tag:blogger.com,1999:blog-73120972890131591.post1708135194264903269..comments2014-03-01T03:06:35.980-08:00Comments on Follow ME in Denmark: Is ME autoimmunoreactive IgGs against lipid raft-associated proteins?Helle Nielsenhttp://www.blogger.com/profile/13779967748632121875noreply@blogger.comBlogger3125tag:blogger.com,1999:blog-73120972890131591.post-47749762630837011252013-05-14T05:42:05.775-07:002013-05-14T05:42:05.775-07:00Thank you very much for your comment. I agree, we ...Thank you very much for your comment. I agree, we need to find the cause of the inflammation and better treatment than Rituximab. And I will be very busy the next days reading about PrPc, endogenous retrovirus and lipid rafts. Until a few hours ago, I didn't know anything about prions, but I am learning... :-))Helle Nielsenhttp://followmeindenmark.blogspot.dk/noreply@blogger.comtag:blogger.com,1999:blog-73120972890131591.post-15106193812370827782013-05-13T16:28:03.529-07:002013-05-13T16:28:03.529-07:00Hi FollowMEinDenmark, may I first congratulate you...Hi FollowMEinDenmark, may I first congratulate you on your excellent blog. I enjoyed reading it, and your past posts.<br /><br />Yes, this Wang et al paper you refer to is very interesting, the Immune system is likely attacking cardiac tissue which would explain non coronary artery disease chest pain (vasospastic angina), and fluctuating symptoms not associated to postural change and not caused by low blood pressure which many physicians are puzzled by or simply don't believe. <br /><br />There are other papers in the past showing autoimmunity in POTS and CFS, involving both Ganglionic and Muscaranic antibodies detected in blood. (NB: Not the same 'muscle' acethylcholine antibodies as Myasthenia Gravis). The autoantibodies in ME & CFS effect the autonomic and sympathetic nervous system, both which are deranged in CFS (ME) and POTS. <br /><br />I would keep a keen eye on PrPC, Endogenous retroviruses and ME and see if you can gather more information on this from your own keen eye.<br /><br />Prion PrpC in ME (normal prion protein) activity is likely altered through the effects of monoclonal antibodies. Rituximab is a monoclonal antibody depletor of CD20 on B cells.<br /><br />I think we will find this is why Rituximab 'works' for ME symptoms. Rituximab is likely negatively affecting prion production, which talk to T cells and which talk to B cells. Therefore Rituximab is affecting T cell function, through the effects of B cells, through the administration of a monoclonal antibody drug.<br /><br />What we need to find out is how to control the cross talk of viruses and PrpC first. Rituximab, although proving the 'cause' (inadvertently, as B cells aren't 'the cause'), is not a realistic long term drug solution.<br /><br />Getting the unique inflammatory process in ME causing the oxidative stress down in ME patients is the primary goal for future ME research. Inflammation drive by infection. If we can do that, we won't have to use Rituximab at all.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-73120972890131591.post-48824942894073318622013-04-27T20:54:26.909-07:002013-04-27T20:54:26.909-07:00Im not sure the paper was brilliant - the cohort o...Im not sure the paper was brilliant - the cohort of patients is only ten for a start and their previous paper included patients with profound orthostatic hypotension, excluding them from the diagnosis of POTS according to the recent consensus statement. <br />Will be interesting to see if they can employ the same technique to examine adrenergic locations since these mechanisms appear closely linked with the etiology of orthostatic intolerance. <br />Personally I think evidence has always suggested that CFS/Fibro/POTS and OI syndromes in general are autoimmune in a large portion of patients has been strong; female/male ratio, acute onset after stressor, etc. Anonymousnoreply@blogger.com