Although copper plays a pivotal role in numerous physiological processes, its deficiency is virtually indistinguishable from subacute combined degeneration due to cobalamin deficiency. Moreover, the co-occurrence of deficiencies in other micronutrients and vitamins is common, making the diagnosis even more challenging. Here, we describe a case of copper deficiency in a 50-year-old woman who presented with altered mental status and bilateral upper and lower extremity weakness, numbness, and paresthesia. She was treated for cirrhosis and hepatic encephalopathy secondary to hepatic injury. While her mental symptoms improved, her physical symptoms continued to worsen, and she was transferred for further evaluation. The neurologic examination was positive for sensory neuropathy including decreased vibration/proprioception and ataxia in arms and legs; complete blood count showed pancytopenia; but infectious workup, cerebrospinal fluid analysis, autoimmune studies, and brain/spine magnetic resonance imaging were normal. A nerve conduction study showed generalized, axonal sensorimotor polyneuropathy. Micronutrient/trace element deficiency was suspected in the setting of gastric bypass surgery, and supplementation was successfully initiated. Though uncommon, clinical copper deficiency is increasingly frequently recognized in the inpatient setting, and permanent neurological damage can occur prior to diagnosis and treatment. Physicians should have an elevated clinical suspicion of copper deficiency in cases of polyneuropathy and pancytopenia in patients with a history of bariatric surgery.
Keywords: bariatric surgery; ceruloplasmin transferrin; copper deficiency; copper myeloneuropathy; polyneuropathy.
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