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Article Abstract
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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12344377 | PMC |
| http://dx.doi.org/10.1111/ene.70308 | DOI Listing |
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