Saline infusions

Binkie4

Binkie4

Senior Member (Voting Rights)
This post has been copied and following posts moved from Open Medicine Foundation (OMF)

I'm interested in the saline trial. I wonder why Dr Feinberg selected it to study.

I've had an experience of being administered saline infusions during a week of inpatient testing for a heart issue. Some of the testing was under a GA, others involved MRIs, CTs.

I would have expected to feel PEM at some point during the week but I didn't at all, nor after stress testing on a treadmill the following week when as an outpatient I had a concurrent saline infusion.
Will be interested to see what emerges.
 
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I don't know how common fluid management issues are in ME. It doesn't seem to be discussed much, so maybe it's something only a minority experience.

In PEM my fluid intake goes up a lot, and in the catastrophic crashes I had before I was diagnosed, it was bizarre. I needed 10 to 12 litres of water a day, and my skin still looked dehydrated. Last time round I even asked our stage manager to get me rehydration salts to add to it, because I was worried about washing out too many nutrients. I don't know whether it made any difference, and the only thing that reduced the need for fluids was when I began to recover.
 
Binkie4 said:
I'm interested in the saline trial. I wonder why Dr Feinberg selected it to study.

I've had an experience of being administered saline infusions during a week of inpatient testing for a heart issue. Some of the testing was under a GA, others involved MRIs, CTs.

I would have expected to feel PEM at some point during the week but I didn't at all, nor after stress testing on a treadmill the following week when as an outpatient I had a concurrent saline infusion.
Will be interested to see what emerges.
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Hi Binkie,

Chris Armstrong here.
We were prompted to assess saline after receiving information from a lot of patients about treatments that were effective, also heard from a lot of clinicians.

I've personally wanted to assess saline for a long time because I noted a lot of treatments that showed promise in me/cfs had saline infusion as part of their mode of delivery and have struggled to overcome a strong placebo (saline). I think it's worth considering that saline may have been part of the reason these treatments to begin with.
A lot of patients display vascular issues and it very well could be the POTS or orthostatic intolerance as a comorbidity that is improving with saline in some patients.

So we want to assess saline for its potential benefits for patients, we want to know which patients it helps to target them and we want to characterise the impact so we don't waste more time on drug trials that use saline infusion as mode of delivery without understanding that it too is helping and should be accounted for early.

Another benefit is that it has rapid impact, which helps us assess the objective measures we are using and also look at omic profile changes in patients. The low dose trials are long and drawn out, a lot of other factors can contribute to changes we might see.

Furthermore, we are assessing saline vs dextrose. The dextrose should be better at directing water to the brain as water follows dextrose in. However, dextrose can be used up and water will leak out again (this is a bit of a layman explanation). This is different to how saline would operate. Hartmann's is a composition that includes lactate. We want to know which types have a more sustained response or improved response on certain areas. This is going to tell us more about the role of volume expansion in patients.
 
Hi Chris @MelbME. Thank you for taking the time to tell us more about the inspiration for the saline study. I also note you writing that it will tell you more about volume expansion which will also be interesting. It seems strange that these possible features of ME have had so little attention paid to them.

I was fortunate to be seeing an ME specialist privately when I was due to have heart testing which was then expected to lead to open heart surgery. He knew I was very concerned about losing functionality because of the testing and wrote me a detailed letter to pass to the heart surgeon recommending saline infusions, avoiding intense activity and spreading out the testing. Fortunately the heart hospital was willing to cooperate and I was able to follow the advice. I didn't go into PEM or lose functionality and felt well throughout the procedures.

We look forward to hearing how the research progresses.
 
Kitty said:
I don't know how common fluid management issues are in ME. It doesn't seem to be discussed much, so maybe it's something only a minority experience.

In PEM my fluid intake goes up a lot, and in the catastrophic crashes I had before I was diagnosed, it was bizarre. I needed 10 to 12 litres of water a day, and my skin still looked dehydrated. Last time round I even asked our stage manager to get me rehydration salts to add to it, because I was worried about washing out too many nutrients. I don't know whether it made any difference, and the only thing that reduced the need for fluids was when I began to recover.
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That's interesting and not the first time I've heard that.

