B Mark Hoffman1, Nuhad Abou Zeid2, Umar Alam3, James B Caress4. 1. Wake Forest School of Medicine, Department of Neurology, One Medical Center Blvd, Winston Salem, NC 27157, USA. 2. Wake Forest School of Medicine, Department of Neurology, One Medical Center Blvd, Winston Salem, NC 27157, USA. Electronic address: nabouzei@wakehealth.edu. 3. Wake Forest School of Medicine, Department of Neurology, One Medical Center Blvd, Winston Salem, NC 27157, USA. Electronic address: ualam@wakehealth.edu. 4. Wake Forest School of Medicine, Department of Neurology, One Medical Center Blvd, Winston Salem, NC 27157, USA. Electronic address: jcaress@wakehealth.edu.
Abstract
BACKGROUND: Alemtuzumab administration is known to cause secondary autoimmune disease but has not been associated with the development of neurologic autoimmune conditions. Lambert-Eaton myasthenic syndrome (LEMS) is caused by autoantibodies directed against calcium channels on the neuromuscular junction. CASE REPORT: We report a case of a patient with relapsing-remitting multiple sclerosis (RRMS) treated with alemtuzumab who develop generalized weakness initially attributed to progression of MS but eventually determined to be due to LEMS. CONCLUSION: Alemtuzumab treatment can result in the development of neurologic autoimmune conditions that could mimic MS progression.
BACKGROUND:Alemtuzumab administration is known to cause secondary autoimmune disease but has not been associated with the development of neurologic autoimmune conditions. Lambert-Eaton myasthenic syndrome (LEMS) is caused by autoantibodies directed against calcium channels on the neuromuscular junction. CASE REPORT: We report a case of a patient with relapsing-remitting multiple sclerosis (RRMS) treated with alemtuzumab who develop generalized weakness initially attributed to progression of MS but eventually determined to be due to LEMS. CONCLUSION:Alemtuzumab treatment can result in the development of neurologic autoimmune conditions that could mimic MS progression.