Autoantibodies to Vasoregulative G-Protein-Coupled Receptors Correlate with Symptom Severity, Autonomic Dysfunction and Disability in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is an acquired complex disease with patients suffering from the cardinal symptoms of fatigue, post-exertional malaise (PEM), cognitive impairment, pain and autonomous dysfunction. ME/CFS is triggered by an infection in the majority of patie...

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Published in:Journal of clinical medicine 2021-08, Vol.10 (16), p.3675
Main Authors: Freitag, Helma, Szklarski, Marvin, Lorenz, Sebastian, Sotzny, Franziska, Bauer, Sandra, Philippe, Aurélie, Kedor, Claudia, Grabowski, Patricia, Lange, Tanja, Riemekasten, Gabriela, Heidecke, Harald, Scheibenbogen, Carmen
Format: Article
Language:English
Subjects:
Age
Catecholamines
Chronic fatigue syndrome
Clinical medicine
Disease
Encephalomyelitis
Infections
Laboratories
Pain
Pathogenesis
Patients
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Summary:Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is an acquired complex disease with patients suffering from the cardinal symptoms of fatigue, post-exertional malaise (PEM), cognitive impairment, pain and autonomous dysfunction. ME/CFS is triggered by an infection in the majority of patients. Initial evidence for a potential role of natural regulatory autoantibodies (AAB) to beta-adrenergic (AdR) and muscarinic acetylcholine receptors (M-AChR) in ME/CFS patients comes from a few studies. Here, we analyzed the correlations of symptom severity with levels of AAB to vasoregulative AdR, AChR and Endothelin-1 type A and B (ETA/B) and Angiotensin II type 1 (AT1) receptor in a Berlin cohort of ME/CFS patients ( = 116) by ELISA. The severity of disease, symptoms and autonomic dysfunction were assessed by questionnaires. We found levels of most AABs significantly correlated with key symptoms of fatigue and muscle pain in patients with infection-triggered onset. The severity of cognitive impairment correlated with AT1-R- and ETA-R-AAB and severity of gastrointestinal symptoms with alpha1/2-AdR-AAB. In contrast, the patients with non-infection-triggered ME/CFS showed fewer and other correlations. Correlations of specific AAB against G-protein-coupled receptors (GPCR) with symptoms provide evidence for a role of these AAB or respective receptor pathways in disease pathomechanism.
ISSN:2077-0383
2077-0383
DOI:10.3390/jcm10163675