Vanderbilt Talk On Pots - Where We Are At

[ramakentesh]

Just dropping to report hte following. This may be of interest in terms of current thinking on pathophysiology:

http://10thintcatsym..._9.11_RAJ.S.pdf

It appears that some have increased Ang II and faulty ang II receptor vasoconstriction

Some have faulty vasoconstriction in their legs due to small fibre neuropathies

Some have acquired (and very rarely genetic) deficets in NET.

[issie]

Just had someone ask me if I thought that POTS would one day be identifiable with genetic testing - my response was anything is possible. Now, if they can figure out the different subsets and genetically figure some of it out ---that will be wonderful. I know, I figured out a good bit of my issues have genetic markers - indicating a possible connection.

It mostly looks like they are talking about the things we've been talking about for a long time. This is mostly laying out the direction they are looking - but, doesn't really give us any solutions ---yet.

Low renin and aldosterone issues with possible high Angiotensin (of course, none of us have yet to have those levels checked - so we don't know if our angiotension levels are high.) Also, I found some articles indicating that angiotension is made in the liver and heart and the levels could be high from that area and not the kidney area ---that is being suggested with the graphs.

Then there is mast cell issues --which many of us have already connected. New treatments we are trying for that.

Then there is the NET issue ---is it too much production of NE or lack of elimination of a normal amount - therefore causing a build-up. Still the same questions ---we've always had.

There's also the autoimmune component that some of us have figured out with ourselves.

But, at least these things are being looked into. Hope they come up with some answers. Thanks for posting ---it gives me hope.

Issie

[corina]

Great article, thanks for sharing Rama!

[HopeSprings]

I'm confused. On p.5 Dr. Robertson says POTS is a "final common pathway of HUNDREDS of genetic and aquired autonomic and cardiovascular entities." This makes it sound impossible for a person to find their individual cause. So they've identified like 10 possible causes, but there are 100's more to be found??? Disturbing. Then on p. 19 they say, "Excitement - The cause of POTS has been found!" Really - WHAT is it???? It's hard to be patient.

[issie]

Naomi,

To me all this is doing is listing things we already know is an issue. It isn't giving any answers. Mostly it shows the things they know are dysfunctional with us in POTS. Hopefully, since they have an outline of the issues ---solutions will be coming?????? Let's hope so.

Issie

[corina]

What makes it great to me is that things are written down on paper, it gives me hope!!!

[diamondcut]

This is true, it is documented and i have just been to see a geneticist today and at least when you can hold in your hand written down proof as to whats going "wrong" with us we habe to be taken seriously, i wanted to see the page where they have come up with new treatments and non side effects drugs for us though, they must have missed that page out by mistake!

[Kellysavedbygrace]

Thx for sharing. I am grateful there are docs and researchers actively working on this.

[Guest Alex]

Great article.

It still looks to me that the medical community has more questions than answers at this point. At least things seem to be moving, and I'm keeping my hopes high...one of these days!

Can't help but point out the awesome slide(s) with the elephant. A picture truly worth 1000 words...

Alex

[Zap]

Well, this is interesting - I found this presentation the other day but I didn't realize it was new. From the data it looks like someone has the capability to test Angiotensin & ACE, as they have test data from a number of patients. I was planning to have either my primary (if she'll do it) or a nephrologist test my renin/aldosterone. I know that I've heard talk of some nephrologists prescribing Florinef in instances where the test data indicates it would be helpful. I wonder if there is anything else that might be helpful.

One huge question this brings up, again - are beta blockers making some problems worse due to their effects, at least in some cases? Propranolol reduces renin. If one already has low renin, that can't be a good thing.

This definitely appears to be making strides in the right direction. The next thing to ponder is if any of these particular issues have genetic connections that 23andme will confirm - or if they are outside what is currently tested.

[Monstrosity]

good read, thanks!

[ramakentesh]

The slideshow suggests that we are reaching a point where the subcatagories of POTS based on pathophysiology are becoming clearer. This will undoubtedly lead to more focused and appropriate treatment protocols in the future.

it also suggests that it is NOW in the realm of possibility that a patient can endevour to have tests conducted that explain where they may sit within this spectrum:

1. A QSART test may suggest or exclude the possibility of selective small fibre neuropathy of the legs. This may inform a doctor about the best treatment for the patient.

2. A serum ANG II level may suggest or exclude the possibility of high ANGII/low aldosterone and the possibility of an underlying hypovolumia which again may change the direction of treatment protocol for a doctor. There is the possibility here that this constitutes a genetic defect of ang II catabolism.

3. And perhaps an MIBG reuptake scan may soon be employed to assess whether there is impaired NE reuptake via an acquired deficit in NET expression rather than a genetic one.

Ofcourse there may be and is likely there are other pathophysiologies but it is nice to read that some consensus is growing on the main subgroups.

And that's it for me for another six months or so or until another interesting study develops...

[abbyw]

Rama, - in your opinion, based on this study, why would SSRIs help people?

Just got this from Wikipedia:

Due to its tendency to increase blood pressure and its modulative effects on the autonomic nervous system, venlafaxine is often used to treat orthostatic intolerance and postural orthostatic tachycardia syndrome.^[18]

Also:

At low doses (<150 mg/day), it acts only on serotonergic transmission. At moderate doses (>150 mg/day), it acts on serotonergic and noradrenergic systems, whereas at high doses (>300 mg/day), it also affects dopaminergic neurotransmission.^[7]

Does that mean that the SSRI/SNRIs are treating the symptoms but not addressing any of the possible underlying causes?

Thanks,

Abby

[HopeSprings]

Let me just say as frustrated as I feel at times, I am grateful for all the research going on. The Doctors at Vanderbilt, in particular, seem very committed to solving the mystery. If you look at their page on current research projects, they're looking at everything - from renal salt handling to genetics to certain neurotransmitter and hormones, and the list goes on. I know they're trying. The pace just feels really slow when you're living with the illness.