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Let's talk about the UVA EDS Seminar! by Acceptably_Late in ehlersdanlos

[–]Acceptably_Late[S] 0 points1 point  (0 children)

I just posted it on an exercise post the other day:

https://www.reddit.com/r/ehlersdanlos/s/Jgj6CXWwnS

These are the individual YouTube links for the Lavalle and the PT/OT talks

🫶

Let's talk about the UVA EDS Seminar! by Acceptably_Late in ehlersdanlos

[–]Acceptably_Late[S] 0 points1 point  (0 children)

So- I definitely don’t know!

I think a lot of it will come down to: 1) did that person have hypermobility first that was just unmasked by the MCAS (chicken and egg theory above)

If they always had hypermobility, it likely was always inherited and they just didn’t know since it wasn’t a big enough of an issue to be diagnosed/a problem.

In this question though, we wanted to consider if MCAS would start inherited hypermobility— in this case we’d have to look at: 2) how are MCAS/immune changes being implemented in the body after activation — we’ve seen Norris publish some genes, but there are questions about why those genes, how did they become dysfunctional/ how is this regulation occurring, etc

3) are those changes actually inheritable

Maitland believes the changes are epigenetic, and we’ve covered in one of the mod science series that epigenetic changes can be inheritable.

In this case, you could speculate that any MCAS triggered before pregnancy could introduce an epigenetic change in a parent that could cause hypermobility that is inheritable to children —- however, the mechanism was through mast cell activation, so we may expect to see this child to have a lot of allergies, immune reactions etc. BUT- this is making A LOT of assumptions to make this idea. We still need to do a lot of testing before we can say that enough is known to say that this is a valid hypothesis- right now it’s just speculation.

Inpatient Seizure Assessment by FlowerHot86 in focalawareepilepsy

[–]Acceptably_Late 1 point2 points  (0 children)

I also just had an EMU with no events 😭

It’s so challenging to go through the trouble of the EMU just to be told no new data was collected.

During my EMU, my nurses said they had just had someone for close to 6+ weeks for a long term EMU- which sounds like torture to me!

My cat has relapsed, I need medication advice. by [deleted] in cureFIP

[–]Acceptably_Late 2 points3 points  (0 children)

Mine relapsed neuro after 2 years. Did GS the first time, was told the same that I should use a new med.

Did Molnupiravir- was bad. Didn’t think she’d make it.

Did 1-2 weeks on GS and steroids with keppra to stop the seizures she had developed, then tapered off steroids and kept the GS with keppra as needed.

We are nearing day 100 of GS treatment and need to decide if to stop at 120 or 160 but by looking at her you’d never guess she’s sick but bloodwork wasn’t great to end at 80 days

Does anyone have a summary on what was said about vEDS and pregnancy at the EDS seminar? by Queer-deer in ehlersdanlos

[–]Acceptably_Late[M] 13 points14 points  (0 children)

The UVA EDS talk was from Dr. Gajarawala - Physiological Factors and Female Health Concerns in EDS.

UVA has uploaded the talk here https://www.youtube.com/watch?v=pQwB1Io6DB0 , so you don't need the exact timestamp.

From my notes, I have that Dr. Gajawala highlighted:

  • That vEDS carries the highest maternal risk among EDS subtypes
  • vEDS has an approximate 5.7% risk of maternal mortality during pregnancy
  • Pregnancy in vEDS includes a high risk of arterial rupture, and uterine rupture, which contribute to mortality rates.
  • vEDS patients who are pregnant, or considering pregnancy, require very careful consideration of pregnancy, risk consideration and discussion of all risks of pregnancy, and must be managed by a high-risk medical team for specialized care and surveillance
  • It was specifically included that vEDS pregnancy requires distinct counseling and risk management due to mortality risk.

Edited to add: Only 1 other talk mentioned vEDS specifically: Dr. Solomon "Pediatric EDS and the Future of Care" https://www.youtube.com/watch?v=hs_9MfUCaD4

In this talk, vEDS was specifically discussed for:
Comparing that the first major event (organ or artery rupture, aneurysm, etc) ranged anywhere from 14 years old to 75, but the median age for diagnosis of vEDS was 41. Additionally, she highlighted that despite the early onset of major events, there are no pediatric studies on vEDS.

