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Everything posted by jangle

  1. 10-40 mg of propanolol is an extremely low dose. The maximum prescription strength is 640 mg, it doesn't start to slow the heart down until about 30 mg and really to slow the heart down doctors prescribe around 160 mg a day. It has been shown in studies that POTS patients don't tolerate beta blockers in higher dosages. This could be what's affecting you, but if it were me I wouldn't worry about heart attacks and/or other serious side effects at that dosage level.
  2. EDIT: The heart autoantibodies and the beta/alpha autoantibodies I don't believe have an explicit blood test yet. The ACHR can be run here: http://www.mayomedicallaboratories.com/test-catalog/Overview/89904 Sorry, I don't believe the bloodwork exists for the newly discovered heart autoantibodies. The antibodies to the nerves are these ones: http://edrv.endojour...bstracts/OR48-1 And of course the ACHR nicotionic antibodies found in 10-25% of POTS patients (which mayo does test for.) I'm currently in the process of getting referred to Mayo Rochester. We were talking about going there and speaking hypothetically if the blood tests for those autoantibodies did exist, which they may very well exist by the time I get to Mayo as it's going to be a few months. I think what she said was reasonable, she has done IVIG on patients with AAG as she's trained at Southwestern with Dr. Vernino. She said she's had about half her patients improve with IVIG that she's done this to, but it's a small pool of patients and they were quite more sick than I was. She said IVIG would be difficult if not impossible to approve through insurance and it is very expensive to continue with a long term treatment. Steroids can also be used, but she would need the bloodwork to indicate that it is even autoimmune and in addition long term steroid use is not all that great either. So even though others have improved with steroids, it might be something that can only be a short term therapy. As for other biologics, they might have a place in POTS treatment, but they're so expensive that we might have to wait for a clinical trial to open up to fund it. I've looked and currently there are no clinical trials employing immunomodulation for POTS. However, I emailed the authors of the heart study from Mayo and they transferred my question to other physicians at Mayo and I will try to find out if there are clinical trials opening up. Hopefully there will be some when I go up to Mayo. Overall she answered my questions very well and made an honest effort to help me out. She herself was on Florinef for another reason and told me of its safety profile and got me on a lower dose. It's just refreshing to have someone with experience to talk to. It's the worst feeling when I ask a POTS question to another doctor and get the dumbfounded, "huh" expression. I especially like how she said, "What were you doing with a cardiologist? There are no cardiologists in Austin who treat POTS, This is in neurology's field." She knows what's up.
  3. Yes actually this doctor is well versed in POTS, she's read many of the studies and seen quite a lot of patients so I'm pleasantly surprised. The bloodwork we were talking about would be the mayo clinic heart autoantibodies as well as the alpha/beta receptor antibodies and achr antiganglionic antibodies associated with POTS. The type of immunosuppression was IVIG/steroids.
  4. I'm currently going to try florinef again this time just taking it 3 days of the week. But I was talking with my new neurologist who's experienced with POTS patients. She said that she would consider immunosuppression if my bloodwork comes back positive and the specialists advise immunosuppression, but that she feels the side effects of immunosuppression can outweigh the severity of POTS. I'm not familiar with immunosuppressant drugs, so I don't know the severity of their side effects. I think for some immuno-modulators like IVIG, the side effects can be short lived and not too intense, but they can certainly vary. Of course if one gets an infection that could have serious complications. I guess any kind of discussion like this would have to accurately measure side effect vs symptoms without treatment. But basically what I took from the conversation is that POTS may very well be an autoimmune disorder, but that doesn't necessarily mean they'll treat the autoimmunity.
  5. Wait what? So can we no longer post links to medical studies we're talking about?
  6. Well according to drugs interaction website, there doesn't seem to be interactions listed. Florinef and Prednisone target different receptors. http://en.wikipedia.org/wiki/Glucocorticoid As you can see in that wikipedia article, Florinef has more than 200 times more affinity to the mineral receptors than Prednisone. It also has 5 times the affinity for gluco-receptors, but the dosage is so small (.025 mg) that this is negligible. However there is no denying that there will be additive effects, and realistically this is something you should ask an expert pharmacist about. Call around different pharmacies, they give you free advice.
  7. For those with the ACHR POTS, it was noted in a case study that disease activity was correlated with ACHR titer. I do think inflammation is important in POTS in the sense of an overall immune mediated reaction, whether the specific autoantibodies are important or not I don't know as there are perhaps other autoantibodies now being shown associated with POTS. However, given that people's experience on this board with Prednisone or hydrocortisone has been good (minus the side effects) I'm liking the evidence for autoimmune pathophysiology.
  8. For the people posting about success with steroid shots - what shots were you using?
  9. With the recent study about autoantibodies being spotted in POTS patients, I was wondering if anyone else has anything to add to this.
  10. The symptoms you reported are consistent with other POTS sufferer's experiences including my own. For me, the nausea and vomiting subsided some years ago, but I still have the headaches and presyncope. To summarize, there are some fundamental theories as to what causes POTS. Dr. Stewart advanced the idea of high levels of angiotensin ii on the assumption that an overactive sympathetic nervous system tends to produce high levels of angiotensin ii. However, the flaw with this theory is that only a few of his POTS patients exhibited measurably high levels of angiotensin ii, and losartan (which is an angiotensin ii blocker) does not seem to be a gold standard for treating POTS. Dr. Levine advanced the idea that a small heart size is responsible for producing POTS. The flaw with this theory is that POTS seems to strike later in life, and is not typically seen present at birth or earliest childhood years. Additionally many people with POTS have a normal stroke volume and heart size as measured by other studies. Dr. Bayles advanced the idea that reduced levels of norepinephrine transporter protein is responsible for POTS. This has the most evidence as studies have shown that blocking NET (norepinephrine transporter) in healthy controls produces POTS in them (That is, they get the rise in heart rate upon standing.) But he did not advance an idea as to what causes this reduced NET. He did rule out mutations as well as methylation. He suggested perhaps a cytokine/inflammatory role. A recent study out of the Mayo Clinic identified autoantibodies to the heart in POTS patients. This might be the underlying cause of the disease. POTS seems to follow a lot of the same traits of other autoimmune illnesses. It has a higher incidence in women (who are more predisposed to autoimmune illness). It has a flare up/remission cycle in some patients (similar to other autoimmune illnesses) and it's triggered often by febrile illness or pregnancy (similar to other autoimmune illnesses).
