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Rapid Development of Severe Copper Deficiency in a Patient With Crohn's Disease Receiving Parenteral Nutrition

Department of Internal Medicine, Division of Gastroenterology, University of California, San Francisco, UCSF-Mount Zion Medical Center

Robert F. Willenbucher, MD

Department of Internal Medicine, Division of Gastroenterology, University of California, San Francisco, UCSF-Mount Zion Medical Center

A 32-year-old man with active Crohn's disease and recurrent small bowel strictures underwent abdominal surgery and was subsequently given total parenteral nutrition (TPN). Severe cholestasis developed and copper was removed from the TPN. Although serum ceruloplasmin levels were within normal limits, 8 weeks after copper removal, he developed pancytopenia. Serum copper levels were severely depressed. Bone marrow biopsy was consistent with copper deficiency; cytoplasmic vacuolization of both myeloid and erythroid precursors, megaloblastic erthropoiesis, and marked hypocellularity were observed. IV replacement with copper sulfate resulted in improvement in the patient's anemia, neutropenia, and thrombocytopenia, but the patient died suddenly from cardiac tamponade. Postmortem examination revealed fibrinous and hemorrhagic pericarditis. Despite the rare occurrence of overt copper deficiency, this case emphasizes the need to recognize copper deficiency as an important etiology of iron-resistant anemia in patients receiving TPN. Furthermore, the relative rapidity with which our patient developed pancytopenia suggests that, in view of the established recommendation that copper be removed from TPN in cholestatic conditions, serum copper levels must be measured periodically. (Journal of Parenteral and Enteral Nutrition 23:169-172, 1999)

Journal of Parenteral and Enteral Nutrition, Vol. 23, No. 3, 169-172 (1999)
DOI: 10.1177/0148607199023003169


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