You probably have an autoimmune disease...

[Martin aka paused||M.E.]

I would get w/ your fellow German CFS'ers (if you haven't already) like @Martin aka paused||M.E. and @Badpack maybe collaboration will help you guys more w/ labs and acquiring drugs and supplements and what not.

I'm happy to help if I can

 

[SWAlexander]

I would get w/ your fellow German CFS'ers (if you haven't already) like @Martin aka paused||M.E. and @Badpack maybe collaboration will help you guys more w/ labs and acquiring drugs and supplements and what not.

I don´t understand your question. Please be more specific.

 

[keepontruckin]

Interesting article out today on German researchers finding early treatment makes big difference in progress of autoimmune diseases.
https://www.sciencedaily.com/releases/2021/09/210927132044.htm

 

[SWAlexander]

Interesting article out today on German researchers finding early treatment makes big difference in progress of autoimmune diseases.
https://www.sciencedaily.com/releases/2021/09/210927132044.htm

Thank you.

 

[Yuno]

H

If it makes you feel any better, I didn't have any symptom improvement at all when my Hashimoto's finally went into remission.

Just too much other stuff going on in my body I suppose.

how did you get your Hashimoto in remission??

 

[Inara]

If you've tested positive for auto-antibodies, please let me know. I

TPO and MAK were elevated several times (some years later they were normal again) - I was told I have Hashimoto's, but ultrasound shows a small, but otherwise normal thyroid. What's interesting is I have a slightly jumping TSH between 0.01 and 1.4 (no change in symptoms).

GAD65 was elevated (it was measured 2 or 3 times). This was not followed-up and I can't say what it means.
(If anyone has an input, I'd be interested.)

I have to add I am not sure if I have ME. It's quite realistic my symptoms are due to all the other stuff.

 

[Inara]

I read on a Renaissance historian's blog that (in her view) autoimmunity is the result of the Black Death (I think 1378 or 1348) and the following Plagues. Because only people with a stronger immune system survived, but a stronger IS comes at the cost of autoimmunity.

I have to specify: The high number of autoimmune cases is the result of...

 

[Gingergrrl]

GAD65 was elevated (it was measured 2 or 3 times). This was not followed-up and I can't say what it means. (If anyone has an input, I'd be interested.)

@Inara I think you and I have discussed this before (in past years) but just in case, I had elevated anti GAD65 in 2016 on Mayo Panel (and it remained elevated on subsequent panels from Mayo & Quest). The number did reduce following my treatment but it never reduced enough to go into the "normal" range.

My Endo ran every test possible for diabetes (which links to GAD65 Abs) and every single one was completely negative. We also ruled out that I did not have SPS (Stiff Person Syndrome) which also links to GAD65 Abs.

In my case, my doctors felt (at that time) that my GAD65 Abs either were b/c of my Hashimoto's (autoimmune thyroid) or b/c of my overall dysautonomia. Some articles that I read at the time included GAD65 Abs with the paraneoplastic autoantibodies but others didn't. I'm not sure if any of this is helpful to you?!

 

[Inara]

Thank you @Gingergrrl! I remember now you told me that before, but not in that detail, and I find it helpful.

 

[kalles]

Thank You!!!! For real, that is so helpful and it saves so much time :Trophäe:. If I had a breakdown like that from everyone, I'd have a comprehensive list to share in no time!

I actually had some of yours documented already. Some I didn't, and they are updated (along w/ some others) in BLUE below. I also updated some of the names and info.

