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Antibodies to ß adrenergic and muscarinic cholinergic receptors in patients with CFS

jimells

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Since our illness appears to be autoimmune, does that suggest it is time for rheumatologists to step up to the plate? How can we make that happen, get stuff published in their society journals, show up at their conferences?

I've been to two rheumatologists, and they couldn't hustle me out of their office fast enough. One tried to claim that my symptoms are caused by COPD, which I don't have, but that didn't seem to matter much.
 

Marco

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I think it does sound simplistic but I suspect there are layers of subtlety underneath and I am quite happy to think this might link to the clinical presentation. Everything in immunology tends to need looking at from a certain sideways angle to see how it really makes sense, but when it does I think it does.
I can't access the full paper but I'm looking forward to further detail/discussion.
 

sillysocks84

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I find it interesting that the B2 and M3 receptors are involved in insulin release and energy production. This might explain the difficulties that patients tend to have in regulating their blood sugar despite the absence of an identifiable endocrine disease.
Yes that would explain why my insulin is always a bit high. My doctor keeps saying to be proactive. But the sugar I get is from my banana smoothies. My weight is average too. But my dang hr is out of control.
 

sillysocks84

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Since our illness appears to be autoimmune, does that suggest it is time for rheumatologists to step up to the plate? How can we make that happen, get stuff published in their society journals, show up at their conferences?

I've been to two rheumatologists, and they couldn't hustle me out of their office fast enough. One tried to claim that my symptoms are caused by COPD, which I don't have, but that didn't seem to matter much.
I feel your pain! I went to a rheumatologist who ordered tests and reordered and sent me to a pulmonologists who did an echo and pft on me. No help
 

Riley

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I feel your pain! I went to a rheumatologist who ordered tests and reordered and sent me to a pulmonologists who did an echo and pft on me. No help
I once saw a rheumatologist that said he would be right back before leaving the room and then never returned. After a while I poked my head out and asked where he was and was told by an office staffer my appointment was over.

Another one I saw pointed at a scar on my knee and told me it was psoriasis and that I therefore probably had psoriatic arthritis. This was in spite of me telling him that it was in fact a scar along with when and how I got it.
 

BurnA

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Since our illness appears to be autoimmune, does that suggest it is time for rheumatologists to step up to the plate? How can we make that happen, get stuff published in their society journals, show up at their conferences?
Rheumatologists or immunologists ? There is overlap but my quick Google search tells me rheumys are more into the musculoskeletal end of things.

Either way we need to educate doctors in general.
 

Gijs

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I think it does sound simplistic but I suspect there are layers of subtlety underneath and I am quite happy to think this might link to the clinical presentation. Everything in immunology tends to need looking at from a certain sideways angle to see how it really makes sense, but when it does I think it does.
I like simplistic qualifications. These findings are not the cause for CFS or ME in general only for a small subgroup especially those with POTS.
 

BurnA

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We further correlated elevated receptor autoantibodies with various clinical symptoms including disease severity, muscle pain, susceptibility to infection and infection triggered disease onset. The only association we observed was of M1 AChR antibodies with dizziness (p=0.05). Data on POTS was available in 8 patients only. Of these 4 patients fulfilled the criteria for POTS and 4 did not. Elevated ß AdR antibodies were present only in two of the latter.
Can someone explain what this means specifically in relation to POTS. ?
 

sillysocks84

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I once saw a rheumatologist that said he would be right back before leaving the room and then never returned. After a while I poked my head out and asked where he was and was told by an office staffer my appointment was over.

Another one I saw pointed at a scar on my knee and told me it was psoriasis and that I therefore probably had psoriatic arthritis. This was in spite of me telling him that it was in fact a scar along with when and how I got it.
Doctors get away with a loto_O
 

jimells

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I once saw a rheumatologist that said he would be right back before leaving the room and then never returned. After a while I poked my head out and asked where he was and was told by an office staffer my appointment was over.
Wow, that has got to be the "best" worst-doctor story I've ever heard. Just unbelievable.
 

snowathlete

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Are they saying that 29.5% of the 268 CFS patients studied had elevated antibodies?
Yes, I think so, but I haven't looked at it since this morning and my brain...well, there are probably autoantibodies causing havok up there.

M3 Receptor:

"However, with respect to vasculature, activation of M3 on vascular endothelial cells causes increased synthesis of nitric oxide, which diffuses to adjacent vascular smooth muscle cells and causes their relaxation and vasodilation."

"The muscarinic M3 receptor regulates insulin secretion from the pancreas[4] and are an important target for understanding the mechanisms of type 2 diabetes mellitus."

"The M3 receptors are also located in many glands, both endocrine and exocrine glands, and help to stimulate secretion in salivary glands and other glands of the body. Other effects are: Increased secretions from stomach, Eye accomodation."

Directly linked to NO syntheses and insulin secretion. Very interesting!!!
Might be an explaination as to why my sebacious glands went haywire when I got ME and started massively over producing for no good reason.

Since our illness appears to be autoimmune, does that suggest it is time for rheumatologists to step up to the plate? How can we make that happen, get stuff published in their society journals, show up at their conferences?

I've been to two rheumatologists, and they couldn't hustle me out of their office fast enough. One tried to claim that my symptoms are caused by COPD, which I don't have, but that didn't seem to matter much.
I saw a Rheumatologist years ago when I first got diagnosed with ME. I was actually seeing him in follow up to a sports injury I had from a number of years earlier, and I mentioned that I now had ME, he asked me about symptoms and he told me he thought it sounded like a rheumatological disease to him. He also told me that he was retiring a few months later. He seemed pretty switched on to me, shame I cant go see him now.
 

Dolphin

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In this paper, elevated levels of an antibody seem to be any values above the 90th percentile of a control group (judging by the descriptions on Tables 2 & 3).

Often normal ranges for tests are the values excluding the top and bottom 2.5% or so or perhaps 5% for scales where results are only abnormal in one direction. However, there can be problems with this e.g. with TSH levels (thyroid hormones, not thyroid antibodies), the thresholds were found to be too strict i.e. people who were classed as having "normal" levels actually often had abnormal functioning.

I don't know enough about autoantibodies or medical testing to know whether using the threshold they used is used much or not.
 
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alex3619

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What's that crackling sound in the distance? Is it... could it be... the Humpty Dumpty of Psychobabble has taken a great fall?

And look... all the King's Horses and Sir Simon's Men couldn't put Humpty together again... :rolleyes:
I little premature maybe. Oh, except that I posted something similar on Facebook, though a bit more tentative. They will still claim everyone else of course. It might be fun watching the spin machine though.
 

msf

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Prof. Edwards, I know this isn´t your view, but how do you think the authors of the paper see these kind of auto-antibodies arising after an infectious trigger?
 
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I haven't read the paper in sufficient detail to comment, but also note that there is an additional 'in press' paper:

Loebel, M., Mooslechner AA, Bauer S, Guenther S, Letsch A, Hanitsch LG, Grabowski P, Meisel C, Volk HD and Scheibenbogen S 2015. Polymorphism in COMT is associated with IgG3 subclass level and susceptibility to infection in patients with Chronic Fatigue Syndrome. Journal of translational medicine in press.

http://www.ncbi.nlm.nih.gov/pubmed/26272340
http://www.translational-medicine.com/content/13/1/264

Keep this in mind when interpreting the IgG3 and IgG4 data in the current paper.