voner
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https://www.ncbi.nlm.nih.gov/pubmed/29618472
other authors include Dr. Satish Raj and Dr. Kem. Seems like a significant finding.
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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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I don’t know the answers to those questions. I doubt there’s any commercial lab that contest for these antibodies yet.
This study was shared some days ago in a german group on facebook, so I already had a look which lab would test these antibodies. I have found one here in Germany, its called "Labor Berlin". Unfortunately you can't just send your blood there but you will need a (I suspect german) doctor who will do that for you.
Celltrend is testing Angiotensin autoantibodies, too. But its the wrong type.
And, if one had these antibodies, what would the treatment be?
Postural orthostatic tachycardia syndrome: a dermatologic perspective and successful treatment with losartan.
Landero J1.
Author information
Abstract
The postural orthostatic tachycardia syndrome is a disease characterized by excessively increased heart rate during orthostatic challenge associated with symptoms of orthostatic intolerance including dizziness, exercise intolerance, headache, fatigue, memory problems, nausea, blurred vision, pallor, and sweating, which improve with recumbence. Postural orthostatic tachycardia syndrome patients may present with a multitude of additional symptoms that are attributable to vascular vasoconstriction. Observed signs and symptoms in a patient with postural orthostatic tachycardia syndrome include tachycardia at rest, exaggerated heart rate increase with upright position and exercise, crushing chest pain, tremor, syncope, loss of vision, confusion, migraines, fatigue, heat intolerance, parasthesia, dysesthesia, allodynia, altered traditional senses, and thermoregulatory abnormalities. There are a number of possible dermatological manifestations of postural orthostatic tachycardia syndrome easily explained by its recently discovered pathophysiology. The author reports the case of a 22-year-old woman with moderate-to-severe postural orthostatic tachycardia syndrome with numerous dermatological manifestations attributable to the disease process. The cutaneous manifestations observed in this patient are diverse and most noticeable during postural orthostatic tachycardia syndrome flares. The most distinct are evanescent, hyperemic, sharply demarcated, irregular patches on the chest and neck area that resolve upon diascopy. This distinct "evanescent hyperemia" disappears spontaneously after seconds to minutes and reappears unexpectedly. Other observed dermatological manifestations of this systemic disease include Raynaud's phenomenon, koilonychia, onychodystrophy, madarosis, dysesthesia, allodynia, telogen effluvium, increased capillary refill time, and livedo reticularis. The treatment of this disease poses a great challenge. The author reports the unprecedented use of an oral angiotensin II type 1 receptor antagonist resulting in remarkable improvement.
Brief Summary:
The investigators study will determine how often blood flow regulation abnormalities and abnormalities of sympathetic regulation produced by nitric oxide, angiotensin-II, and oxidative stress occur in POTS and the mechanism(s) of POTS in individual patients. Specific causes for POTS may vary from patient to patient. Patients will be compared to healthy control subjects. There is a treatment arm with a medication (losartan) that reduces the binding of angiotensin and increases NO. If the investigators know the specific biochemical mechanism the investigators may be able to offer further specific treatments to specific patients.
Condition or disease Intervention/treatment Phase
Postural Tachycardia Syndrome Drug: LosartanDrug: Ascorbic Acid (Vitamin C)Drug: Normal Saline Early Phase 1
Detailed Description:
Chronic orthostatic intolerance due to the postural tachycardia syndrome (POTS) severely impairs daily life in over a million Americans, mostly young women. POTS is defined by symptoms of orthostatic intolerance associated with excessive upright heart rate. While there is general agreement that abnormalities in vascular regulation and autonomic activity account for the tachycardia and symptoms of POTS, its pathophysiology is heterogeneous and only partially characterized.
The key feature of POTS is symptoms which are most prominent when standing. However, in some, findings are present supine (lying down) but worsened standing. Symptoms of POTS include dizziness in all patients, exercise provoked symptoms and thus exercise intolerance, excessive fatigue, nausea and abdominal pain, headache, shortness of breath and deep breathing, weakness, shakiness and postural anxiety, pallor, and neurocognitive loss (difficulty thinking). These occur on a day-to-day basis. The symptoms overlap with the case definition of chronic fatigue syndrome (CFS) and POTS is often found in CFS in the young. Fainting is relatively uncommon during daily life.
