Red blood cell deformability is diminished in patients with Chronic Fatigue Syndrome, Saha et al, 2019

Red blood cell deformability is diminished in patients with Chronic Fatigue Syndrome
Amit K. Saha, Brendan R. Schmidt, Julie Wilhelmy, Vy Nguyen, Abed Abugherir, Justin K. Do, Mohsen Nemat-Gorgani, Ronald W. Davis
Clinical Hemorheology and Microcirculation 71 (2019) 113–116
DOI: 10.3233/CH-180469
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Abstract
BACKGROUND: Myalgic encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a poorly understood disease. Amongst others symptoms, the disease is associated with profound fatigue, cognitive dysfunction, sleep abnormalities, and other symptoms that are made worse by physical or mental exertion. While the etiology of the disease is still debated, evidence suggests oxidative damage to immune and hematological systems as one of the pathophysiological mechanisms of the disease. Since red blood cells (RBCs) are well-known scavengers of oxidative stress, and are critical in microvascular perfusion and tissue oxygenation, we hypothesized that RBC deformability is adversely affected in ME/CFS.

METHODS: We used a custom microfluidic platform and high-speed microscopy to assess the difference in deformability of RBCs obtained from ME/CFS patients and age-matched healthy controls.

RESULTS AND CONCLUSION: We observed from various measures of deformability that the RBCs isolated from ME/ CFS patients were significantly stiffer than those from healthy controls. Our observations suggest that RBC transport through microcapillaries may explain, at least in part, the ME/CFS phenotype, and promises to be a novel first-pass diagnostic test.

Edit: We have 3 threads on related or the same research by the same team:
Erythrocyte Deformability As a Potential Biomarker for Chronic Fatigue Syndrome, Davis et al (2018)
Altered Erythrocyte Biophysical Properties in Chronic Fatigue Syndrome, 2019, Saha, Davis, et al
Red blood cell deformability is diminished in patients with Chronic Fatigue Syndrome, Saha et al, 2019

 

Very interesting part of the puzzle, spent 14% more time in the channels and 18% slower due to being “unusually bigger” with 15% less elongation so stiffer. And RBC do alter their shape with oxidative stress and inflammation and there might be a further impact from the disease process (still to be confirmed…) and which would tie in with a chronic relapsing condition and gradual worsening of overall function or other trajectories. Also meds and supplements not known to cause these changes so some nice contributory evidence towards the microcirculation/perfusion enquiry…and does this oxidative stress/inflammation of the RBC alter the offloading of oxygen to the cell/tissue?

 

It sounds as if it have some effect. Also the Stanford researchers recently said that ME RBCs were much less deformable when hypoxic (unlike normals), which could act to produce positive feedback perpetuation.

It's possible it increases tissue oxygenation (somewhat paradoxically). Please see this post where I talked about a possible two-state mechanism.

ETA: ah think you'd already seen it - sorry

 

When Dr Simpson first found badly shaped RBCs his research was not replicated. He complained that he examined cells as soon as they were removed from patients but the replication studies all stored the cells until they looked at them. This storage process restored the cells to their proper shape.

As usual with ME, nothing was resolved one way or another.

It is interesting that it keeps cropping up.

I have problems with my fingernails and the tips of my fingers which hypoxia would explain.