Acetylcholine Ganglionic Antibodies And Other Possible Autoimmune Targets In Autonomic Disorders

[ramakentesh]

A bit of an oldie, but a goodie. I like the conclusions the most:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2671239/

On POTS:

POTS is arguably the most common syndrome of orthostatic intolerance, characterized by excessive tachycardic response upon standing as well as multiple symptoms in other autonomic (particularly gastrointestinal) and somatic domains. POTS is a syndrome, not a specific disease and a major subtype is the neuropathic variant, associated with impaired sudomotor function (Schondorf et al., 1993; Thieben et al., 2007) and altered peripheral adrenergic vasomotor tone. There is considerable heterogeneity of pathogenetic mechanisms, with venous pooling and abnormal beta-2-receptor sensitivity likely to play key roles.

Approximately 50% of cases report an acute or subacute onset, often following a viral illness, suggesting an immune-mediated process. In a recent review (Thieben, 2007) of 152 cases of POTS seen consecutively by Sandroni and Low, 6 of 42 patients (who had ganglionic antibody measured) had increased levels of antibody. These were consistently of low titer. In our ongoing prospective study, the percent of positive cases we have found a positivity of 25% (unpublished data). Hence we do not provide a firm percent in Table 1. There is no obvious clinical characteristic that seem to differentiate antibody positive from the antibody negative cases, although the issue has not been formally studied.

This is interesting because of recent work on beta 2 receptor autoantibodies in OH.

And the conclusions:

<p class="p p-last">

The take home messages from this brief overview of conditions other than AAG in which G-AchR positivity may be found are:

• the spectrum of autoimmune autonomic disorders is broad and still expanding
  
• clinical suspicion of an autoimmune pathogenesis is higher whenever an antecedent event, subacute onset, evidence of multiple (albeit sometimes subtle) organ/system involvement or of other autoimmune disorder is present
  
• the decision to treat with costly therapies requiring careful monitoring (such as long-term immunosuppressive agents) should probably be entertained whenever the index of suspicion of an autoimmune pathogenesis is high, regardless of the low titer seropositivity or seronegativity, whenever a patient fails to respond adequately to symptomatic therapies. Such decision should be taken in a case by case approach as there is no large study at present to justify otherwise
  
• seronegativity does not exclude autoimmune pathogenesis: it may simply mean the responsible autoantibody has not been yet identified
  
• similar phenotypes may have very different pathogenetic mechanisms and “idiopathic” should not equate “autoimmune”
  

[ramakentesh]

sorry i double posted again!!!

[issie]

Yeah, science is advancing and I bet that they will figure out that allot of things may be autoimmune related. But, figuring out what to do about it - may be another story.

[ramakentesh]

And interesting that Ritixumab seems to work in CFS and Myanthenia gravis:

http://www.medscape.com/viewarticle/750757_4