Some Potential Roles of Fibrin Amyloid (‘Fibrinaloid’) Microclots in Fibromyalgia Syndrome

• Douglas B. Kell

  Department of Biochemistry, Cell and Systems Biology, Institute of Systems, Molecular and Integrative Biology, Faculty of Health and Life Sciences, University of Liverpool, Crown St, Liverpool L69 7ZB, UK

  Author

• Etheresia Pretorius

  Department of Physiological Sciences, Faculty of Science, Stellenbosch University, Stellenbosch, Private Bag X1 Matieland, 7602, South Africa

  Author

Fibromyalgia syndrome (FMS) is a complex multisystem disorder that, like many other chronic diseases with an infectious origin, is commonly accompanied by inflammation, oxidative stress, autoimmunity (not least antiphospholipid antibodies), endothelial dysfunction, pain, fatigue and other symptoms that can vary significantly between individuals, and that can interact in multiple and complex ways. As well as ‘primary’ fibromyalgia, such disease comorbidities include rheumatoid arthritis, myalgic encephalomyelitis/ chronic fatigue syndrome (ME/CFS) and long COVID. Such disorders are also commonly accompanied by microclots in blood plasma, that we refer to as fibrinaloid microclots since they both contain fibrin and stain with amyloid stains, and also by platelet activation. Following an original proposal by Berg in 1999, and our own findings of the fibrinaloid microclots in such diseases, we here develop the idea in a prospective review (with much evidence) that these fibrinaloid microclots may in fact be a substantial contributor to the aetiology of fibromyalgia. This would open up a number of useful and valuable therapeutic approaches to the treatment of FMS, including the use of anticoagulants, antiplatelet therapy, fibrinolytic enzymes, and/or other natural products.

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