Biomarkers for POTS

[Sarah Tee]

A very interesting new study, and a decent cohort size!

https://www.youtube.com/watch?v=S6v2rQ7u2Do

I imagine some of these biomarkers will turn out to be present in other forms of dysautonomia as well.

[Sarah Tee]

By the way, for anyone excitedly looking up the various biomarkers like I am, there is a mistake in one of the slides in regards to the inflammatory ones. It refers to "beta-2 macroglobulin". It should read "beta-2 microglobulin".

It's correct in the published paper, which you can find here:

https://www.nature.com/articles/s41598-022-24729-x

[MikeO]

1 hour ago, Sarah Tee said:

By the way, for anyone excitedly looking up the various biomarkers like I am, there is a mistake in one of the slides in regards to the inflammatory ones. It refers to "beta-2 macroglobulin". It should read "beta-2 microglobulin".

It's correct in the published paper, which you can find here:

https://www.nature.com/articles/s41598-022-24729-x

This look very interesting hopefully there will be some promising findings in the future.  

[MTRJ75]

This has become a popular theory in recent years, so I'm happy to see them continuing to make progress. 

This, in the discussion portion of the paper caught my eye, considering there's another recent thread concerning the possibility of enlarged hearts in some of us: 

Quote

We observed downregulated expression of TSP-4 in POTS. In vivo mouse models have shown that TSP-4 deficient mice develop pronounced cardiac hypertrophy, fibrosis together with left ventricular dilatation, and depressed systolic function²⁴. These defects in adaptation to chronic pressure overload, result in chamber dilation, reduced cardiac function, and increased cardiac mass²⁴.

And if these AI processes are triggered by persistent viral assaults, as also asserted in this paper, it seems like lots of work is being done to more easily identify that as well. 

Fatigue and deconditioning. This paper hits all the marks. 

[Sarah Tee]

A quick summary of the study:

Researchers took 65 people who had been diagnosed with POTS and had been unwell for more than six months and matched them with 65 healthy controls. They analysed their blood for biomarkers, looking for any that were up or down regulated in the POTS group compared to the control group.

They identified 393 biomarker proteins, 30 of which were expressed differently in the POTS group.

These differences pointed to the following in POTS:

• hypercoagulable state
• proinflammatory state
• enhanced cardiac contractility and hypertrophy
• skeletal muscle expression
• adrenergic activity.

"These findings support the hypothesis that POTS may be an autoimmune, inflammatory and hyperadrenergic disorder."

(The researchers note that they did not detect any difference in biomarkers between the male patients and matched male controls. This may have been due to having fewer male subjects included in the study.)

[Sarah Tee]

I was surprised by the "hypercoagulable state" one. I had not heard of this connection before.

The authors linked to a paper on this topic:

https://link.springer.com/article/10.1007/s12264-018-0295-6

You can read the full paper through Sci-Hub. Basically it says that orthostatic stress in the lower extremities causes changes in the body's coagulation system. The authors conclude that:

"Abnormal coagulation is an important component of OI."