I think reduced production of ATP per second (per second should be emphasised) is underlying fatigue and brain fog (a combination of vascular and central carbon metabolism issues varying between patients). There are a number of studies that show this in immune cells and that occurring inherently would impact immune cell function, especially functions dependent on amino acid or ATP availability. What happens to a neurons function with slightly less ATP, what happens to an immune cell, a muscle cell, a liver cell, a kidney cell, etc. If ATP production inefficiency is occurring then is it occurring in all tissues or different tissues depending on the person (heterogeneity)? In the case of the kidney, reduced ATP would mean less renal absorption, could you have rapid fluid and metabolite loss at certain times? Perhaps there is a threshold below which you get shutdown of important processes and this is what PEM is. Very little attention has been paid to the kidney in these diseases because it's hard to study.

What you describe is polydipsia, there is likely some negative outcome to drinking that much water a day. ORS would have absolutely made a difference. Can't comment on the cause as many possibilities.
 
MelbME said:
In the case of the kidney, reduced ATP would mean less renal absorption, could you have rapid fluid and metabolite loss at certain times? Perhaps there is a threshold below which you get shutdown of important processes and this is what PEM is.
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A number of us get oedema in PEM. If you look at photos of people with PEM, they often have puffy faces, swollen eyelids. So, that's an interesting thought, that the kidney is on a 'go slow', resulting in poor management of hydration. Gastroparesis could be another example of a reduction in body processes.
 
MelbME said:
In the case of the kidney, reduced ATP would mean less renal absorption, could you have rapid fluid and metabolite loss at certain times?
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(I developed LC/ME at the end of 2020/Jan 2021, from a prior position of excellent health and fitness.) Although I had no idea what was going on then, I had a warning moderate PEM crash six months before I crashed out to severe, but the second crash was astonishingly dramatic. One of its features was a sudden massive diuresis and I simply could not keep up with the losses. I would drink water but I would pee it out within 15-20 minutes - faster than I would expect one could absorb, but maybe it was the previous glass. This was much more than I'd ever experienced with bog standard past viral illnesses. Eventually this stabilised but it seemed obvious to me that I was now intravascularly depleted in status quo. That improved at around 6 months, either just with time +/- helped along by supplements. Renal function in terms of eGFR has remained normal.
 
Dehydration and polyuria has been a common PEM symptom for me. One year I had nocturia as well, and got up once or twice every night to pee. But that only occured for one year nearly on the mark. Since it was a new symptom I had it checked out and nothing was found. Since I had the history of polyuria with PEM I have assumed there was a connection although I don't know why the nocturia stopped. The polyuria is very frustrating as it makes it so I can't sit down for a while when in PEM, but have to get up often to go to the bathroom and expend energy I don't have.

Edit: Forgot to add that I can also get oedema when I overexert myself.
 
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Hutan said:
A number of us get oedema in PEM. If you look at photos of people with PEM, they often have puffy faces, swollen eyelids. So, that's an interesting thought, that the kidney is on a 'go slow', resulting in poor management of hydration. Gastroparesis could be another example of a reduction in body processes.
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Yes it could.

Actually there's a gastroenterologist in Queensland that thinks gastroparesis is getting misdiagnosed in people that have POTS group, she has seen many of these patients and finds they actually have gastroptosis. Something that can only be seen if you have a standing up X ray of your stomach after a meal. The weight of the food stretches the stomach down and the food struggles to get out. Kind of similar to CCI but instead of stretchy ligaments in the neck it's stretchy ligaments around digestive organs. I wonder if this happens in ME patients, it would be significantly under diagnosed. So many of these issues rely on stand up imaging services, which are rarer.
 
Hutan said:
A number of us get oedema in PEM. If you look at photos of people with PEM, they often have puffy faces, swollen eyelids. So, that's an interesting thought, that the kidney is on a 'go slow', resulting in poor management of hydration. Gastroparesis could be another example of a reduction in body processes.
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I wasn't aware of this. Interesting. I'm the complete opposite. My face looks sunken in and my eyes are hollow during PEM.

