TY - JOUR
T1 - Pancytopenia after removal of copper from total parenteral nutrition
AU - Fuhrman, M. Patricia
AU - Herrmann, Virginia
AU - Masidonski, Patricia
AU - Eby, Charles
PY - 2000
Y1 - 2000
N2 - Patients who develop cholestatic jaundice during chronic total parenteral nutrition (TPN) can develop significant hematologic complications due to hypocupremia if copper supplementation is withheld. A 36-year-old female with short bowel syndrome developed progressive liver dysfunction 6 months after initiation of TPN. Trace elements were omitted from her TPN because of cholestasis and persistent hyperbilirubinemia. Despite chronic diarrhea, absorption of some dietary copper was anticipated from her oral diet. Fifteen months later, the patient became red cell transfusion dependent, and her neutrophil and platelet counts steadily declined. After 19 months of receiving TPN without trace elements, her serum copper level was 25 μg/dL (normal 70 to 155 μg/dL). Provision of trace elements for 2 months was associated with increased serum copper, neutrophil and platelet counts and independence from red cell transfusions. When the serum copper level reached 186 μg/dL, copper supplementation was discontinued. Over the next 3 months, serum copper level fell to 10 μg/dL, neutrophil and platelet counts fell precipitously, and red cell transfusions were resumed. Once again, copper, neutrophil and platelet levels promptly rebounded with parenteral copper supplementation. Although anemia and neutropenia are well-recognized hematologic consequences of copper deficiency, thrombocytopenia rarely has been reported. This is the first report of pancytopenia secondary to TPN-related copper deficiency in which the association was confirmed when hypocupremia recurred.
AB - Patients who develop cholestatic jaundice during chronic total parenteral nutrition (TPN) can develop significant hematologic complications due to hypocupremia if copper supplementation is withheld. A 36-year-old female with short bowel syndrome developed progressive liver dysfunction 6 months after initiation of TPN. Trace elements were omitted from her TPN because of cholestasis and persistent hyperbilirubinemia. Despite chronic diarrhea, absorption of some dietary copper was anticipated from her oral diet. Fifteen months later, the patient became red cell transfusion dependent, and her neutrophil and platelet counts steadily declined. After 19 months of receiving TPN without trace elements, her serum copper level was 25 μg/dL (normal 70 to 155 μg/dL). Provision of trace elements for 2 months was associated with increased serum copper, neutrophil and platelet counts and independence from red cell transfusions. When the serum copper level reached 186 μg/dL, copper supplementation was discontinued. Over the next 3 months, serum copper level fell to 10 μg/dL, neutrophil and platelet counts fell precipitously, and red cell transfusions were resumed. Once again, copper, neutrophil and platelet levels promptly rebounded with parenteral copper supplementation. Although anemia and neutropenia are well-recognized hematologic consequences of copper deficiency, thrombocytopenia rarely has been reported. This is the first report of pancytopenia secondary to TPN-related copper deficiency in which the association was confirmed when hypocupremia recurred.
UR - http://www.scopus.com/inward/record.url?scp=0033744391&partnerID=8YFLogxK
U2 - 10.1177/0148607100024006361
DO - 10.1177/0148607100024006361
M3 - Article
C2 - 11071596
AN - SCOPUS:0033744391
VL - 24
SP - 361
EP - 366
JO - Journal of Parenteral and Enteral Nutrition
JF - Journal of Parenteral and Enteral Nutrition
SN - 0148-6071
IS - 6
ER -