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Hi All,
I’m new to the site. Joined because I adore Dr. Driscoll. 🙂 She is a compassionate pioneer in this triad of diseases. I have autonomic neuropathy, elevated (tryptase) mast cells and hypermobility, and orthostatic intolerance, but have noticed that a lot of the posts are for POTS. Do these theories also pertain to someone with my issues, even though I don’t have POTS. I did have POTS for a few years, about 2006 to 2009, due to a serious infection. But not so much anymore. I do have some BP that goes up on bad days but now pain in joints is biggest symptom and my neck.
Thanks All,
MaiysaI don’t think it matters really what our ‘groups of symptoms’ are classified as, what does matter however, is what’s CAUSING them. Like I was at one point, I suppose many visitors to this website have no diagnosis whatsoever. POTS, does seem to be a common consequence of the likely ‘Cause’, that Dr Driscoll has proposed.
Just for the record, I wondered if POTS was a phase that you either went ‘through’, or went ‘in and out of’ because now (some 8 years down the line since POTS reared it’s ugly head) I notice that, even though I still cannot stand up for long, my heart no longer races to 30 beats more when I stand. My blood pressure doesn’t drop however, instead it continues to rise, so maybe I’m not true POTS anymore, more Neurally Mediated Hypertension (NMH) now? Maybe this raised blood pressure is just another mechanism that the human body recruits to try and deal with the difficult situation it finds itself in.
I’m curious that you say you HAD POTS but don’t have it now, what makes you say you don’t have it now?
Regards
Barbara
(UK)I would definitely think it applies. The authors of this medscape paper say POTS patients seem to suffer from a type of autonomic neuropathy. http://www.medscape.com/viewarticle/717904_5
“These patients seem to suffer from a mild type of autonomic neuropathy; the peripheral vessels cannot constrict when there is orthostatic stress. In many patients symptoms start abruptly following viral infections, trauma, surgery and after pregnancy. Serum auto-antibodies to alpha-3-acetylcholine receptors of the peripheral ganglia have been detected in some patients with a post-viral presentation. In some cases, there is a hyperadrenergic state[8] leading to increased noradrenaline due to impaired clearance or decreased uptake of noradrenaline by the synaptic cleft. These patients suffer from profuse sweating, anxiety, tremulousness, tachycardia and high blood pressure. This variety usually runs in families and is thought to be due to an underlying genetic disorder. The secondary form of the disorder is seen in conditions associated with autonomic neuropathy, e.g. diabetes mellitus or amyloidosis, and in conditions that may be associated with intrinsic abnormalities in capacitance vessels, e.g. hypermobility syndromes. In other conditions the underlying pathogenesis is less clear, e.g. Sjögren’s syndrome.”
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