Adrenergic Autoantibody‐Induced Postural Tachycardia Syndrome in Rabbits, 2019, Li et al

Jonathan Edwards said:
“I hope you are not going to say muscarinic”.
Click to expand...
I don't think these authors are saying 'muscarinic'. They worked with adrenergic autoantibodies. As far as I can see they are different things.

Hutan said:
The authors suggest that these have autoantibodies been found in all POTS patients tested by one group in small studies. and that it isn't known if healthy individuals are just as likely to have the antibodies to adrenergic receptors.

Is the latter point, that the prevalence of these adrenergic autoantibodies isn't known in healthy people, correct?
Click to expand...

What evidence have you seen Jonathan that suggests the levels of adrenergic autoantibodies in people with ME and healthy people are similar? I expect there is something, but it would be good to be reminded what it is.

Jonathan Edwards said:
It is possible that there are different antibodies in ME but then the assays are not showing that up so the ME antibodies might be any sort of antibodies, unrelated to adrenergic or muscarinic receptors- so we are back to first base.
Click to expand...
My question that prompted this answer wasn't whether there are different antibodies, but whether the same antibodies, and even the same levels of the same antibodies, might have different effects in healthy people and people with ME. Maybe if there was something different about the receptors, or what happens when the antibodies bind to the receptors?
 
So i looked up a lot of studies again for graves disease and rituximab. For me it still seems to only help with the graves opthalmopathy and not the disease itself. Also it seems strange to me why you would prefer a medical removal of a life dependant gland instead of trying to treat it with other options like rituximab if it would work that great. Because why would you prefer to make a patient lifelong dependant on medical substitution when you could save the organ otherwise. Also its a strange coincidence that a lot of patients in graves disease start with a normal infection just like so many cfs patients report. I still stand by my assumption that graves disease and cfs have a lot in common in how they operate as a disease. You get a normal viral / intracellular bacterial infection, the body wants to help you but builds autoantibodies who act like hormones in the process via molecular mimicry.
 
Last edited:
For what it's worth, and it's probably not worth much, I have euthyroid Graves opthalmopathy. It preceded the ME/CFS; I've had a few flares it. Thyroid function has been fine whenever checked. I've had a couple of operations to lower an eyelid.

It started after a work trip to a remote and swampy part of South America, staying in a camp where there was an active typhoid outbreak, malaria was rife and I got bitten by a very large number of tick nymphs (which is to say there was a lot of exposure to all sorts of diseases). Just prior to the trip I had had a number of vaccinations including for yellow fever and typhoid. I recall that I developed what I would now call orthostatic intolerance; I had a lot of trouble with the up and down of pilates, being lightheaded and with my vision clouding over, when prior to the trip I had had no trouble. And my voice became oddly nasal. After a year or so, that resolved itself. Another aftermath of the trip was a granuloma annulare which was fixed with, I think, hydrocortisone injections.
 
My husband developed a thyroid storm after a bad flu. It looked as if the flu caused it but when we thought about it he had had symptoms for a good while before but they were not severe enough to recognize at the time. There are a few people in his family with overactive thyroid so we should have noticed but you look back at things and wonder how you missed it.

The flu had let the disease develop into a life threatening emergency but had not caused it. This may be what happens in some cases of ME but it does not explain the epidemics.
 
Badpack said:
So i looked up a lot of studies again for graves disease and rituximab. For me it still seems to only help with the graves opthalmopathy and not the disease itself. Also it seems strange to me why you would prefer a medical removal of a life dependant gland instead of trying to treat it with other options like rituximab if it would work that great. Because why would you prefer to make a patient lifelong dependant on medical substitution when you could save the organ otherwise. Also its a strange coincidence that a lot of patients in graves disease start with a normal infection just like so many cfs patients report. I still stand by my assumption that graves disease and cfs have a lot in common in how they operate as a disease. You get a normal viral / intracellular bacterial infection, the body wants to help you but builds autoantibodies who act like hormones in the process via molecular mimicry.
Click to expand...

The study I remember was from a group in Copenhagen. T4 levels and autoantodies reduced with rituximab. But the focus has been on ophthalmopathy because it does not respond to radioiodine or thyroid surgery.

Thyroid surgery is far preferable to rituximab. It produces a lon term solution, the main downside is the need for simple replacement of T4 in some cases. Repeated use of rituximab means you are constantly under a specialist clinic life long, needing infusions and likely running into IgG level problems after 10 years. I have not met a physician who thought rituximab would ever be preferable for the T4 levels.
 
Hutan said:
I don't think these authors are saying 'muscarinic'. They worked with adrenergic autoantibodies. As far as I can see they are different things.

What evidence have you seen Jonathan that suggests the levels of adrenergic autoantibodies in people with ME and healthy people are similar?

My question that prompted this answer wasn't whether there are different antibodies, but whether the same antibodies, and even the same levels of the same antibodies, might have different effects in healthy people and people with ME. Maybe if there was something different about the receptors, or what happens when the antibodies bind to the receptors?
Click to expand...

A lot of people in this field, like Dr Scheibenbogen, have looked at adrenergic and muscarinic cholinergic antibodies in parallel. People coming from the POTS side may just do adrenergic.

I went over Dr Scheibenbogen’s data with her before a prepublication presentation to IiME a while back. My memory may be wrong but what I remember is that she looked at both and differences between ME and control was a tiny statistical shift. That is not what you get with antibodies known to be pathogenic.

The is huge heterogeneity in terms of antibody binding and effect so your lat point is theoretically valid. However, in cases where we know antibodies are important it shows up on simple tests (even those of the 1940s) like a sore thumb. I have seen hundreds of studies all sorts of antibodies supposed to be important in diseases with minor shifts. None of them have turned out to be of interest.
 
You must log in or register to reply here.
Back
Top Bottom