Thrombocytopenia in the reported cases improved as early as 2–6 weeks after supplementation. In one patient, pancytopenia developed 8 weeks after the removal of copper from PN. Anemia and neutropenia were the first signs of copper deficiency after an average of 11 months. summarized 14 case reports of PN-related copper deficiency and in addition to neutropenia and/or anemia, 3 of the 14 patients also had thrombocytopenia. This highlights the difficulty in interpreting serum copper levels in the setting of inflammation.Ĭlinical manifestations of copper deficiency are pancytopenia (including hypochromic anemia unresponsive to iron supplementation), skeletal abnormalities, myocardial disease, depigmentation of hair, and neurologic abnormalities.
In a recent study of 166 patients, copper levels had no correlation with C-reactive protein (CRP) levels, unlike zinc, selenium, and albumin, which were negatively correlated with CRP. Additionally, as ceruloplasmin is an acute phase reactant, ceruloplasmin and copper levels can be elevated in inflammatory states even in the setting of marginal copper deficiency. In copper deficiency, serum copper and ceruloplasmin levels are low but if the deficiency is not severe, these levels can be normal and thus do not reflect copper status in the body. In the context of PN, copper may have increased urinary excretion, as copper is complexed to amino acids. Eighty percent of copper is excreted in the bile and the remainder is excreted in the urine. More than 90% of copper in the blood is bound to ceruloplasmin and the rest is bound to albumin and amino acids. The aim of this paper aims to summarize the most recent recommendations to help guide the clinician prescribing PN in acute care and long-term settings.Ĭopper is essential as an enzymatic cofactor in processes involving connective tissue formation, iron metabolism and hematopoesis, and central nervous system function. The following is a review of TEs that are currently supplemented in PN, and a brief review on TEs that are not routinely added in North America but whose importance should not be overlooked. Many of these still contain doses of TEs that are not in keeping with the current recommendations from expert groups. There are currently a variety of pre-mixed multi-TE combinations that are commercially available for addition to parenteral nutrition (PN) solutions. Despite expert agreement that copper, manganese, and chromium doses be reduced, the FDA has not updated the 1979 guidelines. Conversely, in conditions of organ dysfunction, certain reductions in trace elements are recommended. In critical illness, the processes of inflammation, infection, and oxidative stress increase the metabolic requirements for certain trace elements. In the following decades, as more information came from toxicity and balance studies, as well as reports in the literature of PN contamination, further adjustments to recommended doses were made.
As patients were maintained on home parenteral nutrition (HPN) for longer durations of time, additional light was shed on TEs. A few years later, selenium was added to a subsequent review. In 1979, the Nutrition Advisory Group of the American Medical Association (NAG-AMA) published guidelines submitted to the Food and Drug Administration (FDA) for daily TEs considered essential for human health in parenteral nutrition: zinc, copper, manganese, and chromium. There are TEs that are well established as essential in human physiology, and other TEs whose roles and requirements have yet to be defined. Trace elements (TE) are essential components of complexes required for fundamental processes such as enzymatic reactions.
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