Red Blood Cell Morphology Is Associated with Altered Hemorheological Properties and Fatigue in Patients with Long COVID, 2024, Grau

https://www.mdpi.com/2079-7737/13/11/948

Red Blood Cell Morphology Is Associated with Altered Hemorheological Properties and Fatigue in Patients with Long COVID
by
Marijke Grau
1,*,
Alena Presche
1,
Anna-Lena Krüger
1,2,
Wilhelm Bloch
1 and
Björn Haiduk
2

Simple Summary

SARS-CoV-2 alters the properties of oxygen-carrying red blood cells (RBCs) through a possible deterioration of hemorheological properties, such as aggregation and deformability.

However, long-term changes in these properties and a possible association with morphological abnormalities remain unknown.

Therefore, this study aims to investigate changes in the above-mentioned RBC properties in Long-COVID (LC). Venous blood was collected from n = 30 diagnosed LC and n = 30 non-Long-COVID controls (non-LC).

Hematological parameters were measured, as well as the aggregation, deformability, and morphology of the RBCs and the mechanical sensitivity index (MS), which reflects the functional capacity of RBCs to deform.

The results indicate that hematological parameters were not altered in LC.

However, LC showed higher overall aggregation parameters.

RBC deformability was higher in LC compared to non-LC; however, MS was limited in this group.

LC showed a higher percentage of RBCs with abnormal shapes, which was related to MS and to fatigue, which is considered the leading symptom of LC.

It is concluded that the symptoms of LC and changes in the blood flow determining the properties of RBCs are related to the morphological changes in RBCs.

Future studies should investigate the underlying causes in order to develop appropriate therapies for this relatively new disease.

Abstract

Background:

SARS-CoV-2 infection adversely affects rheological parameters, particularly red blood cell (RBC) aggregation and deformability, but whether these changes persist in patients suffering from Long-COVID (LC) and whether these changes are related to RBC morphology remain unknown.

Methods:

Venous blood was collected from n = 30 diagnosed LC patients and n = 30 non-LC controls and RBC deformability, RBC aggregation, and hematological parameters were measured.

In addition, RBCs were examined microscopically for morphological abnormalities.

The mechanical sensitivity index (MS) was assessed in n = 15 LC and n = 15 non-LC samples. Results: Hematological parameters did not differ between the groups.

However, LC showed higher aggregation-related parameters.

Although RBC deformability was higher in LC, MS, reflecting the functional capacity to deform, was limited in this group.

RBCs from LC showed significantly more morphological abnormalities.

The extent of morphological abnormalities correlated with MS and the FACIT-Fatigue score of the LC patients.

Conclusion:

RBCs from LC show a high degree of morphological abnormalities, which might limit the blood flow determining RBC properties and also be related to fatigue symptomatology in LC.

Approaches are now needed to understand the underlying cause of these alterations and to ameliorate these permanent changes.

 

RBC's are less deformable
aggregates are formed
oxygen binding to hemoglobin is problematic
oxygen extraction is problematic
viscosity is higher
turnover rate of RBC's is higher, more immature RBC's,
lower blood volume
blood flow is hampered
CO2 retention
Krebs cycle needs oxygen and it ain't getting (enough of) it

And we still wonder why we are so exhausted?

Could PEM be caused by (more) dehydration and worsening of the mentioned problems?

 

interesting - is this similar to what happens in me/cfs ? I’ve heard of the less bendy red blood cells but checking on the rest?

How battered up do our less morphable red blood cells get when eg exertion of whatever call might cause them to go round the body more (and does anything like speed or constriction or angularity of any corners change)?

and what does that leave behind? Is it a case of needing a clean up operation, having bruised’ rbc mixed in or are they ‘broken’ ones in some sense and would that be worse for being in less plasma as some sort of slurry?

could all of that happen without affecting oxygen levels whilst still making people feel ill and awfully manky?

does all of this malfunctioning vs a system without this mean a bigger energy drain ? If so where would that come from and would eventually it lead to an enforced pause from a big crash?

notice the kerbs cycle but and assuming there might be a switch of energy source if possible but what toll does getting the system back in order involve at the same time?

would you eventually maybe end up with more red blood cells being made than normal from bone marrow as you get for example from living at altitude (is it a ‘switch ’ between things like storing as iron vs produce rbc ?) in some that could mean different downstream findings/symptoms in different groups?