Amiodarone
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Neuromyopathy: case report An 87-year-old woman developed neuromyopathy during treatment with amiodarone for atrial fibrillation. The woman, who had atrial fibrillation, started receiving treatment with oral amiodarone 200mg three times a day for 14 days in April 2019, followed by 200mg daily. Additionally, she started receiving anticoagulant therapy with apixaban for atrial fibrillation. Also, she was receiving treatment with insulin and sitagliptin concomitantly. Shortly after the initiation of amiodarone, she developed bilateral leg weakness and pain. The pain was migratory and progressive though it was limited to her lower extremities. Before the initiation of amiodarone, she was able to ambulate independently and without a gait aid. Subsequently, she was admitted. When admitted she could not ambulate and need two-person assist for transfers from sit-to-stand. This was following approximately 2 months of amiodarone therapy. Physical examination revealed hip flexor and extensor strength of 2/5 bilaterally while knee flexor and extensor strength were 4/5 and 3/5, respectively. Plantarflexor and ankle dorsiflexor strength were 5/5 bilaterally. Pinprick sensation was compromised to the mid-distal level bilaterally. The physical medicine and rehabilitation service carried out nerve conduction studies and EMG (electromyography). Only the left lower extremity was tested because EMG and nerve conduction studies were terminated prematurely due to bleeding associated with apixaban. Her studies revealed slightly decreased amplitude of the tibialis anterior and borderline normal amplitude but decreased conduction velocity on tibial motor testing. The overall idea was that she had an axonal length-dependent polyneuropathy of the left lower extremity, sensory greater than motor, which was graded as severe. Evidence of myopathic changes to the left iliopsoas muscle without frank denervation was observed. Based on these findings and clinical presentation an amiodarone-induced neuromyopathy was diagnosed [time to reaction onset not clearly stated]. The woman’s treatment with amiodarone was discontinued in June 2019. The rate control with a beta-blocker was started. With active rehabilitation, she gradually started to regain lower extremity function. By the end of October 2019, she started using a fourwheel walker gait aid and was independent with ambulation and transfer. She was discharged home at her pre-amiodarone level of functional abilities and mobility. At a Follow-up in March 2020, she showed no recurrence of leg weakness or pain. Stanton MM, et al. Amiodarone-induced neuromyopathy in a geriatric patient. BMJ Case Reports 13: No. 11, 4 Nov 2020. Available from: URL: http://doi.org/10.1136/ 803518528 bcr-2020-236620
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Reactions 5 Dec 2020 No. 1833
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