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

@Hutan maybe you want to watch this.

https://www.youtube.com/watch?v=XHaDCBXWArU

 

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.

 

@Hutan that sounds absolutely plausible to me. Maybe also want to look into this. OI and POTS after vaccination.

https://www.youtube.com/watch?v=pyMTYzgN78I

 

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.

 

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.

 

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.

 

@Badpack did you try plasma exchange?

 

@butter. 7 plasma exchanges over the time of 10 days. Nothing.