The Occurrence of Hyperactivated Platelets and Fibrinaloid Microclots in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).
Nunes, Jean M, Kruger, Arneaux, Proal, Amy et al. · Pharmaceuticals (Basel, Switzerland) · 2022 · DOI
Quick Summary
This study found that people with ME/CFS have blood clotting abnormalities similar to those seen in Long COVID. Researchers discovered that ME/CFS patients have overactive platelets (blood cells involved in clotting) and tiny clots made of a protein called fibrin scattered throughout their blood plasma. These microscopic clots may block small blood vessels and reduce oxygen delivery to tissues, potentially explaining fatigue and other ME/CFS symptoms.
Why It Matters
This research identifies objective, measurable biomarkers in ME/CFS blood that could improve diagnosis and understanding of disease mechanisms. The findings suggest that existing anticoagulant or antiplatelet drugs might help reduce symptoms, potentially opening new treatment avenues for patients with limited therapeutic options.
Observed Findings
ME/CFS plasma samples showed significantly increased hypercoagulability compared to healthy controls using thromboelastography of both whole blood and PPP.
Fibrinaloid microclot area in ME/CFS PPP was commonly more than 10-fold greater than in healthy controls, both in untreated and thrombin-treated samples.
Platelets from ME/CFS patients showed increased activation markers (PAC-1 and CD62P binding) with a mean spreading score of 2.72 ± 1.24 compared to 1.00 in healthy controls.
The degree of microclot formation in ME/CFS was substantial but notably less than previously observed in Long COVID/PASC samples.
Inferred Conclusions
ME/CFS is accompanied by measurable coagulopathy, platelet hyperactivation, and fibrinaloid microclot formation.
Fibrinaloid microclots may contribute to ME/CFS symptoms (particularly fatigue) through temporary microvascular blockade and resulting tissue ischemia.
These clotting abnormalities and microclots represent potential therapeutic targets using existing anticoagulant drugs or nutraceutical interventions.
Remaining Questions
Do fibrinaloid microclots directly cause or merely correlate with ME/CFS symptoms, and can their reduction improve clinical outcomes?
What triggers platelet hyperactivation and microclot formation in ME/CFS—is it an infection, immune dysfunction, endothelial damage, or another mechanism?
What This Study Does Not Prove
This study does not prove that fibrinaloid microclots directly cause ME/CFS symptoms—it only shows a correlation between their presence and the disease. The research is observational and cannot establish whether microclots are a primary cause, secondary consequence, or coincidental finding. It also does not demonstrate that treating these clotting abnormalities will improve patients' symptoms.