A major subset of POTS has increased peripheral resistance and low blood flow(LFP) related to increased angiotensin-II (Ang-II), and decreased nitric oxide (NO). NO deficits are reversed by Ang-II type-1 receptor (AT1R) blockade, ascorbic acid (AA) and tetrahydrobiopterin in skin suggesting the importance of oxidative stress. Preliminary data also suggest that the coupling of sympathetic nerve activity to blood vessel contraction is enhanced via ↑Ang-II and ↓NO. We hypothesize that this is due to activation of reactive oxygen species (ROS) including superoxide, which scavenges NO to generate peroxynitrite, and hydrogen peroxide. Combined measurements in the skin and the systemic circulation will be combined with local measurement of ROS production and sympathetic nerve activity will enable us to determine precisely how the autonomic nervous system is affected by the illness. Methods include cutaneous microdialysis to measure ROS, skin biopsy and blood tests to measure gene expression of nitric oxide synthase and Ang-II receptors, and peroneal microneurography to measure muscle sympathetic nerve activity (MSNA). Combined with ultrasonic femoral artery blood flow this will yield assessment of the interactions of nerves with the blood vessels that they control.
If we discover specific biochemical mechanisms of POTS in patients, then we may be able to specifically treat the defect.
@voner Wow, thanks for finding this stuff and I am definitely going to read the study and research Losartan. I Googled Losartan and POTS and a lot of stuff came up. I have some reading to do and don't know enough about this to even comment yet.
In 5+ years, I have been recommended just about every med on the planet for POTS by different docs but no one has ever even mentioned Losartan! Is this a new medication?
Wikipedia says it’s a little over 20 years old and it’s inexpensive.
I suspect it is just a German lab and from my research the labs in Germany are much more advanced than other countries re: testing for autoantibodies and in some other medical procedures.
Is that a new test that Cell Trend recently added? When I did the Cell Trend testing, they offered nine different autoantibody tests and I did all nine. Do you know if the angiotensin autoantibodies is something new? Also, when you said it is the "wrong type" does that mean it is not the one from @voner's article that potentially correlates with POTS?
So, after trying olmesartan and then telmisartan for over a year, I finally decided they were doing nothing to reduce my blood pressure which runs high, or POTS
I don‘t want to get too excited yet... but I googled again for the Angiotensin-Autoantibodies at Celltrend and found they seem to not only test the wrong type (by which I meant the TYpe 2 not the Type 1 which was used in the study) but also the Angiotensin II Receptor 1 autoantibodies. Which should be the „right“ type.
Oh and I really have to remind myself of that we have advanced labs here in Germany and that it is quite a lucky situation. I often feel dismissed as a patient when you just can‘t get things tested but need a doctor who agrees that you get stuff tested. But not all labs are doing it like that and I feel like things are getting a little more patient-friendlier.
Sorry @Gingergrrl, I'm not good in explaining what I mean because of the language barrier. I googled again after you've asked about Celltrend. And I think they are also testing the antibodies from the study.
As I remember, Vanderbilt tested for this but probably only on patients in their Autonomic clinic--might be worth checking though.Satish Raj used to be at Vanderbilt – who has a well published dysautonomia faculty.
I thought I had heard of every POTS med & treatment that existed (beta blockers, CA+ Channel blockers, Midodrine, Droxidopa, Mestinon, IV saline, Salt tablets, etc).
Here is an important point: there are a number of causes for POTS and while decreased NO is an important subset, it is probably not true for the majority. (increasing NO is Julian Stewart's usual treatment choice). If you increase NO, you increase vasodilation. The majority of POTS patients seem to respond better to vasoconstriction (hence Midodrine works). So it looks like testing is very important to determine treatment. For instance, testing showed that I was low in norepinephrine in the synapses. This is also a subset but not the majority. So I responded extremely well to Strattera, a norepinephrine reuptake inhibitor.A major subset of POTS has increased peripheral resistance and low blood flow(LFP) related to increased angiotensin-II (Ang-II), and decreased nitric oxide (NO). NO deficits are reversed by Ang-II type-1 receptor (AT1R) blockade, ascorbic acid (AA) and tetrahydrobiopterin in skin suggesting the importance of oxidative stress.