ME RÁÐSTEFNA 28. SEPTEMBER 2017 - aukaefni
ME CONFERENCE - FURTHER INFORMATION
Dr. Daniel Peterson, helstu rannsóknir
Title: Therapeutic intervention and disease mechanisms in ME/CFS.
Øystein Fluge, MD, PhD, consultant in oncology and researcher, Dept. of Oncology, Haukeland University Hospital.
Ingrid Gurvin Rekeland, MD, physician in oncology training and research fellow, Dept. of Oncology, Haukeland University Hospital.
In 2004-2007 we observed patients with long-standing ME/CFS who was diagnosed with lymphoma, and who experienced relief of ME/CFS symptoms after lymphoma therapy with chemotherapy and/or the therapeutic antibody rituximab.
We have since then performed research in ME/CFS and explored the therapeutic principle of B-cell depletion using the monoclonal anti-CD20 antibody rituximab in ME/CFS. First, a case series of three ME/CFS patients was performed, then a small randomized phase-II trial, and thereafter an open-label phase II study using prolonged B-cell depletion with rituximab maintenance treatment.
These studies indicate that a subgroup of ME/CFS patients may benefit from B-cell depletion therapy. To verify or refute the findings from these initial trials, a multi-center, randomized, double-blind phase III trial (rituximab maintenance versus placebo) with 151 ME/CFS patients is ongoing in Norway (finished by October 2017).
In addition, after observing ME/CFS patients who got breast cancer and who reported improvement of ME/CFS symptoms after cytotoxic chemotherapy for breast cancer, an open-label phase II clinical trial exploring cyclophosphamide infusions in 40 ME/CFS patients is now finished.
Analyses of both the rituximab (RituxME) and cyclophosphamide (CycloME) trials will be performed in autumn 2017.
Basic research is performed to elucidate possible disease mechanisms in ME/CFS, using biobank samples from patients included in the clinical trials. Using a metabolomics approach, our data indicate that ME/CFS patients have an “obstruction” in the central energy pathway, with inadequate use of glucose as energy source and early accumulation of lactic acid upon limited exertion, and with compensatory use of alternative sources (amino acids, fatty acids) for energy metabolism and oxidative phosphorylation.
Dr. Rekeland and dr. Fluge will during their talks give an overview of the clinical trials and of the laboratory work.