Zinc is an essential nutritional requirement that serves as a cofactor for more than 70 different enzymes including carbonic anhydrase, alkaline phosphatase, lactic dehydrogenase and both RNA and DNA polymerase. Zinc facilitates wound healing, helps maintain normal skin hydration and the senses of taste and smell.
Zinc resides in muscle, bone, skin, the kidney, liver, pancreas, retina, prostate and particularly in the red and white blood cells. Zinc binds to plasma albumin, a2-macroglobulin, and some plasma amino acids including histidine, cysteine, threonine, glycine and asparagine. Ingested zinc is excreted mainly in the stool (approximately 90%), and to a lesser extent in the urine and in perspiration. Providing zinc during TPN helps prevent development of deficiency symptoms such as: Parakeratosis, hypogeusia, anorexia, dysosmia, geophagia, hypogonadism, growth retardation and hepatosplenomegaly.
The initial manifestations of hypozincemia in TPN patients are diarrhea, apathy and depression. At plasma levels below 20 mcg zinc/100 mL, dermatitis followed by alopecia has been reported for TPN patients. Normal zinc plasma levels are 100 ± 12 mcg/100 mL.
Copper is an essential nutrient that serves as a cofactor for serum ceruloplasmin, an oxidase necessary for proper formation of the iron carrier protein, transferrin. Providing copper during TPN helps prevent development of the following deficiency symptoms: Leukopenia, neutropenia, anemia, depressed ceruloplasmin levels, impaired transferrin formation and secondary iron deficiency.
Normal serum copper values range from 80 to 163 mcg/100 mL (mean, approximately 110 mcg/100 mL). The serum copper level at which deficiency symptoms appear is not precisely defined. The daily turnover of copper through ceruloplasmin is approximately 0.5 mg. Excretion of copper is through the bile (80%), directly through the intestinal wall (16%) and in urine (4%).
Manganese is an essential nutrient that serves as an activator for enzymes such as polysaccharide polymerase, liver arginase, cholinesterase and pyruvate carboxylase.
Providing manganese during TPN helps prevent development of deficiency symptoms such as nausea and vomiting, weight loss, dermatitis and changes in growth and color of hair. Under conditions of minimal intake, 20 mcg manganese/day is retained. Manganese is bound to a specific transport protein, transmanganin, a b1-globulin. Manganese is widely distributed but concentrates in the mitochondria-rich tissues such as brain, kidney, pancreas and liver. Assay for manganese in whole blood results in concentrations ranging from 6 to 12 mcg manganese/liter. Excretion of manganese occurs mainly through the bile, but in the event of obstruction, ancillary excretion routes include pancreatic juice, or return into the lumen of duodenum, jejunum or ileum. Urinary excretion of manganese is negligible.
Trivalent chromium is party of glucose tolerance factor, an essential activator of insulin-mediated reactions. Chromium helps to maintain normal glucose metabolism and peripheral nerve function. Providing chromium during TPN helps prevent deficiency symptoms including impaired glucose tolerance, ataxia, peripheral neuropathy and a confusional state similar to mild/moderate hepatic encephalopathy.
Serum chromium is bound to transferrin (siderophilin) in the b-globulin fraction. Typical blood levels for chromium range from 1 to 5 mcg/liter, but blood levels are not considered a meaningful index of tissue stores. Administration of chromium supplements to chromium-deficient patients can result in normalization of the glucose tolerance curve from the diabetic-like curve typical of chromium deficiency. This response is viewed as a more meaningful indicator of chromium nutriture than serum chromium levels.
Excretion of chromium is via the kidneys, ranging from 3 to 50 mcg/day. Biliary excretion via the small intestine may be an ancillary route, but it is believed that only small amounts of chromium are excreted in this manner.