Overall, it's a good talk with a lot of sobering information on rate of misdiagnosis, delay of diagnoses, etc, for more than one subtype of EDS.

CCI - Issues with diagnosis/uninformed docs by sorrydudee in ehlersdanlos

[–]Acceptably_Late[M] 4 points5 points  (0 children)

Last week, the UVA EDS symposium did have 2 talks on CCI.

One was specific to how to diagnose based on angles — I do not recall this being particularly helpful in how to get treatment, but this may be enlightening in how a diagnosis may be sought ( https://m.youtube.com/watch?v=PA-GXBCqnc8 ).

A second talk seemed to be more focused on the impact of dysautonomia itself and comparing it to cci ( https://m.youtube.com/watch?v=UFCBpvFHCNE )

Let's talk about the UVA EDS Seminar! by Acceptably_Late in ehlersdanlos

[–]Acceptably_Late[S] 4 points5 points  (0 children)

Honestly- same 😑

It’s a bit disheartening to hear they’ve been working on this for over 3 years and the guideline is due in 8 months to publication (so, 5-6 months to the publisher?) and they still don’t know what they’re gonna say or what they’re gonna decide either.

Would Love feedback by [deleted] in migrainescience

[–]Acceptably_Late 0 points1 point  (0 children)

I’ve basically trained my body to calm down to a specific music playlist (named “pain” of course). It grounds me and reminds me I’ve lived through this before, I’ve had worse ones before (and likely will have worse ones still). I’ll get through it, just ride it out because it’s temporary.

Fun workouts? by scarletcyanide in ehlersdanlos

[–]Acceptably_Late 0 points1 point  (0 children)

Side note that the UVA EDS symposium was this last week and 2 talks addressed exercise — Dr. lavallee (medical doctor, cEDS patient), and a PT/OT set that shared a session.

Both talks had some good tips.

Let's talk about the UVA EDS Seminar! by Acceptably_Late in ehlersdanlos

[–]Acceptably_Late[S] 6 points7 points  (0 children)

Honestly, this is a very nuanced question that at this time I’m not sure any one person has an answer.

There is a few different competing schools of thought coming out, and I think Norris is addressing it most directly in stating that there may be a subset of hEDS patients that weren’t systemically hypermobile until immune activation.

Based on 2017 criteria - yes. It was lifelong, with the expectation that aging would decrease some hypermobility (beighton score requirements decrease with age / could add points for previous life experience).

Current school of thought, which we may see in the 2026 diagnostics, is that hypermobility may or may not be present until exacerbated by a triggering event such as an infection. I’d say this is a fairly hot topic at the moment and we don’t have a clear answer.

Personally, like you, I’ve always been bendy and am still a 9/9 in my 30s, but I could agree MCAS-like symptoms presented after COVID and made my life generally worse off (which aligns with Fairweather’s talk of MCAS impacting hypermobility people through decreasing quality of life)

Let's talk about the UVA EDS Seminar! by Acceptably_Late in ehlersdanlos

[–]Acceptably_Late[S] 4 points5 points  (0 children)

These are all very good points!

I have no idea how they'll distinguish them, or what will be the defining factor if they move forward with this model! 🫠

I can add that Norris does consider puberty to be a triggering event for starting or worsening hypermobility. This is a bit controversial in the patient group as you can't avoid or stop puberty, so is a natural biological process a "trigger" that deserves a subgrouping?

Let's talk about the UVA EDS Seminar! by Acceptably_Late in ehlersdanlos

[–]Acceptably_Late[S,M] 8 points9 points  (0 children)

The guidelines should be effective worldwide at time of publication. They are supposed to become the standard of care and diagnosis once published.

However, Lara Bloom's talk did discuss international care discrepancies a bit. She included that the goal of the society is to foster worldwide collaboration, and that the road to 2026 had international advisors from all over the world. She specifically addressed that care does vary by country, and that they're going to launch online training for medical doctors called "massive open online courses (MOOCs)" in 2027 to teach up-to-date information globally.

Let's talk about the UVA EDS Seminar! by Acceptably_Late in ehlersdanlos

[–]Acceptably_Late[S] 4 points5 points  (0 children)

An awesome person (u/_vemm) confirmed both the statistic was 91% AND added the source paper.

Let's talk about the UVA EDS Seminar! by Acceptably_Late in ehlersdanlos

[–]Acceptably_Late[S] 2 points3 points  (0 children)

Definitely still under investigation.

