Abstract
Copper is an essential micronutrient necessary for the hematologic and neurologic systems. Acquired copper deficiency in humans has been described, causing a syndrome similar to the subacute combined degeneration of vitamin B12 deficiency. Copper deficiency is being increasingly recognized in adult populations due to various causes including high zinc levels, copper chelating agents and after gastric bypass surgery. We present a case patient with sever hypocupremia leading to profound neurological symptoms to stress the importance of this clinical entity and its early diagnosis and treatment. We present a 52 year-old white male who had Roux-en-Y gastric bypass surgery. He was maintained on multivitamin supplements including Vitamin B12, iron and zinc. Fifteen years after his gastric bypass he started having worsening sensory ataxia and worsening paresthesias of the lower extremities, and was hospitalized for severe weakness in his lower extremities. On admission his nutritional evaluation revealed normal serum levels for Vitamin B12, zinc and iron. However he was found to have an extremely low serum copper level. MRI of the spine showed T-2 hyperintensity within the dorsal spinal cord from C2 through C5 which has been described in patients with copper deficiency. The patient was started on copper supplements, showed significant clinical improvement, and was maintained on copper supplements after his discharge. Copper deficiency is a rare complication following gastric bypass surgery. Copper is primarily absorbed from stomach and proximal small bowel. It is not clear why copper deficiency occurs in some but not all patients after gastric surgery. Iron and zinc have been described to inhibit copper uptake in the proximal bowel. Zinc and copper compete for absorption in the digestive tract so that a diet that is excessive in one of these minerals may result in a deficiency in the other. Bariatric procedures such as gastric bypass surgery result in a similar functional anatomy of the proximal gut and may place more patients at increased risk of copper deficiency. Early recognition and therapy with copper supplements may lead to a decrease in both neurologic and other known hematologic consequences of hypocupremia. Oral copper should to be taken in a different time preferably earlier to the oral multivitamins or oral zinc to prevent the chelating effect of zinc on copper.
Published Version
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