember about what the cost was and turn around time for results? Mayo won't tell me, they said they have to speak with the doctor to order it.
I honestly don't know b/c I never dealt w/Mayo's Lab directly. In early 2016, I saw a neuromuscular specialist at Stanford and he ordered 3-4 Mayo Panels (PAVAL, Myasthenia Gravis, MuSK, anti GAD65, and maybe others?) along w/a bunch of other (non Mayo) bloodwork plus I had full autonomic testing (TTT, QSART, etc) and an exam.

Stanford confirmed in advance that they took my (former) insurance but then the ENTIRE thing was denied and I got a bill for all of it which I had to appeal and then apply for financial aid. So I have no idea what portion of the total bill was the Mayo Panels.

Later in 2018, my main doctor ordered the Mayo DYS1 Panel which I did it at Quest who sent the blood to Mayo. It was billed properly that time and was fully covered by my insurance. So, I actually have no idea. I wish Mayo could tell you what the panels cost :bang-head:!
 
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Thx for confirming. Did your daughter do any treatments for autoimmunity or was she positive for any autoantibodies outside of the Cell Trend Panel?
She was mildly positive for anti AT1R and anti ETAR. She's taking Fludrocortisone, Pyridostigmine, Propranolol, Midodrine and Potassium Chloride for her POTS. Last week, increased dosages finally got her heart rate increase down to 40 in a lean test.
 

Gingergrrl

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She was mildly positive for anti AT1R and anti ETAR.
When I did the Cell Trend Panel twice (in 2016) it was before they offered these two newer tests (Anti AT1R and Anti ETAR). But when I repeated it last year, I was able to do all eleven tests (including those two) and I was "at risk" for Anti AT1R at 16.1 (positive was 17.0) and I was positive for Anti ETAR at 18.9 (and positive was above 17.0).

She's taking Fludrocortisone, Pyridostigmine, Propranolol, Midodrine and Potassium Chloride for her POTS.
I take Atenolol & Midodrine and did not tolerate Fludrocortisone or Mestinon. I also take prescription Potassium (Klor Con) but not specifically for POTS vs. that I have low potassium on tests without it. In my case, the Atenolol & Midodrine provide symptom relief but it was not until I did treatments for autoimmunity that the POTS significantly improved.
 

Learner1

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I don't know why some autoimmune diseases fail in Rituximab trials, but it happens.
But even in these diseases, there was anecdotal reports of rituximab suc
I had high a1 and m4 antibodies. I am trying Rituximab on the basis of those results. From what i understand, the trials that were done did not select ME/CFS patients so specifically for autltoimmunity. I've talked with 2 doctors who believe Rituximab dies work snd has helped certain patients who had autoimmunity. Rituximab doesn't necessarily help every patormts for the on label autoimmune problems its approved for. So, it's a matter of trying it on autoimmune patients and then a little bit of luck on top of that. I've taken other drugs that don't work on everyone either...
 
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it was not until I did treatments for autoimmunity that the POTS significantly improved.
Sorry for my ignorant response to your original question. Please tell me more about how you were treated for autoimmunity. I don't think she's been offered that option yet.
 

Belbyr

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I will add this to my original post but this paragraph is very interesting from Dr Grubb:

We have previously reported a comorbidity in POTS that could explain many of these clinical symptoms; platelet delta granule storage pool deficiency with diminished serotonin levels appears to be frequent in our experience.12 We have not proposed delta granule storage pool deficiency as an etiology of POTS; however, the deficiency might be acquired by autoantibodies, perhaps against enteric cells that produce serotonin in the gut that is stored in platelet granules.
 

pattismith

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I will add this to my original post but this paragraph is very interesting from Dr Grubb:

We have previously reported a comorbidity in POTS that could explain many of these clinical symptoms; platelet delta granule storage pool deficiency with diminished serotonin levels appears to be frequent in our experience.12 We have not proposed delta granule storage pool deficiency as an etiology of POTS; however, the deficiency might be acquired by autoantibodies, perhaps against enteric cells that produce serotonin in the gut that is stored in platelet granules.
isn't Dr Phair's trap theory that implies too much serotonin in the brain and not enough in the gut?
 

Belbyr

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I'm not sure on that one.

I did pretty good on low dose Elavil 25mg for about 2.5 years then I started noticing the side effects going away, then the benefits went away shortly after. I know it is supposed to boost serotonin and my gut it my worst.

My personal uneducated opinion of the 'something in the blood' is an autoantibody or several stirring all this mess up. I know Dr. Davis is trying to look upstream of autoimmunity, but I think there is no doubt we have autoantibodies to all kinds of receptors, some maybe yet discovered. The evidence is too robust now approaching year 2020.
 

Gingergrrl

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Sorry for my ignorant response to your original question. Please tell me more about how you were treated for autoimmunity. I don't think she's been offered that option yet.
Your response was not ignorant at all! I was just curious if your daughter had tested positive for any autoantibodies in addition to the Cell Trend testing (and I might have missed it). I had also wondered if she had done any treatments specifically for autoimmunity in addition to symptom management for POTS. The treatments in my case were high dose IVIG and then Rituximab (for the autoimmunity).

