Erythrocyte Deformability As a Potential Biomarker for Chronic Fatigue Syndrome, Davis et al (2018)

I would like to know if the selected pts had post lyme or long term antibiotic treatments.

Apparently malaria and co-infections for lyme (bartonella and babesia) alter RBC.
 
Forbin said:
Any idea why this has a different title, is in a different journal and has one less author than before? The text is also different, though it covers the same ground. Was the original merely an "article," while this is the "paper?"
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Was the first an extended abstract from a conference proceedings while the latest is the actual paper with all the details?
 
Forbin said:
Any idea why this has a different title, is in a different journal and has one less author than before? The text is also different, though it covers the same ground. Was the original merely an "article," while this is the "paper?"
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Well, we knew from this post, https://s4me.info/threads/erythrocy...rome-davis-et-al-2018.6938/page-3#post-125283, that the original text was "an online abstract for the @ASH_hematology conference", which might explain some of the differences, but other than that I'm no wiser than you. I was aware that there were differences but, given that it certainly was on the same subject, assumed that was due to it being the full paper now.
 
I've been wondering for some time - presuming reduced deformability of RBCs and this way of measuring them pans out as a biomarker, and it's useful for diagnosis, could, for example, being a sickle cell carrier (ie asymptomatic for sickle cell but with a low percentage of deformed RBC's) affect this method? I don't suppose they've given thought to it as it's early days, however people in this category do exist. Hence my curiosity.

Hope this makes sense, it's not a good brain day.
 
I found this interesting since I had high oxidative stress (when tested), and low antioxidant status. All those healthy foods, juices and supplements I take do nothing in my body?


 
Andy said:
Well, we knew from this post, https://s4me.info/threads/erythrocy...rome-davis-et-al-2018.6938/page-3#post-125283, that the original text was "an online abstract for the @ASH_hematology conference", which might explain some of the differences, but other than that I'm no wiser than you. I was aware that there were differences but, given that it certainly was on the same subject, assumed that was due to it being the full paper now.
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Thanks! For some reason, I thought the original article was an "abstract" and that the full paper was either behind a paywall or had been embargoed all this time. As you pointed out, the original article looks like it appeared in the "proceedings" of a blood conference. I wonder if this was an example of Ron Davis' desire to disseminate important information quickly, rather than to endure the delays of the sometimes lengthy publication process.
 
Forbin said:
Thanks! For some reason, I thought the original article was an "abstract" and that the full paper was either behind a paywall or had been embargoed all this time. As you pointed out, the original article looks like it appeared in the "proceedings" of a blood conference. I wonder if this was an example of Ron Davis' desire to disseminate important information quickly, rather than to endure the delays of the sometimes lengthy publication process.
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I read both again. The first abstract from the conference has a lot of interesting information not covered in the full text paper e.g. low ESR and zeta potential to name a few. It seems as if the full text paper was limited to just "deformability" and the data to support that, but for the conference I'm guessing they could talk about a lot more. I read on PR that they were pressured to shorten the paper by the publishing editor...........
 
wigglethemouse said:
I read both again. The first abstract from the conference has a lot of interesting information not covered in the full text paper e.g. low ESR and zeta potential to name a few. It seems as if the full text paper was limited to just "deformability" and the data to support that, but for the conference I'm guessing they could talk about a lot more. I read on PR that they were pressured to shorten the paper by the publishing editor...........
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Perhaps they'll publish a second paper later? Low ESR is certainly something I want to know more about (it has been mentioned before).

Especially because our first task on the NICE committee (in February and March) is settling on diagnostic criteria and tests that may support diagnosis.

ESR is done as part of the standard battery of tests performed, so would be helpful in that sense, but the evidence for low ESR is mostly anecdotal at this stage.
 
Many patients think magnesium is helpful for their condition. Magnesium seems to increase RBC deformability.

https://www.ncbi.nlm.nih.gov/pubmed/16036387

A clinical trial also reported that magnesium improved symptoms in most CFS patients.
https://www.ncbi.nlm.nih.gov/pubmed/1672392

One study reported no lack of magnesium in RBCs of CFS patients and concluded that there was no role for magnesium supplementation, which may explain why this treatment approach was not investigated further https://www.ncbi.nlm.nih.gov/pubmed/7832571

In my view if it improves symptoms then it may have a role, even if the mechanism of action is not correction of a deficiency. The mechanism could be improvement of microcirculation by increasing RBC deformability.
 
