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

• Published in: Medicina (Kaunas, Lithuania) Vol. 59; no. 5; p. 978
• Main Authors: Wirth, Klaus J, Löhn, Matthias
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 18.05.2023; MDPI
• 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; small fiber neuropathy; dysmenorrhea; endometriosis; orthostatic intolerance; cerebral blood flow; MCA; long COVID; brain fog; ME/CFS; β2-adrenergic receptors
• ISSN: 1648-9144; 1010-660X; 1648-9144
• DOI: 10.3390/medicina59050978

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.