For example, there's an excellent article from Massachusetts General Hospital entitled
Autoimmunity may underlie newly discovered painful nerve-damage disorder. The subtitle to this article is "Immunoglobulin infusions improve pain and function in 75 percent of patients thought to have autoimmune small-fiber polyneuropathy."
@zzz I finally had a chance to read the article you linked and it was really interesting. First, I had no idea that there was a study that showed that 75% of patients with autoimmune SFN got improvement in pain and functioning from IVIG! That is amazing in and of itself. But this part that I am quoting below also stood out to me:
SFPN involves widespread damage to the tiny nerve fibers that carry pain signals and control internal functions such as heart rate, blood pressure and sweating. Patients often develop chronic pain, fatigue, weakness or fainting when standing, rapid heart rate or gastrointestinal problems.
I had always thought of "neuropathy" as pain and numbness (or "pins and needles") in the hands and feet. But this article is referring to SFN as everything from the internal functions that control heart rate, blood pressure, and sweating (all of which were grossly abnormal for me on multiple autonomic tests prior to IVIG and Rituximab).
Our doctor (Dr. K) did not have me do a muscle biopsy for SFN because he suspected that it would be positive based on my other failed tests (TTT, QSART, etc) and I already had multiple diagnoses including "Autoimmune POTS" and "Autoimmune Dysautonomia" and he said that it would not change my treatment plan no matter what it showed. But reading your link I now have a better understanding of why he thought I also had SFN (even though I did not have numbness in my hands or feet).
In SFN, does it mean that autoantibodies are attacking the tiny nerve fibers that control HR, BP, and sweating? Do we know which autoantibodies they are?
I was unaware of this effect when I started treating myself with one gram of SCIG once a week. To my shock and surprise, one day after my second treatment, my SFN completely disappeared.
Is that what you took/take? gamunex-C? I've been offered scig by my rheum (i asked for it; they preferred iv, but i asked for sub q)
I know you were asking zzz, but in case it is helpful, my two years of IVIG were also Gamunex-C. I was curious why you prefer SCIG to IVIG
@vision blue? Can you remind me of your main symptoms?
I thought for autoimmunity they use a very high dose - higher than someone needing replacemetn for example -
In general, for autoimmunity, it would be high dose IVIG which is what I had (vs. a much lower dose for immune deficiency). Although many people have both autoimmunity & immune deficiency (although in my case, I only had autoimmunity by the point that I started IVIG in 2016). But there are definitely people like
@zzz who have benefitted from very low dose of SCIG as well. I wish there were more interest in formal studies on IVIG for ME/CFS and co-related disorders.
I think most rheums are familiar with it as well- tho i expect some in dark ages who don't know about IG for rheum related diseases might not be.
Yes, many rheumys & neuros are in the dark ages and I could not find one in 2016 who was willing to prescribe IVIG (vs. my main doctor, who is an ME/CFS specialist, and also my MCAS specialist, who is an allergist/ immunologist, felt without question that it was the best treatment for me and both advocated with my insurance for the opportunity to try it).
and makes sense as well, IG supresses ones own immune system, so if ones own immune system is currently responsible for the symptoms of PN, then shutting it off would also shut off symptoms. Takes a while though since the autoantibodies still in circulation have to die off a natural death I think.
This makes sense although I constantly hear from my doctors that IVIG is an "immune modulator" (vs. immune suppressant) and that no one truly understands how it works in autoimmunity. Without question it works, even if science does not understand the exact mechanism yet. Also, IVIG does not stop new autoantibodies from being produced which is partially why I was prescribed Rituximab (once it was crystal clear that I was a responder to high dose IVIG) so that it would kill the B-cells and stop new autoantibody production, which IVIG alone cannot do.
My doctor (Dr. Kaufman) has thought from the beginning that I have an autoimmune problem, but he still thought that the one gram SCIG treatment was worth trying. Nevertheless, I was still rather astounded when it worked as well as it did.
I was astounded by your results, too, and am so curious to hear what happens next!
I think it could all be neuropathy.
This was also really interesting to me
@alex3619 b/c I never thought of "neuropathy" as related to having trouble swallowing but it makes sense if you think of neuropathy as numbness or weakness. I have never actually had trouble swallowing BUT my worst symptom prior to treatment was shortness of breath which turned out to be due to muscle weakness of the lungs and diaphragm. (I also had POTS and MCAS which affected my breathing for the trifecta... but that was a completely different experience than the muscle weakness).
We ultimately felt (in my case) that it was due to autoantibodies (the LEMS/CA+ Channel autoantibodies and anti-muscarinic/cholinergic) but now I am wondering if SFN played a role? I wish I could understand this all better b/c all of these symptoms are in remission and I currently do not have breathing issues or muscle weakness (beyond the now de-conditioning from 3.5 years of using wheelchair). I am constantly concerned if my remission is permanent or temporary (which no one can know) but the more I learn, the more I try to put all the puzzle pieces together.
