Ixekizumab-associated transverse myelopathy in a patient with psoriatic arthritis (P14-3.017)

Abstract

<h3>Objective:</h3> We present the case of a woman with acute-onset myelopathy who presented with sensory symptoms and ataxia. We discuss her diagnosis of monoclonal antibody-induced short-segment transverse myelopathy and the potential mechanisms mediating this adverse reaction. <h3>Background:</h3> Monoclonal antibodies have provided novel therapeutic avenues for several disorders in oncology, rheumatology, and neurology. These treatments, however, have been noted to carry a rapidly growing host of adverse reactions, many of which involve the nervous system. <h3>Design/Methods:</h3> N/A <h3>Results:</h3> A 57-year-old right-handed woman with psoriatic arthritis on monthly ixekizumab injections (a humanized monoclonal antibody directed against interleukin 17A) was admitted for a two-day history of progressive dysesthesias, which ascended from her feet to the lower abdomen. Her neurologic examination showed patellar and ankle hyperreflexia with large-fiber modality length-dependent sensory loss and preserved small-fiber modalities. The workup was notable for normal B12, homocysteine, copper, and zinc levels. No abnormal protein bands were identified on serum protein electrophoresis. A lumbar puncture yielded a bland CSF with two white cells, glucose of 65, protein of 43.5, and 0 oligoclonal bands. Serum ANA was positive with homogeneous with a 1:320 titer, reflecting to positive dsDNA and Scl70. A broad infectious workup was negative for HSV, VZV, CMV West Nile virus, Lyme, syphilis, HIV, and HTLV-2. MRI of the neuraxis was remarkable for a short-segment T2 hyperintense lesion of the dorsal column spanning T7–9. In the context of unrevealing etiological work-up, she was diagnosed with ixekizumab-induced transverse myelopathy and the biologic drug was stopped. She continued to improve during the following year without recurring CNS symptoms. <h3>Conclusions:</h3> We report the first case of ixekizumab-induced thoracic transverse myelopathy which we stipulate may result from dysregulation of the T-helper pathways given the antagonism of IL-17A. As shown by this clinical presentation, neurologists need to be aware of the adverse reactions of monoclonal antibodies. <b>Disclosure:</b> Dr. Rosso has nothing to disclose. Dr. Milano has received personal compensation in the range of $500-$4,999 for serving as an Expert Witness for Jackson kelly. Dr. Gleichgerrcht has nothing to disclose.