Case report and review: IVIg and efgartigimod in Guillain-Barré with Graves disease and thyroid cancer

Guillain–Barré syndrome (GBS) is an acute immune-mediated peripheral neuropathy typically characterized by a monophasic course; however, atypical or relapsing presentations suggest that sustained immune dysregulation contribute to disease heterogeneity. We report a 33-year-old man with progressive limb weakness diagnosed as motor-predominant acute inflammatory demyelinating polyradiculoneuropathy (AIDP), supported by albuminocytologic dissociation and demyelinating features on nerve conduction studies with preserved sensory conduction. Immunological evaluation revealed B lymphocyte expansion, elevated interleukin-6 and interleukin-8 levels, and strong thyroid autoantibody positivity consistent with Graves’ disease, while anti-ganglioside and paraneoplastic antibodies were negative. The clinical course was marked by immune-triggered relapses and the patient responded well to intravenous immunoglobulin (IVIg) and FcRn inhibition with efgartigimod. Further investigation identified papillary thyroid carcinoma harboring a BRAF V600E mutation, after which neurological symptoms stabilized following thyroidectomy. This case illustrates a rare concurrence of relapsing AIDP, Graves’ disease, and papillary thyroid carcinoma, and supports the hypothesis that persistent systemic immune activation underlies relapsing GBS, rather than a chronic demyelinating process. Clinically, it highlights the importance of considering underlying autoimmune and neoplastic conditions in atypical or relapsing GBS to guide individualized management.