Clinical Manifestations of Copper Deficiency: A Case Report and Review of the Literature

Copper is a mineral that is absorbed in the stomach, duodenum, and jejunum. Gastric bypass surgery, gastrectomy, and short-bowel syndrome commonly lead to copper malabsorption. Copper deficiency primarily presents with hematological and neurological sequelae, including macrocytic anemia and myelopathy. Although hematological disturbances often correct with copper supplementation, neurological manifestations of copper deficiency may be irreversible. We present the case of copper deficiency secondary to malabsorption and management strategies to prevent irreversible neurological sequelae.

A 48-year-old female with a history of hypothyroidism, ischemic stroke, and Crohn's disease, complicated by subtotal colectomy and small-bowel resections, was admitted for fatigue and progressive neurological deficiencies. Her vital signs were stable, and physical examination was remarkable for weakness of both upper and lower extremities, ataxia, and upper extremities paresthesia. Computed tomography scan of the head without contrast was unremarkable. Magnetic resonance imaging enterography revealed a focal area of narrowing of the remaining small bowel. Copper level was low at 39 µg/dL. After 5 days of intravenous replacement using trace element within parenteral nutrition, her copper level corrected to 81 µg/dL. Her ataxia improved after intravenous copper supplementation and did not recur.

Our patient presented with copper deficiency secondary to malabsoprtion. This case highlights the importance of copper testing in the bariatric surgery population and in patients with short-bowel syndrome. Given the irreversible nature of neurological symptoms when compared with the expense of nutrition supplements, routine copper testing should be considered in patients with malabsorptive states or altered anatomy, regardless of initial presentation.