Immunoadsorption in ME/CFS and PCS

Dr. Elisa Stein gave an overview of immunoadsorption (IA) studies conducted at her institution and of ongoing randomised controlled trials in Germany. The underlying hypothesis is that, in a subgroup of post-infectious ME/CFS patients, elevated autoantibodies against G protein-coupled receptors (GPCRs) — in particular β2-adrenergic receptors — contribute to symptom development, and that filtering them out via IA leads to clinical improvement. In the observational study published in 2025, 20 patients with post-COVID ME/CFS meeting the Canadian Consensus Criteria and elevated β2-adrenergic receptor autoantibodies were treated with five IA cycles using an IgG-binding adsorber, achieving an IgG depletion of 80–90%. The primary endpoint — improvement in SF-36 physical function — was met, alongside improvements in fatigue, pain, PEM duration, and autonomic symptoms. The effect lasted around six months; a repeated IA course produced a comparable but equally time-limited benefit. Immunological profiling in collaboration with Birgit Sawitzki's group identified distinct B-cell and plasma-cell patterns between responders and non-responders. A follow-up observational study in piMECFS included 15 patients with post-infectious ME/CFS diagnosed at the Charité Fatigue Center, aged 18 to 65 years and with elevated β2-adrenergic receptor autoantibodies; five IA cycles were again used, and the primary endpoint was an increase of at least 10 points in SF-36 physical function at week 8. Seven patients were classified as responders and six as non-responders, with some apparent late responses emerging only after several months. The multicentre IMPACT study, using the same protocol within the National Clinical Study Group, has been ongoing since March 2026 and no results are yet available. Stein also provided an overview of ongoing randomised IA trials in Germany, including sham-controlled studies in Hanover, Mainz, and Berlin. She concluded that IA is effective for a subgroup of patients with elevated autoantibodies, but that the effect is time-limited and the mechanisms underlying non-response require further investigation.