Background & aims: Copper absorption in humans probably occurs in the stomach and duodenum. Copper is essential for the structure and function of the nervous system and acquired copper deficiency in humans has been recognized to cause a myelopathy that resembles vitamin B12 deficiency. Acquired copper deficiency is not a well-recognized complication of gastric surgery. In Menke's disease a defect in enterocyte transport of absorbed copper results in increased copper content in the duodenal mucosa and hypocupremia.
Methods: We report 2 patients who developed neurologic deficits with copper deficiency many years after gastric surgery. In 2 other patients with hypocupremic myelopathy but no history of gastric surgery, colonic copper was measured to determine if an absorptive defect similar to that seen in Menke's disease may be responsible for hypocupremia.
Results: In all 4 patients copper deficiency was identified as the cause of the myelopathy. In 2 patients the copper deficiency occurred after gastric surgery. Eight additional patients with copper deficiency after gastric surgery were identified from the literature. Six of these 8 patients also had neurologic manifestations. Colonic mucosa copper content was increased in the 2 patients with hypocupremia without prior gastric surgery.
Conclusions: Acquired copper deficiency may be a delayed complication of gastric surgery and may result in a myelopathy similar to that seen with vitamin B12 deficiency. In some patients with acquired copper deficiency no cause for the hypocupremia may be evident and a primary absorptive defect should be considered.