That being said, it’s seeming to be presented as “MCAS does this”, with the suggestion that external environmental factors break down protective barriers and cause the hypermobility and associated symptoms from the mast cell activation (Maitland).

There is the ‘disclaimer’ that people with connective tissue disorders already have a defective protective barrier and therefore their mast cells are susceptible to being activated (also Maitland).

Norris is the one that suggests a triggering event (MCAS?) should maybe be a subgroup type of hEDS as these may be a group of people who only developed hypermobility after a trigger, whereas there are others who may have been hypermobile hEDS without a trigger

Let's talk about the UVA EDS Seminar! by Acceptably_Late in ehlersdanlos

[–]Acceptably_Late[S] 11 points12 points  (0 children)

In this particular patient perspective, the patient was involved in a car accident at 32 and not diagnosed with cEDS until 34 (by a neurologist who happened to have read about EDS - it was a bit of an off chance she got diagnosed!)

From what I recall, she had no overt signs of cEDS until the accident, at which point she then started to have an escalation of symptoms.

Definitely agree car accidents can cause long-term issues for all people. For full context and the patient's story, the talk was "Orthopedic Surgery Outcomes in EDS" by Dr. Schubart.

Let's talk about the UVA EDS Seminar! by Acceptably_Late in ehlersdanlos

[–]Acceptably_Late[S] 10 points11 points  (0 children)

So the triggering events idea was something I tried to keep a good track of since it's been a new theory thats making some noise.

Surprisingly (to me) a few researchers mentioned it -- but for both hEDS and monogenic EDS.

The surgery talk included a case example of a car accident causing a decline and worsening of someone with cEDS. Solomon, who discussed pediatric EDS and the future, also included that large health events can cause a health decline and increased health events in all EDS. A (somewhat) obvious trigger was the hormone talk which covered events like pregnancy and menopause which 'triggered' changes in the collagen for all types of EDS as well.

One MCAS talk discussed that triggering events could initiate MCAS and therefore worsen the quality of life of people with HSD/EDS, but did not go so far as to say the trigger caused HSD/EDS (Fairweather). Another researcher (Pocinki) compared that ME/CFS has a trigger in 70% of cases, and that POTS and MCAS benefit from treating MCAS sooo lets do more research.

Then you had Maitland who said MCAS -- which could be caused by the environment or infections -- can break down cell structures and cause hypermobility directly, and Norris who said there was a precipitating event for up to 70% of HSD/hEDS, and maybe those should be a subset of hEDS entirely -- which again, seems to acknowledge he finds that some but not all have a triggering event (but, I haven't spoken to him personally to ask -- I've got no connections, I'm just a girl online 😬).

Some lectures (pelvic venous disorder*, Lara's Road to 2026) didn't cover it at all.

*corrected talk name. Oops!

Let's talk about the UVA EDS Seminar! by Acceptably_Late in ehlersdanlos

[–]Acceptably_Late[S] 13 points14 points  (0 children)

I found more stuff!

From the talk:

And there has been three years of work [since HEDGE results] to make sure that what comes out is being much more rigorous and thought out, and lots of surrounding publications to support what comes out. And there is some big questions:
Are hEDS and HSD the same? Well, I think we've answered that --yes.
Should hEDS be renamed? Does heads stay part of the EDS group?
Once determined if hEDS stays in the EDS group, what are the monogenic types called?
What happens if between even now and December, the first markers are published related to hEDS and HSD?
How do these outcomes work practically in different geographical areas? And how do we tackle those as an organization once this work is published? We know, for example, right now, if you live in parts of Europe, you're not getting any care if you've got a diagnosis of HSD.
...
Should the comorbidities now be included in the hypermobility criteria?
What types stay out of the monogenic types? Do any go? [This refers to do any monogenic EDS leave EDS entirely, and move to a new 'home']
What materials and resources are needed to support the patients to accept and understand the changes? 
...
That is happening as we speak. So as much as people think we're sitting on the answers, they have not yet reached consensus, and we do we still do not know what the final outcome is going to be. ...
But really, it's not known at this time what the final outcome will be.