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strategist said:
Many patients think magnesium is helpful for their condition. Magnesium seems to increase RBC deformability.

https://www.ncbi.nlm.nih.gov/pubmed/16036387

A clinical trial also reported that magnesium improved symptoms in most CFS patients.
https://www.ncbi.nlm.nih.gov/pubmed/1672392

One study reported no lack of magnesium in RBCs of CFS patients and concluded that there was no role for magnesium supplementation, which may explain why this treatment approach was not investigated further https://www.ncbi.nlm.nih.gov/pubmed/7832571

In my view if it improves symptoms then it may have a role, even if the mechanism of action is not correction of a deficiency. The mechanism could be improvement of microcirculation by increasing RBC deformability.
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Magnesium is the one supplement we have that is noticed if a dose is missed.
My understanding is that the body works hard to keep a consistent % in the blood, but like many elements, most is in tissues etc.

ATP needs magnesium bound to it to work . The ATP profiles test done for my daughter showed low levels of this which may explain why it has an effect.

My aunt's magnesium injections have significantly reduced heart palpitations.

Is magnesium like calcium in that if it is low in the blood it is pulled from tissues/ bones? (If so this may go some way to explaining the severity of my aunt' s illness)
 
Andy said:
Link isn't to the same thing as the subject of this thread, yours/OMFs goes to a study with the title, "Abnormal rheological properties of red blood cells as a potential marker of Gulf War Illness: A preliminary study".
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Study is titled: "Red blood cell deformability is diminished in patients with Chronic Fatigue Syndrome" and it's available here:
https://content.iospress.com/articles/clinical-hemorheology-and-microcirculation/ch180469
I uploaded the wrong web address in my previous post

Here's an extract from the paper which @wigglethemouse has (understandably) drawn our attracted to:
"By comparing the change in cell diameters normalized to the width of the test channel before (L 1/d) and after (L 2/d) entry, Fig. 1D clearly demonstrates that RBCs from ME/CFS patients deform 7-fold less compared to those from the HC."
Three times baseline noise was an old rule I remember from chemistry. I.e. three times baseline noise is a significant measurable change from background. 7 times looks good in terms of a possible diagnostic test*. Also, this doesn't require a mass spectrometer* (MS) [MS - expensive + skilled operators required].


*Extract from an email from OMF:
"OMF-funded Red Blood Cell Deformability Research Study Published
Written by Ronald W. Davis, PhD
This paper documents that red blood cells are less deformable in ME/CFS patients compared to healthy controls. It potentially could be a biomarker, and we are proceeding to design new devices that will make a clear distinction between patients and healthy controls. These devices will be hand-held and easy to use by doctors in their offices, or in clinical testing labs. Past work has looked primarily at the shape of red blood cells, which is difficult to quantitate. Our approach will give a clear quantitative number. It measures the ability of red blood cells to deform while squeezing into a capillary, something that blood cells must do for healthy flow. We measure hundreds of cells from each patient, so, because of this, even though the number of patients is low, we get a very statistically significant distinction between patient and healthy cells' deformability. We are putting our energy into developing the new devices as soon as possible."
 
wigglethemouse said:
I read both again. The first abstract from the conference has a lot of interesting information not covered in the full text paper e.g. low ESR and zeta potential to name a few. It seems as if the full text paper was limited to just "deformability" and the data to support that, but for the conference I'm guessing they could talk about a lot more. I read on PR that they were pressured to shorten the paper by the publishing editor...........
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This is Amit's response when asked about sharing the extra details in the first "Blood" abstract
 
adambeyoncelowe said:
Thanks. I've asked Amit if there's any interim data that can be shared with NICE.
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It sure would be nice if the NHS could do a search of records for ESR data for patients that have an ME/CFS diagnosis. But what I hear from folks in the UK is that the health records are a mess, and tests are not even available for review by patients. ESR patient data must be available somewhere to be mined.
 
wigglethemouse said:
It sure would be nice if the NHS could do a search of records for ESR data for patients that have an ME/CFS diagnosis. But what I hear from folks in the UK is that the health records are a mess, and tests are not even available for review by patients. ESR patient data must be available somewhere to be mined.
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It would make sense to pool this data in a trial to see if it does correspond to patient experiences. However, as the full paper seems to show, patients in a remission seem to have normal ESRs, so you'd have to control for that.
 
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