My personal uneducated opinion of the 'something in the blood' is an autoantibody or several stirring all this mess up. I know Dr. Davis is trying to look upstream of autoimmunity, but I think there is no doubt we have autoantibodies to all kinds of receptors, some maybe yet discovered. The evidence is too robust now approaching year 2020.
@Belbyr, do you mean that your theory is that all of ME/CFS is an autoimmune disease, or that there is an autoimmune sub-group, or something else? My own illness is now determined to be autoimmune (even though it started off with viral and mold as the triggers but then shifted into autoimmunity). I now have four separate issues that are all autoimmune but I no longer feel that I had ME/CFS. But until there is a bio-marker, I cannot say this with 100% certainty b/c the beginning of my illness was very different than when it later shifted into autoimmunity.
 

Belbyr

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I think between Dr Systrom's findings of 1/2 of all patients have small fiber neuropathy (autoimmune)
+
Orthostatic Intolerance now looks to be autoimmune (which Dr Klimas says more than 95% of her patients have)
+
I found this, Patients that meet the criteria for 'JAGA' are being given IVIG at Johns Hopkins https://www.hopkinscim.org/breakthrough/holiday-2017/autoimmunity-and-the-gut/

I could keep posting resources, but I'm really starting to think we all have something autoimmune going on. Maybe not every single case, but a majority.
 

Gingergrrl

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I found this, Patients that meet the criteria for 'JAGA' are being given IVIG at Johns Hopkins https://www.hopkinscim.org/breakthrough/holiday-2017/autoimmunity-and-the-gut/
That was interesting and I had not heard of "JAGA" before. I am copying this from your link:

Recently, Pasricha has described a new syndrome based on his team’s observations of a particular subgroup of patients. He’s dubbed this syndrome “JAG-A,” for the conditions it encompasses. The acronym stands for:

  • Joint hypermobility or any type of connective tissue disease, such as Ehlers-Danlos syndrome
  • Autonomic dysfunction such as postural orthostatic tachycardia syndrome, or POTS, which involves an abnormal heart rate increase upon standing
  • Gastrointestinal dysmotility such as gastroparesis or slow-transit constipation
  • Autoimmunity or predisposition to any underlying autoimmune disease
In my case, I do not have any joint hypermobility or GI issues but I have hard-core autonomic dysfunction and autoimmunity.

I could keep posting resources, but I'm really starting to think we all have something autoimmune going on. Maybe not every single case, but a majority.
I agree that there is a large group of us with "Autoimmune Dysautonomia" but I wonder if that will turn out to be a sub-group of ME/CFS or a completely different group who was initially misdiagnosed with ME/CFS but do not have it (plus a group who have BOTH ME/CFS and Autoimmune Dysautonomia).

Thanks. Those are on the list. Her doc is currently building a case so the insurance will pay for the IVIG :thumbsup:
Best wishes to your daughter with getting IVIG approved.
 
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I had a few 'at risks' on the test but nothing in the 'positive' range. Apparently other POTS patients are testing negative too. I wonder what's up?
I’m similar. My positives were pretty weak even though I have pretty severe POTS. I started blacking out from my POTS when I was a kid (11-12) and it’s only gotten progressively worse (I’m 29 now). My heart rate ranges from 37-210!

My tilt table test was very positive and my heart rate was still climbing after 30 minutes.
I’ve been encouraged to repeat the CellTrend but it’s so expensive. I’d rather just save the money for trying IVIG.

Plus my insurance would not consider the CellTrend results or my positive skin biopsies showing small fiber neuropathy. If a clearer CellTrend would change their minds then I’d repeat it but they view it as meaningless 😤
 

pattismith

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"Researchers screened the patients' blood for autoantibodies against nine receptors. A handful of patients showed elevated levels against all nine. But it was the prevalence of adrenergic A1 subtype receptor autoantibodies that make their findings so intriguing.


"I think that we have identified a biomarker. We now might have the ability to diagnosis this, or at least have an inkling. Like other autoimmune disease, we can take a blood sample and detect if there are increased levels of autoantibodies present. According to our results, autoantibodies against this particular receptor should be present in about 90 percent of patients with POTS," said Dr. William Gunning, a professor of pathology in the UToledo College of Medicine and Life Sciences, and the paper's lead author."
Unfortunately we don't have any info about the prevalence of these antibodies in non-pots population (non control group).
Also people with Joint hyperflexibility were 72.7% of the POTS patients, but I can't find how hyperflexibility was evaluated.

"The symptom of hyperflexibility was not evaluated using the current diagnostic criteria to categorize hypermobile Elhers‐Danlos syndrome.33
Our experience using the Beighton 9‐point scoring system for joint hypermobility is much lower, with 20% to 30% of our POTS patients having scores of 6 or more.
Given that we did not include the criteria to diagnose Elhers‐Danlos syndrome in this study, any correlation with detection of autoantibodies was therefore not evaluated.

With the heterogeneity of symptoms associated with POTS, a variety of proposed etiologies have been suggested, yet no conclusive basis or mechanism has been established.7, 20, 21, 34, 35

The less‐frequent primary form of POTS (hyperadrenergic POTS) has been described as a form of β‐adrenergic receptor hypersensitivity with many of these patients experiencing true migraine headaches, including onset with photophobia and nausea.36
A secondary form of POTS resulting from peripheral autonomic deinnervation, but with maintained cardiac innervation, is usually associated with underlying disease states with diabetes mellitus the most common. Hypermobile Elhers‐Danlos syndrome has also been considered as secondary form of POTS. Our results support the hypothesis that POTS may be an autoimmune disorder affecting the autonomic nervous system."