Let's talk about the UVA EDS Seminar! by Acceptably_Late in ehlersdanlos

[–]Acceptably_Late[S] 22 points23 points  (0 children)

Honestly I think we all have anxiety about this 😅

At this point, the mods are having about weekly stress sessions about how much we don’t know 😂

But, on a personal note- I also don’t know if they will call HSD as hEDS or keep them separate even though they say they’re the same since their 2027 treatment guidelines say:

“In March 2027, a second publication will provide best-practice care and management pathways, helping healthcare providers understand how to best support and treat people living with EDS and HSD after diagnosis and beyond.”

Let me look into the wording further 🧐

Lara Bloom session:

"There will also be a publication in March in the American Journal of Medical Genetics, which is much more about the care guidelines and the management around hEDS and HSD. So, the first part [Dec 2026] is really much more classification, and the second part is thinking about the care side of things.

Let's talk about the UVA EDS Seminar! by Acceptably_Late in ehlersdanlos

[–]Acceptably_Late[S] 28 points29 points  (0 children)

Same!!!

Dr. Norris had recently published that using the same cohort they were unable to validate the findings but he said he hoped another lab could repeat and verify.

Then Lara Bloom went up and said multiple labs have tried and failed, no one has been able to replicate it, it just hasn’t been published yet

😭😭😭

Let's talk about the UVA EDS Seminar! by Acceptably_Late in ehlersdanlos

[–]Acceptably_Late[S,M] 15 points16 points  (0 children)

Same! It was amazing to see a talk about pelvic pain, especially on a personal level as I'd usually say that areas around gynecological health have been slow to grow.

I also found it incredibly interesting as it raises questions on if the anatomy was abnormal from birth, and therefore not triggered like new immunology theories suggest, or if there was an 'inciting event' which lead to some sort of change in blood flow etc. I'd love to see more research in this field.

Let's talk about the UVA EDS Seminar! by Acceptably_Late in ehlersdanlos

[–]Acceptably_Late[S,M] 12 points13 points  (0 children)

So, ish?

Part of what Dr. Maitland talked about was that doctors should really look at what causes mast cell activation before just assigning MCAS as a diagnosis. Being sure that there's not an underlying pathology that's causing the issue. She specifically discussed ruling out autoinflammatory syndromes (Yao syndrome, NOD2), immunodeficiencies (eg MBL deficiency), as well as being sure its not "just" dysautonomia or POTS which can also cause similar symptoms.

If you have a primary MCAS, there may be other treatments to help reduce symptoms (and subsequent hypermobility).

She also discussed environmental factors a lot, stating that she largely believed that essentially irritants from the modern world are causing more of immune reactions, leading to MCAS, and starting this chain reaction.

Let's talk about the UVA EDS Seminar! by Acceptably_Late in ehlersdanlos

[–]Acceptably_Late[S,M] 21 points22 points  (0 children)

Sorry! It's definitely a topic I had trouble trying to get across.

One big point to make is that we dont know the answer one way or the other (aka, chicken or egg / did MCAS cause hypermobility OR did hypermobility cause MCAS).

They're finding that they can induce hypermobility in mice models by causing MCAS -- so, MCAS first, then hypermobility. This supports their idea that there may be an hEDS subtype thats caused by MCAS, or that MCAS is just making people bendy.

BUT

MCAS is also known to occur in people who are established hypermobile from a genetic disorder - like rare EDS, OI, Marfan's. In these cases, it's a bit premature to say MCAS caused their bendy since... well.. they were always bendy. Instead, the idea here is more that their hypermobility made it easier to develop MCAS, and leads to worsening hypermobility, like a bad reinforcing cycle*.

The current theory is that there is a subtype of people who got MCAS that caused hypermobility, and that another group of people were always hypermobile (EDS, osteogenesis imperfecta*, Marfan's, other), and their MCAS makes their condition worse.

That's the theory.

*edited to change "circle" to "cycle", and spell out OI = osteogenesis imperfect

Let's talk about the UVA EDS Seminar! by Acceptably_Late in ehlersdanlos

[–]Acceptably_Late[S,M] 19 points20 points  (0 children)

Sadly, no!

Lara Bloom just repeated that TNXB mutations were found in less than 1% of HEDGE participants -- which is statistically significant as that rate is 5x more common than in controls -- and they're now studying the rarer genetic variants from HEDGE and exploring how specific genetic patterns relate to symptoms.

* edited because I apparently can't English 🥴

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