Efgartigimod as Add‐On Treatment in Refractory Guillain–Barré Syndrome: A Case Report

Background and Aims Guillain–Barré Syndrome (GBS) is an autoimmune disease that can cause flaccid tetraplegia. Efgartigimod, a monoclonal antibody that inhibits the neonatal receptor (FcRn), increases IgG degradation. Methods A 60‐year‐old lady was admitted with acute flaccid tetraparesis, requiring mechanical ventilation within 12 h. Nerve conduction studies were compatible with acute inflammatory demyelinating polyneuropathy (AIDP). No anti‐ganglioside or anti‐nodal/paranodal antibody could be identified in serum. Despite receiving standard treatment with plasma exchange (PLEX), the patient remained severely tetraparetic, bedridden, and mechanically ventilated. Human immunoglobulin 2 g/kg was given, without obtaining significant improvement. One month after disease onset, the patient received efgartigimod (10 mg/kg intravenously) weekly for four doses. Results We report the results of this treatment on muscle strength, patient disability, and nerve conduction studies. The tolerability profile was satisfactory, and the patient was able to walk alone after 4 months from disease onset. Interpretation The potential role of efgartigmod in GBS should be explored in future clinical trials.