Thank you so much for posting this study
@Belbyr and I had not seen it before. It really has a lot of credibility and Dr. Blair Grubbs is one of the top POTS specialists in the world.
"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 was going to copy this quote from the article but you beat me to it, Patti! When they said that the patients blood was screened for nine autoantibodies against receptors, do you or Belbyr know if they used the Cell Trend Panel from Germany or another lab?
I was positive for seven out of nine autoantibodies in early 2016 on the Cell Trend Panel (done twice to be sure) and then after IVIG and Rituximab, I re-did the panel in 2018 and I was only positive for four of the seven. However, one of the four that remained positive even after treatment was the a1-adrenergic autoantibody like in this study (and the majority of symptoms that remain for me are POTS related). But unlike the people in the study, I have other autoimmune diseases besides POTS.
"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,"
I believe that some day it will be shown not only that there is an autoimmune sub-set of POTS but that POTS itself is an autoimmune disease (like this study presents). Perhaps the 10% of people who test negative for the alpha-1 adrenergic autoantibody are sero-negative (like in other illnesses, there is often a sero-negative group).
My daughter's anti alpha-1-adrenergic antibodies are almost 16 (with greater than 7.0 being positive).
@Sad Dad Was your daughter tested through Cell Trend in Germany or another lab? My a-1 adrenergic autoantibodies were always in the 20's. We did the test 3x total and they were 27, 22, and 29.
But, if these antibodies are so rampant in POTS & many CFS patients, why did the Rituximab CFS trials fail? Rituximab should have knocked out those bad antibodies, correct?
My personal opinion is that the alpha and beta adrenergic autoantibodies reflect POTS and not ME/CFS. I think if a trial had been done in patients with POTS with these autoantibodies, it would be very different than a trial of people with ME/CFS who may or may not have POTS and/or autoimmunity.
I don't know why some autoimmune diseases fail in Rituximab trials, but it happens.
I have written to an insane length in other threads re: my opinion of why the Fluge and Mella Ritux trial did not succeed so I don't want to take this thread off track.
But even in these diseases, there was anecdotal reports of rituximab success which is very confusing.
Absolutely, there were individual responders.
I guess that reminds me of rituximab failing in lupus trials
Even in RA (which Ritux is FDA approved to treat), there are non-responders.