Trial Report Low Vasopressin in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, 2024, Huhmar/Bragée/Polo

https://www.neurology.org/doi/10.1212/WNL.0000000000205761

GENERAL NEUROLOGY: NEUROIMMUNOLOGY
April 9, 2024
Free Access

Low Vasopressin in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (P4-4.006)

Helena Huhmar, Lauri Soinne, Per Sjögren, Bo Christer Bertilson, Per Hamid Ghatan, Björn Bragée, and Olli Polo
AUTHORS INFO & AFFILIATIONS
April 9, 2024 issue
102 (17_supplement_1)
https://doi.org/10.1212/WNL.0000000000205761

Abstract

Objective:
To shed light on the pathophysiology of water homeostasis in patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), classified by WHO as a neurological disease (ICD 10 code G933).

Background:
The complex symptomatology of ME/CFS includes signs suggesting abnormal water homeostasis and hypovolemia. Since many patients report polyuria-polydipsia, we conducted an observational series of plasma and urine osmolality as well as plasma levels of vasopressin (VP) in consecutive patients diagnosed with ME/CFS according to the Canadian Consensus Criteria.

Design/Methods:
Plasma and urine osmolality (P-Osm and U-Osm, respectively) and plasma VP levels were measured in 111 patients after overnight fasting and 10-hour fluid deprivation. The clinical routine also included brain MRI and blood chemistry.

Results:
Following the fluid deprivation P-Osm was above normal (>292 mOsm/kg) in 61 patients (55.0%) and U-Osm below normal (< 750 mOsm/kg) in 74 patients (66.7%). VP-levels were below the level of detection (<1.6 pg/mL) in 91 patients (82.0%). A normal level of VP in relation to their P-Osm was found in 11 patients (9.9 %). The state resembling a central type of diabetes insipidus (cDI) would in the absence of hypophyseal imaging findings and blood chemistry consistent with any other hypophyseal hormonal defect be classified as idiopathic.

Conclusions:
Our findings suggest that deficiency of vasopressin secretion is a fundamental measurable part of the disease mechanisms, which may underlie a number of symptoms in ME/CFS, including the common complaint of orthostatic intolerance.


Disclosure: Helena Huhmar has nothing to disclose. Dr. Soinne has nothing to disclose. The institution of Prof. Sjögren has received research support from Patient-led Research Collaboration, US. Prof. Sjögren has received publishing royalties from a publication relating to health care. The institution of Dr. Bertilson has received personal compensation in the range of $50,000-$99,999 for serving as a Consultant for Medect Clinical Trial AB. The institution of Dr. Bertilson has received personal compensation in the range of $50,000-$99,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Medect Clinical Trials AB. The institution of Dr. Bertilson has received research support from ME UK. Dr. Bertilson has received intellectual property interests from a discovery or technology relating to health care. Dr. Bertilson has received personal compensation in the range of $500-$4,999 for serving as a teacher with Region Stockholm. Dr. Ghatan has nothing to disclose. Dr. Bragée has nothing to disclose. Dr. Polo has nothing to disclose.

 

Can't tell much from the abstract. Reading between the lines I'm guessing the cohort may just have been regular patients coming through their clinic. Which raises the question if they then treated those they found deficient in vasopressin with vasopressin, and to what effect.

Curiously, for me this phenomenon is very specific to early-phase PEM:
sudden unexplained thirst = entering mild PEM
sudden unexplained thirst + suddenly peeing like a horse every half hour = entering bad PEM

 

If plasma osmolality changes wouldn’t this potentially have all sorts of effects on other chemical processes throughout the body?

 

I produced too much urine from before 2000, and benefited greatly from desmopressin. Then, recently, a while after having had some dental work including the extraction of an infected tooth, I stopped needing it.

My blood pressure also normalised, when I had been taking the beta blocker Nebivolol since 2014, and an ACE inhibitor before that.

I am almost 71, and have had ME since about 1995. No medication needed now except to help me sleep!

https://www.s4me.info/threads/diarrhoea-caused-by-too-much-desmopressin.36981/#post-521077

 

Has anyone been able to access the actual poster presentation? It doesn't seem accessible yet through the Berkeley library.

 

I’ve had periods where the peeing a lot is an early phase stage, then my body suddenly decides it needs to catch up and rehydrate and after that other PEM stuff. And periods where I’ve been stuck in that state for a prolonged time, generally when very bad.

 

You can request a full PDF text here
https://www.researchgate.net/public...phalomyelitisChronic_Fatigue_Syndrome_P4-4006

 

Thanks, that’s the sort of thing I was thinking. My biology knowledge is poor and chemistry/physics better but rusty.

But if there’s changes to how things cross the cell membrane one can imagine how various systems would get upset and behave in odd ways.

As others say, interesting paper, lots of questions.

 

Could it be helpful to take some salt first thing in the morning?

https://www.sciencedirect.com/science/article/pii/S2211124721001807

Highlights

• •
  High dietary salt increases the osmoresponsiveness of vasopressin neurons in vivo
  
  
• •
  Salt loading and AngII-salt both increase the mEPSC amplitude in vasopressin neurons
  
  
• •
  AngII-salt increases glutamate release probability and overall network excitation
  
  
• •
  Salt loading increases stiffness and intrinsic osmosensitivity of vasopressin neurons

 

“Dietary sodium may stimulate vasopressin secretion through extracellular osmolality or even by a direct effect of extracellular sodium on periventricular receptors.“

https://pubmed.ncbi.nlm.nih.gov/391...acellular sodium on periventricular receptors.

 

With SARS-CoV-2 being associated with a loss of sense of smell and taste could a virus cause a loss of sense of thirst?
Could this be anything to do with what's being discussed in this paper?
Some pwME say they have been helped with IV saline infusions though Jonathan Edwards says just drinking water should have the same effect.

 

I drink cold water which is what some cardiologist recommend.