This post is not about Myalgic encephalomyelitis (ME), but about the ME comorbidity Postural Orthostatic Tachycardia Syndrome (POTS).
POTS is a form of dysautonomia, and a description af the syndrome can be read at Dysautonomia International.
A precise pathogenisis of POTS remains elusive, but an autoimmune aetilogy is suspected in some cases.
And POTS is also seen as a side effect after injection of the HPV vaccine Gardasil Postural tachycardia syndrome after vaccination with Gardasil
This is interesting - a immune system trigger as a vaccine, can cause POTS!
Gardasil contains Virus Like Particles (VLP). These VLP are captured by endocytosis via lipid rafts:
Synthetic Virus-Like Particles Target Dendritic Cell Lipid Rafts for Rapid Endocytosis Primarily but Not Exclusively by Macropinocytosis
Please take a quick look in the Wikipedia: Endocytosis
Now it is almost unbearable exciting, because POTS is suspected to be an autoimmune attack on lipid rafts: Autoimmunoreactive IgGs against cardiac lipid raft-associated proteins in patients with postural orthostatic tachycardia syndrome
I don't know what it means, but it calls for more research in POTS and the autoimmune suspicion.
I have found a few more pieces of information that might fit in!?!
Lipid Raft and Blood Brain Barriere are conntected: Functions of lipid raft membrane microdomains at the blood-brain barrier
And the receptor TRPA1 is found in lipid rafts in the brain: Endothelium-Dependent Cerebral Artery Dilation Mediated by TRPA1 and Ca2+-Activated K+ Channels Activation of TRPA1 causes vasodilation.
And TRPA1 and vasodilation is connected: Evidence for the pathophysiological relevance of TRPA1 receptors in the cardiovascular system in vivo
"TRPA1 is involved in mediating vasodilation. TRPA1 can also influence changes in blood pressure of possible relevance to autonomic system reflexes and potentially to vasovagal/neurocardiogenic syncope disorders"
Gardasil "fingerprints" have been found in the cerebral vasculature in post mortem samplesGardasil Fingerprints Found in Post-Mortem Samples
Death after Quadrivalent Human Papillomavirus (HPV) Vaccination: Causal or Coincidental?
And now for some other pieces of information about POTS:
Idiopathic postural orthostatic tachycardia syndrome: an attenuated form of acute pandysautonomia?
Acute pandysautonomia and nicotinic acetylcholine receptor antibodies: "Acute pandysautonomia is an idiopathic, acute or subacute autonomic neuropathy, which diffusely affects pre- and post-synaptic, and sympathetic and parasympathetic nerves. The recent discovery of serum autoantibodies against the nicotinic acethylcholine receptor (nAChR) on autonomic ganglia has led to a better understanding of its pathogenesis as well as the emergence of a new disease entity named autoimmune autonomic ganglionopathy (AAG). Based on the detection of these antibodies in various dysautonomic conditions, AAG is considered a broad-spectrum disease entity that includes acute pandysautonomia as well as secondary autonomic neuropathy, restricted forms of dysautonomia (postural tachycardia syndrome and chronic intestinal pseudoobstruction), and chronic dysautonomia, mimicking pure autonomic failure. "
More about dysautonomia: Autoimmune Dysautonomia Evaluation
Limited dysautonomia: "With limited dysautonomia the symptoms are confined to one or just a few of the domains mentioned in the last slide. These symptoms are often milder and may include sicca manifestations, postural orthostatism, cardiac arrhythmias, bladder dysfunction, or gastrointestinal dysmotility"
Postural orthostatic tachycardia syndrome: the Mayo clinic experience:
“…In a preliminary study, we found ganglionic (α3) acetylcholine receptor (AChR) antibody in 10% of patients with POTS, suggesting that some cases represent a limited form of autoimmune autonomic neuropathy.”
“In 13.8% of patients, onset was subacute, and ganglionic acetylcholine receptor antibody was detected in 14.6%, suggesting an autoimmune origin in at least 1 in 7 patients.”
“CONCLUSION: Our findings suggest a neuropathic basis for at least half the cases of POTS and that a substantial percentage of cases may be autoimmune. Hyperadrenergic and hypovolemic correlates are likely compensatory or exacerbating.”
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