Zinc
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Acquired copper deficiency exacerbation leading to myeloneuropathy secondary to zinc toxicity: case report A 42-year-old woman developed acquired copper deficiency exacerbation leading to myeloneuropathy secondary to zinc toxicity while receiving zinc for cold prophylaxis [duration of treatment to reaction onset not stated; not all outcomes stated]. The woman presented to a neurology clinic with progressive pain and numbness of lower extremities. She reported worsening of symptoms (initially started on knees and later spread to feet and fingertips) of some underlying neuropathy which she had for several years. Her neurological examinations was significant for mild weakness of finger abduction, hip flexors, deltoids and foot plantar flexion. Further, sensory examinations were significant for decreased vibration and proprioception in the toes. Pinprick and light touch sensation were preserved. Broad based gait, diffuse hyporeflexia, unsteady station and decreased ability to stand on heels and toes were also noted. Previously, she had been treated for an unexplained severe anaemia. Further, bilateral lower extremity electromyography (EMG) revealed left-sided tibial neuropathy. Subsequent bilateral upper extremity EMG showed a mild prolongation of right median sensory distal peak latency suggestive of residual median sensory neuropathy (consistent with past diagnosis of Carpal tunnel syndrome). An MRI of cervical spine indicated increased signal intensity of the dorsal spinal cord from C2-C6 suggestive of myelitis. CSF analysis was significant for a minor increase in protein level. Serological examination was significant for herpes simplex virus (HSV) IgG positivity (due to prior exposure). Her past medical history was significant for anaemia, hypertension, type II diabetes mellitus, attention deficit disorder, bipolar disorder, pulmonary embolus, fibromyalgia, migraine headaches and chronic pain. Anamnesis revealed that, at the age of 33 years, she had undergone gastric bypass, oesophagogastrojejunostomy and umbilical herniorrhaphy. Further, at the age of 34 years, she had undergone right sided carpal tunnel release. At the time of the presentation, she had been receiving multiple medications for her comorbidities. Based on the initial findings, copper deficiency or zinc toxicity was suspected. Further investigations also revealed that, she had been receiving over the counter oral zinc [natural zinc] 50mg 4 times a day for several years for cold prophylaxis. Subsequent laboratory findings showed elevated zinc and decreased ceruloplasmin and copper levels. Hence, the diagnosis of exacerbation of copper deficiency secondary to zinc toxicity was confirmed. Her myeloneuroapathy was attributed to exacerbation of acquired copper deficiency due to previous bariatric surgery. The woman’s treatment with zinc was stopped, and she received 5 days of parenteral copper chloride. Thereafter, cupric chloride [copper chloride] was switched to oral copper supplements. At the time of follow-up neurological examinations, partial im
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