Abstract Details

Title Brentuximab-induced sensorimotor polyneuropathy with acquired demyelinating features resembling chronic inflammatory demyelinating polyneuropathy (CIDP)

Topic Neuromuscular and Clinical Neurophysiology (EMG)

Presentation(s) Neuromuscular and Clinical Neurophysiology (EMG) Posters (7:00 AM-5:00 PM)

Poster/Presentation
Number 073

Objective

To describe a case of brentuximab-induced sensorimotor polyneuropathy with acquired demyelinating features resembling chronic inflammatory demyelinating polyneuropathy (CIDP).

Background

Chemotherapy-induced polyneuropathy (CIPN) is a recognized complication of microtubule-disrupting agents (MDA).¹ Brentuximab vedotin (BV), an anti-CD30 biologic linked to the MDA monomethyl auristatin-E, is an effective treatment against Hodgkins lymphoma, anaplastic large cell lymphoma, and CD30+ cutaneous T-cell lymphoma.¹ The common reported neurological side effect is sensory neuropathy (SN) with axonal injury on electrodiagnostics.^1-4 More recently, reports are emerging of Brentixumab treatment associated with acquired demyelinating features resembling acute and chronic inflammatory demyelinating polyneuropathy (CIDP).⁵

Design/Methods NA

Results A 39-year-old man with recurrent cutaneous T-cell lymphoma presented with painful paresthesia and significant distal weakness in all limbs. Several years prior he was diagnosed with mycosis fungoides, the common form of cutaneous T-cell lymphoma. Initial treatment consisted of total skin irradiation and weekly BV which was discontinued due to development of a painful sensory neuropathy. His disease course had several recurrences and he was retreated with BV. All recurrent BV treatments were terminated early due to re-emergence of painful SN and he went on to develop bilateral foot and wrist drop with atrophy of the distal muscles. Examination demonstrated distal greater than proximal weakness, decreased vibration and pinprick sensation to the knees, and areflexia. MRI of the brain and C-spine did not identify culprit lesions. Nerve conduction study (NCS) showed absent responses from right peroneal and tibial motor nerves with evidence of partial conduction block in bilateral median and right ulnar nerves, with the right ulnar motor study also showing temporal dispersion. EMG of tested muscles showed acute and chronic denervation changes with decreased recruitment. He was treated with intravenous immunoglobulin (IVIg) and had notable improvement in strength.

Conclusions This case demonstrates that BV may produce a CIDP phenotype which can potentially be treated with IVIg.

Authors/Disclosures
Adeel Zubair, MD (Yale University School of Medicine) PRESENTER	Dr. Zubair has received personal compensation in the range of $500-$4,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for The MedNet.
Melissa J. Rethana, MD	Dr. Rethana has nothing to disclose.
Benison Keung, MD, F�鶹��ýӳ�� (Yale University School of Medicine, Dept of Neurology)	Dr. Keung has nothing to disclose.

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