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

Abstract

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.

Clinicopathological Analysis of Hematological Disorders in Tube-Fed Patients with Copper Deficiency

“…Copper deficiency has been observed in adult patients with inflammatory bowel disease (19,20), total parenteral nutrition (21,22), massive zinc ingestion (11) (6,(8)(9)(10)(11)(12)(13)(14)(15). Cytoplasmic vacuoles have also been found in patients with acute alcoholic intoxication (23), chloramphenicol toxicity (24), pancreatic dysfunction (25) and myeloproliferative syndromes (26).…”

Cocoa Supplementation for Copper Deficiency Associated with Tube Feeding Nutrition

“…Although it is unclear why gender distribution of our patients showed more women than men (12 versus 1) (19)(20)(21)(22)(23), those with short bowel syndrome (24,25), and those with partial gastrectomy (12,26,27). In addition, sporadic case reports also suggested that inadequate diet alone or genetic disorders affecting proteins of copper metabolism could cause copper deficiency (28)(29)(30), including Menkes disease and occipital horn syndrome (10) …”

Concomitant Immune Thrombocytopenic Purpura and Crohn’s Disease

“…Several conditions causing thrombocytopenia in CD patients have been reported: 1) ITP (autoimmune platelet destruction); 2) druginduced thrombocytopenia, believed to induce autoimmunity or bone marrow suppression, reported following the use of anti-tumor necrosis factor (TNF)-alpha antibodies (i.e., infliximab) [6,7], 5-aminosalicylic acid [8], azathioprine [9], and low-molecular-weight heparin [10]; 3) the presence of thrombotic thrombocytopenic purpura (TTP) or hemolytic-uremic syndrome (HUS) in patients with CD [11][12][13]; 4) hematological malignancies [14] or portal hypertension (hypersplenism); and 5) deficiencies in minor elements, such as copper, during nutrition therapy for CD [15].…”