Autoantibodies in forum…

AChR Binding (acetylcholine receptor)
1x
Carbonic Anhydrase VI (CA VI) – Early Sjogren's Syndrome
1x
Myelin
2x
Basal Ganglia (ABGA)
1x
Myocardial Peptide
1x
Voltage-Gated Calcium Channel, N-Type (VGCC) - Lambert-Eaton myasthenic syndrome
1x
Beta-1 Adrenergic Receptor (β1AR) - Dilated cardiomyopathy
2x
Beta-2 Adrenergic Receptor (β2AR)
6x
Alpha-1 Adrenergic receptor (α1AR)
14x
Alpha-2 adrenergic receptor (α2AR)
5x
Ganglionic (alpha-3) Acetylcholine receptor (α3-AChR) - Autoimmune autonomic ganglionopathy
1x
Phosphatidylserine - Antiphospholipid Syndrome
1x
Endothelin-Receptor-A (ETAR)
7x
Angiotensin-II-Receptor-1 (AT1R)
7x
Muscarinic acetylcholine receptor, M1 (mAChR)
1x
Muscarinic acetylcholine receptor, M2 (mAChR)
5x
Muscarinic acetylcholine receptor, M3 (mAChR) - Primary biliary cholangitis/cirrhosis
3x
Muscarinic acetylcholine receptor, M4 (mAChR)
9x
N-methyl-d-aspartate (NMDA) receptor - (NMDA) Receptor Encephalitis
1x
Parotid Specific Protein (PSP) - Early Sjogren's Syndrome
1x
Dopamine Receptor 1 (DRD1)
1x
Tubulin
1x
Phospholipid - Antiphospholipid Syndrome
1x
Gliadin - Celiac disease
3x
Cardiolipin (aCL) - Antiphospholipid Syndrome
3x
ANA (Antinuclear Antibodies) - Lupus, Scleroderma, Sjögren's syndrome, Rheumatoid arthritis, etc
9x
Scl-70 (topoisomerase) - Scleroderma, Connective Tissue Disease
1x
SS-A/Ro (Sjögren's-syndrome-related antigen A) - Sjögren's-syndrome
3x
TPO (Thyroid peroxidase) - Hashimoto's
11x
Saccharomyces cerevisiae (ASCA) - Crohn's Disease
1x
CCP (cyclic citrullinated peptide) - Rheumatoid arthritis
3x
Parietal Cell - Pernicious anemia
3x
Smooth Muscle (SMA) - Primary biliary cholangitis, Autoimmune hepatitis
2x
GAD65 (glutamic acid decarboxylase 65) - Type 1 Diabetes
1x
Jo-1 (Anti-histidyl tRNA synthetase) - Myositis
1x
Proliferating cell nuclear antigen (PCNA)
1x
Mitochondrial (M7) (<< heart) - Myocarditis
1x
GABABR (gamma-aminobutyric acid B receptor) - GABABR encephalitis
1x
Salivary Protein 1 (SP-1) - Early Sjogren's Syndrome
1x
Thyroglobulin (TgAb) - Hashimoto's
4x
Beta-2-Glycoprotein I (β2GPI) - Antiphospholipid Syndrome
2x
Rheumatoid Factor
2x
Neurofilament
1x
RNP (Ribonucleoprotein)
1x

hey I have beta 1, beta 2 and M2

 

[SWAlexander]

Since I have a final diagnosis: lupus and antiphospholipid syndrome, I would like to share this, because it could also relate to ME/CFS:

Prothrombotic autoantibodies in serum from patients hospitalized with COVID-19

Casting an autoantibody NET in COVID-19
Patients with severe COVID-19 are at high risk for occlusion of blood vessels of all sizes. This prothrombotic phenotype is reminiscent of patients with lupus and antiphospholipid syndrome, who have long-lived circulating antiphospholipid autoantibodies. In new work, Zuo et al. measured eight types of antiphospholipid antibodies in serum from patients hospitalized with COVID-19 and found at least one antibody in half of patients. Antibody levels were associated with neutrophil and coagulation pathway activation. Purified antibodies from some patients activated neutrophils in vitro and potentiated thrombosis when injected into mice. Together, these findings suggest that autoantibodies are a potential therapeutic target in severe COVID-19.

Abstract
Patients with COVID-19 are at high risk for thrombotic arterial and venous occlusions. Lung histopathology often reveals fibrin-based blockages in the small blood vessels of patients who succumb to the disease. Antiphospholipid syndrome is an acquired and potentially life-threatening thrombophilia in which patients develop pathogenic autoantibodies targeting phospholipids and phospholipid-binding proteins (aPL antibodies). Case series have recently detected aPL antibodies in patients with COVID-19. Here, we measured eight types of aPL antibodies in serum samples from 172 patients hospitalized with COVID-19. These aPL antibodies included anticardiolipin IgG, IgM, and IgA; anti–β2 glycoprotein I IgG, IgM, and IgA; and anti-phosphatidylserine/prothrombin (aPS/PT) IgG and IgM. We detected aPS/PT IgG in 24% of serum samples, anticardiolipin IgM in 23% of samples, and aPS/PT IgM in 18% of samples. Antiphospholipid autoantibodies were present in 52% of serum samples using the manufacturer’s threshold and in 30% using a more stringent cutoff (≥40 ELISA-specific units). Higher titers of aPL antibodies were associated with neutrophil hyperactivity, including the release of neutrophil extracellular traps (NETs), higher platelet counts, more severe respiratory disease, and lower clinical estimated glomerular filtration rate. Similar to IgG from patients with antiphospholipid syndrome, IgG fractions isolated from patients with COVID-19 promoted NET release from neutrophils isolated from healthy individuals. Furthermore, injection of IgG purified from COVID-19 patient serum into mice accelerated venous thrombosis in two mouse models. These findings suggest that half of patients hospitalized with COVID-19 become at least transiently positive for aPL antibodies and that these autoantibodies are potentially pathogenic.
continue: https://www.science.org/doi/10.1126/scitranslmed.abd3876