I feel dehydrated when I'm actually not. Nothing can replenish the way I feel.
 
Trish said:
@MelbME are you likely to test a comparison group between intravenous delivery of saline etc and the equivalent quantity of the same solution orally? Is there something specific about bypassing the stomach and going straight to the bloodstream?
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Yeah we are controlling for variation by using direct infusion. We are definitely interested in ORS as a longterm solution for patients.
 
SNT Gatchaman said:
I would drink water but I would pee it out within 15-20 minutes - faster than I would expect one could absorb,
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Midnattsol said:
polyuria
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I think these need more attention.

Pretty sure I have some form of disruption to the water cycle. I seem to process water faster than before, and have had a few bouts of some form of polyuria, even when my bladder is clearly empty, typically lasting a few hours. Whatever the opposite of urinary retention is.

Importantly none of this existed before getting ME/CFS.
 
Milo said:
You are correct, trying to get the immune modulators and cytotoxic drugs approved by a research ethics board would be next to impossible particularly when the rest of the world including the researchers at large, the peer reviewers only view Me/cfs as a simple fatigue problem with no biomarker. Finding objective endpoints can be hard too.

This said I would be very willing to try the big guns drugs for a simple chance of recovering my life as I knew it. But ethics boards do not look at it this way.

So very sorry you are also encountering difficulties getting approved for the saline intervention. It sounds to me like a logical next step that is very worthy of trying particularly for those who are more severe on the spectrum.

We as a disease (said it before and will say it again) are facing barriers of access to health care, research funding, government and insurance benefits and legitimacy. It’s still going on.
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We will get through ethics but there are a lot of hoops. I could see at many steps it would be even more difficult if the treatment had high risks.
 
Sean said:
I think these need more attention.

Pretty sure I have some form of disruption to the water cycle. I seem to process water faster than before, and have had a few bouts of some form of polyuria, even when my bladder is clearly empty, typically lasting a few hours. Whatever the opposite of urinary retention is.

Importantly none of this existed before getting ME/CFS.
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We are exploring this area a little actually and you will see it in a future publication this year. Several of our other studies are set up to monitor this phenomenon and they should be published in 2025.
 
MelbME said:
That's great thank you.

Rituximab and Cyclo both used infusion as mode of delivery, I think they're aware of the problems with volume expansion in the placebo. Interestingly Dara uses subcutaneous injection. I am interested to see if Dara proved to be impactful.

I do recall Campath and Arzerra were 2 of the other B cell depletion drugs being discussed around the time Rituximab kicked off. They could be interesting.

I wonder how you could build up enough rationale to justify a human trial of these drugs to an ethics board without actually having access to patients that had it in combination with another disease like Fluge+Mella did. Especially in a post-pandemic world.

We're having some difficulties just trying to get Saline as an intervention through, something relatively low risk. We're new to the clinical trial area though.
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Welcome and great to have you joining us as a researcher.

The Norwegians should be aware of, at least the possibility that the Saline IV could be seen as "treatment" in ME/CFS, I e-mailed that question to them. Placebo group feeling better too, because of the Saline IV?
I'm really surprised that getting Saline through an ethics board is so difficult. Most doctors give it post-op to most patients, almost without thinking about it. And in a lot of research it is given as a placebo.
I tried ORS for a couple of months, but I went back to just extra sodium and enough fluids. 2+ liters on normal days, extra when I'm using more muscles. Cramps to me = drink more! Wriggely eyes = more fluids now!!
 
Turtle said:
The Norwegians should be aware of, at least the possibility that the Saline IV could be seen as "treatment" in ME/CFS, I e-mailed that question to them. Placebo group feeling better too, because of the Saline IV?
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As improvement occurred only several months after infusions were given I think it's unlikely that any outcomes measured an actual effect of Saline IV or volume expansion?

(Apologies -- in skimming-mode only so in case it hasn't been discussed in this thread yet: How could there be any long term effect of volume expansion via infusions? Wouldn't you need to receive them daily?)
 
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