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Pathomechanisms and possible interventions in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)
Øystein Fluge, … , Karl J. Tronstad, Olav Mella
Øystein Fluge, … , Karl J. Tronstad, Olav Mella
Published July 15, 2021
Citation Information: J Clin Invest. 2021;131(14):e150377. https://doi.org/10.1172/JCI150377.
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Pathomechanisms and possible interventions in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)

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Abstract

Authors

Øystein Fluge, Karl J. Tronstad, Olav Mella

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Figure 1

Proposed model for ME/CFS pathomechanisms.

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Proposed model for ME/CFS pathomechanisms.
We suggest three principal st...
We suggest three principal steps underlie the initiation and maintenance of ME/CFS. (i) Immune response after infection serves as a triggering event, with a role for B cells/plasma cells and autoantibodies in the underlying pathology. (ii) The vascular system and possibly GPCRs are potential targets for autoantibodies, which may affect endothelium or neurovascular control and autonomic small nerve fibers. The autoantibodies could be pathogenic IgGs or functional autoantibodies that normally occur after infection, but persist and fail to resolve over time. This disturbed homeostasis involves endothelial dysfunction in large and small arteries, impaired venous return and preload failure, and arteriovenous shunting, presumed to result in impaired autoregulation of blood flow and tissue hypoxia on exertion. (iii) Secondary compensatory efforts may add to the clinical presentation and symptoms. They include autonomic adaptations, often with increased sympathetic tone, and metabolic adaptations aiming to restore energy supply. Possible strategies for clinical trials targeting these pathways are also indicated.

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ISSN: 0021-9738 (print), 1558-8238 (online)

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