 

[Gingergrrl]

Since I have a final diagnosis: lupus and antiphospholipid syndrome, I would like to share this, because it could also relate to ME/CFS:

I apologize if you have already posted this and I missed it but I was curious which autoantibodies you have that led to your final diagnosis as lupus & antiphospholipid syndrome? Thanks!

 

[SWAlexander]

I apologize if you have already posted this and I missed it but I was curious which autoantibodies you have that led to your final diagnosis as lupus & antiphospholipid syndrome? Thanks!

Gingergrrl
There were many tests before where lupus was mentioned, but I insisted on testing for microclots. These results caught my hematologist's attention.

Transl: Meaning: high Lipoprotein-associated with Phospholipase A2 LP-PLA2 activity.

she ordered more tests: (5 pages)
First and the most important test is von Willebrand Factor (FII, FV, F9).

You may like to listen to:
Antiphospholipid Syndrome (APS) Case Files (Gut, Tinnitus, and Migraine) - Prof Graham Hughes

 

[SWAlexander]

Now and finally (I´m saying this for the last 10 years!!) science is closing in on the X factor reg. ME/CFS and COVID!
"Systrom’s invasive exercise studies provided powerful indirect support when they suggested that the blood vessels are leaking either just before they reach the muscles, or after they’ve left the muscles."

The Endothelial Dysfunction Story in ME/CFS

The idea that something has seriously gone wrong with the blood vessels in ME/CFS has been around at least since 2012 when Newton found evidence of it in both the large and small arteries. With three recently published ME/CFS hypotheses (Fluge et. al.; Wirth and Scheibenbogen; Sfera et. al.), that focus heavily on blood vessel dysfunction that idea has been picking up steam.

Systrom’s invasive exercise studies provided powerful indirect support when they suggested that the blood vessels are leaking either just before they reach the muscles, or after they’ve left the muscles.

A couple of studies have also found direct evidence of endothelial dysfunction, including a recent one that linked disease severity to it. Several more studies have implicated endothelial cell dysfunction in different ways: via miRNA levels, via plasma effect in the lab (this one).

We’ve seen this pattern – in spades – before: studies, most of them small, take stabs at an issue and slowly build up evidence that it’s present – yet with no money to produce definite large studies no conclusions are reached. With three hypotheses showing up in ME/CFS, with this study adding the mysterious X-factor to the equation, and with studies implicating endothelial dysfunction in long COVID as well, this time it feels a bit different.

In a best-case scenario, studies like this would trigger large-scale investigations into both the X-factor and endothelial functioning- and perhaps kill two birds with one stone. The NIH-funded ME/CFS research centers may be our best hope for large, definitive blood vessel studies. Thus far, the centers have been focusing on other matters but the next generation of centers may decide to probe this emerging topic. Let’s hope the NIH really gets with the program – recognizes that ME/CFS’s time has come – and finally supports them with robust levels of funding.

Large endothelial long-COVID studies seem almost certain to come and they provide a superb opportunity to study long COVID and ME/CFS side by side. Since the NIH has decided that it will not allow people with ME/CFS to participate in its Congressionally funded long COVID research studies, we’ll have to look to other groups to include ME/CFS patients in their long COVID research efforts.
https://www.healthrising.org/blog/2022/02/11/x-factor-blood-vessel-chronic-fatigue-endothelial/

 

[CSMLSM]

31 of 364 ME/CFS patients tested positive for at least 1 of 4 autoantibodies in this study for small-fiber polyneuropathy.

Those 31 patients have pretty much identified the cause of their fatigue.

So you think, "well that's less than 10%, so I'm not likely part of that group". Wrong.

You might not have those specific auto-antibodies, but the majority of those w/ ME/CFS have auto-antibodies to something important. Something that probably causes the symptoms you have.

-------EDIT--------
I wanted to come back and edit this. I want to make this very clear. I am 100% confident in the idea, but I don't want it to be misconstrued.