  11. Ya that's what I was thinking as well, I did a preliminary talk with my cardiologist's nurse, and she said that an immunologist would treat that and that the role of the cardiologist would be to oversee the structural integrity of the heart. I told her to forward the question to the cardiologist. I'll see what he says, however from his first message, he basically told me to go to mayo so I'm going to guess his answer would be not cardiologists.
  12. I will admit I have not looked too much into Mast Cell yet, however one fundamental flaw with that theory is that it seems that MCAS presents with fluctuating intensity. There are flares as well as remissions, and these flares seem to be provoked by environmental stimuli. For myself, my symptoms are constant, and do not seem to be exacerbated by allergenic substances. Could there be a connection between mast cells and cytokines? Certainly, but I don't believe we'd be able to get more specific than just using the word, inflammation - which isn't helpful. Inflammation is probably the key and of course the obvious question what is causing the chronic inflammation. I'll have to read more into autoantibodies and autoimmune illness in general. I posed an interesting question to my cardiologist - if this does turn out to be important in POTS, what specialty would treat it? Immunology or Cardiology? Autoantibodies attacking the heart. That's a tough one. In neurology, it's predominately neurologists who treat MS, despite it being an autoimmune disorder. So it will be interesting to see what college of medicine takes it up.
  13. Issie, I read the data from this article, the way the data supplement made it seem - everyone with POTS has autoantibodies. Whether they show up on other tests or not is becoming less relevant. I myself do have a positive ANA, but I believe these auto antibodies are specific to cardiac tissue, and so are not typically targeted by conventional blood tests.
  14. Usually it's the insurance company wanting to save money by having you talk to one of their nurses in an effort to organize your treatment plan so as to attempt to cut down on doctors visits. You can't be dropped due to overuse.
  15. I purchased the full text of this article, however it didn't really give any more details than the abstract which was disappointing. I sent the abstract to my cardiologist who then told me to go to Mayo clinic. I'm going to see what my new neurologist says, but if it does just come around back to "go to Mayo" then I'm probably going to be waiting quite a while before I get anything going on this front. Where is my Dr. House?
  16. It's a symptom of a malfunctioning medical system. Not just tertiary care, which for POTS patients means >6 months to get into POTS specialists but even for regular specialists it's quite a wait. Case in point, I booked for the first available for my neurologist on Sept 14, and I'm not getting in until Oct 11. So even though I've waited so long, I still have like 2 weeks before I'll get in. I dislike waiting.
  17. Ya I remember a more pronounced form of my symptoms followed by excessively going to the bathroom when I stopped Florinef. You should feel back to normal soon.
  18. diamond, I made the appointment to see that neurologist, but it takes a month to get in, so I'm still waiting.
  19. Ask your doctor, as it could be an increase in cytokines after exercise. http://jp.physoc.org.../3/949.full.pdf It's well known that exercise will lead to a substantial transient increase in both inflammatory and non inflammatory cytokines. The logical leap is that in POTS and CFS patients who might already be undergoing an autoimmune disorder, this increase is sufficient to increase symptoms substantially, or perhaps the rise is even more dramatic in these patient populations. Just a theory.
  20. "Since POTS will make you look crazy." Oh gosh, I hope that doesn't mean POTS is being viewed as negatively as fibromyalgia. I don't want to open that conversation, but frankly people with fibro are screwed because the majority of the medical community sees them as crazy and/or latent munchausens/attention seekers. Which means little funding for research and little healthcare for them. I was optimistic when my cardiologist gave his unsolicited opinion, "Fibro is fake, POTS is real" so I was thinking that doctors are at least willing to say that POTS is a physical illness, but I hope hope hope hope hope that it's not starting to roll into psychogenic territory. Because once that's established, like as in Fibro - it won't go away easily. I mean it MIGHT with CFS, but I don't think CFS ever got as bad a rep as Fibro did. You can read on doctor's twitters/blogs, it's a running joke about fibro patients. It scares me honestly. Anyways, welcome to the forum, there is quite a resource of knowledge here, and although there are still many answers left to discover, it does seem that lately there's been a lot of meaningful research being published.
  21. So if the class of autoimmune antibodies are IgG, then what treatments are available? I see IVIG treatments has had some limited success, but I've been looking around the internet and am having trouble locating IgG treatments. Probably something for an immunologist to answer.
  22. http://www.ncbi.nlm.nih.gov/pubmed/23002038 I'm going to go to campus so I can get the full article.
  23. I have my ways, but it appears I was beaten to the most exciting POTS research to come out - which was the autoimmunity study just published this week.
  24. well, it is true that the population size is small, however, this is further evidence that autoimmunity is implicated with POTS, which has been my major suspicion since this past July. This study will help me IMMENSELY in securing doctors on my side to pursue the autoimmune pathway.
  25. Interesting. I'd write more, but I gtg to work. It is new though, it says it was published sept 24
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