Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Comorbidities: Linked by Vascular Pathomechanisms and Vasoactive Mediators?

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is often associated with various other syndromes or conditions including mast cell activation (MCA), dysmenorrhea and endometriosis, postural tachycardia (POTS) and small fiber neuropathy (SFN). The causes of these syndromes and the reason...

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Bibliographic Details
Published in:Medicina (Kaunas, Lithuania) Lithuania), 2023-05, Vol.59 (5), p.978
Main Authors: Wirth, Klaus J, Löhn, Matthias
Format: Article
Language:English
Subjects:
Adenosine
Asthma
Cardiac arrhythmia
Chronic fatigue syndrome
Comorbidity
Coronaviruses
COVID-19
Dengue fever
Disease
dysmenorrhea
Dysmenorrhea - complications
Edema
Encephalomyelitis
Endometriosis
Endometriosis - complications
Fatigue Syndrome, Chronic - complications
Fatigue Syndrome, Chronic - epidemiology
Female
Histamine
Humans
Hypotheses
Hypothesis
Infections
Influenza
Ischemia
long COVID
MCA
ME/CFS
Medical research
Medicine, Experimental
Metabolism
Musculoskeletal system
orthostatic intolerance
Pain
Physiology
Severe acute respiratory syndrome coronavirus 2
Urticaria
Uterus
Viral infections
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Summary:Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is often associated with various other syndromes or conditions including mast cell activation (MCA), dysmenorrhea and endometriosis, postural tachycardia (POTS) and small fiber neuropathy (SFN). The causes of these syndromes and the reason for their frequent association are not yet fully understood. We previously published a comprehensive hypothesis of the ME/CFS pathophysiology that explains the majority of symptoms, findings and chronicity of the disease. We wondered whether some of the identified key pathomechanisms in ME/CFS are also operative in MCA, endometriosis and dysmenorrhea, POTS, decreased cerebral blood flow and SFN, and possibly may provide clues on their causes and frequent co-occurrence. Our analysis indeed provides strong arguments in favor of this assumption, and we conclude that the main pathomechanisms responsible for this association are excessive generation and spillover into the systemic circulation of inflammatory and vasoactive tissue mediators, dysfunctional β2AdR, and the mutual triggering of symptomatology and disease initiation. Overall, vascular dysfunction appears to be a strong common denominator in these linkages.
ISSN:1648-9144
1010-660X
1648-9144
DOI:10.3390/medicina59050978