I am not saying that auto-antibodies and autoimmunity are the sole cause of symptoms. What I am saying, is that the majority of those w/ "ME/CFS" have autoimmune genetic predispositions, and that auto-antibodies and autoimmunity plays a significant role in the development, perpetuation, and exacerbation of the persons unique set of conditions.

While auto-antibody treatment can potentially relieve symptoms, it's important to remember a single treatment isn't likely to cure symptoms elicited by a complex multi-faceted set of conditions.
-------EDIT--------

The small-fiber polyneuropathy study looked at (4) autoantibodies, two cholinergic and two adrenergic receptors. But in this specific category of receptors they are looking at, there are twice as many that could cause symptoms of CFS.

Maybe 10% of us have autoantibodies to the 4 they were looking at. Maybe 10% more of us have autoantibodies to the others.

But that's nothing. There are dozens of other auto-antibodies that can mistakenly attack your own body that could cause fatigue, pain, PEM, autonomic dysfunction, etc.

There are conflicting studies on viral (and non-viral) infections in ME/CFS. But when they do auto-antibody studies in ME/CFS, they often come up w/ definitive evidence.

Antinuclear antibodies (ANA), ganglionic receptor (alpha 3) antibodies, TPO antibodies for Hashimoto's, TRab antibodies for Graves disease, all the antiphospholipid antibodies, serotonin antibodies (5-HT), Heat shock protein antibodies, NMDA receptor antibodies, Anti-IgLON5 antibodies.

Guys, I'm telling you right now. Any one of these can cause the fatigue, pain, GI dysmotility, or dysautonomia symptoms you're feeling. And there are way more than the ones I just mentioned that can cause your symptoms. That, AND, they are still finding new auto-antibodies. There are still antibodies attacking important parts of the human body that haven't been discovered.

If you put all this together, all the auto-antibody studies and what-not, you'll see that autoimmunity in ME/CFS is close to 90%.

Hi sometexan84 my name is Daniel.

I believe you are right about this.

The underlying immune dysfunction leads to an activated adaptive immune response that itself is dysfunctional in nature.

Adaptive immunity is responsible for you developing memory of some infections and creates antibodies in response to this.

So this dysfunctional activated immune state leads to antibodies being dysfunctionally produced in response to you.

Plenty of you to react to and make antibodies based on you.

So to sum it up ME/CFS is not caused by autoimmunity it causes it, as a byproduct to the underlying issue- immune dysfunction caused by an underlying EBV infection or similar type of virus using similar mechanisms as EBV to persist in latency (stay infected past initial infection).

This is what I understand from my vast research over 20 years as a patient with ME/CFS and is my opinion.

Hope you find this interesting,
if you would like to know more I have some threads about my recovery ect you could take a look at.

Daniel

Daniel

 

[SWAlexander]

I wanted to come back and edit this. I want to make this very clear. I am 100% confident in the idea, but I don't want it to be misconstrued.

I am not saying that auto-antibodies and autoimmunity are the sole cause of symptoms. What I am saying, is that the majority of those w/ "ME/CFS" have autoimmune genetic predispositions, and that auto-antibodies and autoimmunity plays a significant role in the development, perpetuation, and exacerbation of the persons unique set of conditions.

While auto-antibody treatment can potentially relieve symptoms, it's important to remember a single treatment isn't likely to cure symptoms elicited by a complex multi-faceted set of conditions.

This is a very important factor and we need to find out why auto-antibodies remain high.
For me, the question is:
are the T-cells going rough,
or are the macrophages overloaded and malfunctioning,
or if the lysosomes don´t empty the collected waste.
all this can lead to inflammation.

 

[Gingergrrl]

@Gingergrrl There were many tests before where lupus was mentioned, but I insisted on testing for microclots. These results caught my hematologist's attention.

Transl: Meaning: high Lipoprotein-associated with Phospholipase A2 LP-PLA2 activity.

I'm not sure if I understood it all and wanted to clarify - were any of your positive results (that led to your diagnoses) part of the Anti Phospholipid Syndrome panel?

 

[SWAlexander]

I'm not sure if I understood it all and wanted to clarify - were any of your positive results (that led to your diagnoses) part of the Anti Phospholipid Syndrome panel?

At first, they tested only von Willebrand Factor and fond indicators for "some kind of" lupus.
Then I ask for a citrat-fibrin test.

Here is a small part of the results of the test.
Left my results - right normal results.

 

[Thebirdman333]

Think I set a record here @sometexan84

 

[Treeman]

Think I set a record here

Where did you do the testing?