Brentuximab vedotin treatment associated with acute and chronic inflammatory demyelinating polyradiculoneuropathies.

Brentuximab vedotin (BV) is an antibody-drug conjugate composed by an anti-CD30 monoclonal antibody and the anti-microtubule agent monomethyl auristatin E, used for the treatment of relapsed/refractory Hodgkin's lymphoma and non-Hodgkin's lymphoma. Peripheral neuropathy is a frequent adverse event of BV treatment, affecting up to 60% to 70% of patients.1 It usually consists of a mild axonal, length-dependent, sensory neuropathy, characterised by numbness and tingling of fingers and toes,1 2 related to the toxic effect of monomethyl auristatin E on axonal microtubules.3 Nonetheless, immune-mediated peripheral neuropathies characterised by prominent motor impairment have also been described,4 suggesting that, similarly to other antineoplastic agents, BV might have the potential to induce or exacerbate inflammatory polyradiculoneuropathies. The aim of this study was to assess the characteristics of inflammatory demyelinating polyradiculoneuropathy associated with BV treatment. ### Patients and methods We performed a retrospective research in seven French neurology departments, for all patients who were admitted between January 2013 and December 2019 to investigate a peripheral neuropathy appeared during BV treatment. We selected patients meeting Sjevar et al criteria for the diagnosis of Guillain-Barre syndrome (GBS) (level 1 of diagnostic certainty) or meeting ‘definite’ criteria for chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) according to 2010 European Federation of Neurological Societies/Peripheral Nerve Society guideline. We considered the onset as acute, subacute or chronic if the disease nadir was reached within 4 weeks, between 4 to 8 …