Modulation of Beta-Adrenergic Autoantibodies Over Time in Post-Viral ME/CFS is Related to Fatigue and Pain Symptoms

Abstract

BACKGROUND: Myalgic encephalomyelits/chronic fatigue syndrome (ME/CFS) is an acquired disease with symptoms of fatigue and pain. In pathogenesis, the  induction of autoantibodies (AAB) against G-protein coupled receptors (GPCR),  such as β-adrenergic receptors (β-AdR), has been suspected. GPCR-AAB correlate  with symptom severity and autonomic dysfunction in ME/CFS. Objectives: To  describe symptoms and treatment of a patient presenting with infection-triggered  ME/CFS demonstrating that levels of β-AdR-AAB underlie modulation over time,  correlating with the severity of symptoms. METHODS: At T1 and T2, GPCR-AAB were  measured and questionnaires assessing symptom severity were completed.  TSHDS-IgM-AAB were tested, and SF density was analyzed via skin probe. RESULTS:  At T2, elevated levels of β-AdR-AAB were found, corresponding with an aggravation  of fatigue and pain symptoms. Elevated TSHDS-IgM-AAB were found, which  corresponded with reduced fiber density from the skin probe. CONCLUSIONS: The  levels of β-AdR-AAB in post-infectious ME/CFS can be modulated. Future studies  might target interventions to reduce these AAB.