Trace element loss in urine and effluent following traumatic injury.

BACKGROUND: Few data are available to establish recommendations for trace element supplementation during critical illness. This study quantified the loss of several elements and assessed the adequacy of manganese and selenium in parenteral nutrition (PN). METHODS: Men with traumatic injuries were grouped by renal status: adequate (POLY; n = 6), acute failure with continuous venovenous hemofiltration (CVVH; n = 2), or continuous venovenous hemodiafiltration (CVVHD; n = 4). PN supplied 300 microg/d manganese and 60 microg/d selenium. Urine and effluent (from artificial kidneys) were collected for 3 days and analyzed for boron, manganese, nickel, and silicon using inductively coupled plasma atomic emission spectrometry, and for selenium using atomic absorption spectrometry. RESULTS: POLY manganese and selenium excretion averaged (standard deviation [SD]) 7.9 (3.3) microg/d and 103.5 (22.4) microg/d, respectively. All elements except selenium were detected in dialysate (prior to use). CVVHD effluent contained 3.5 and 7.3 times more manganese and nickel than CVVH ultrafiltrate, respectively. Loss of manganese averaged 2.6%, 21%, and 73% of PN amounts for POLY, CVVH, and CVVHD groups, respectively. DISCUSSION: Minimal loss of manganese compared with the amount in PN suggests that excessive amounts are retained. POLY patients excreted more selenium than was in PN, indicating negative balance. POLY losses of boron and silicon were less than that published for healthy adults, reflecting less than typical intake, whereas loss during CVVH was in the normal reference range, possibly because of added intake from boron contamination of replacement fluids. All patients lost more nickel than amounts published for healthy adults. CONCLUSIONS: Current guidelines of 60-100 microg/d of parenteral manganese may be excessive for trauma patients. The uptake of manganese and nickel from contaminants in CVVHD dialysate should be investigated.

A single 60-mg iron dose decreases zinc absorption in lactating women.

This study determined whether a single 60-mg dose of ferrous sulfate interferes with fractional zinc absorption (FZA) at 7-9 wk of lactation. In a crossover design, 5 exclusively breast-feeding women were given either a single 60-mg iron supplement or no supplement. FZA was measured by analyzing zinc stable isotope tracers ((70)Zn and (67)Zn) in urine samples collected for 7 d after isotope dosing. A 0.7-micromol intravenous (IV) infusion of (70)Zn as ZnCl(2) in saline was followed by a 0.03-mmol oral dose of (67)Zn as ZnCl(2) given with a standardized meal. After a 7-d wash-out period, the supplement given was reversed and a second FZA measurement was taken. FZA was calculated from isotopic enrichments in urine measured by inductively coupled plasma mass spectrometry. Hemoglobin, plasma ferritin and transferrin receptor, and plasma 5'-nucleotidase, plasma zinc and erythrocyte zinc did not differ before the two measurements of zinc absorption. When women were given a single iron supplement, FZA was significantly lower, 21.7 +/- 1.7% compared with 26.9 +/- 2.6% when no supplement was given (P = 0.032). A single 60-mg iron dose significantly decreases FZA during early lactation.

Carotenoid composition of human milk during the first month postpartum and the response to beta-carotene supplementation.

BACKGROUND: Information is lacking regarding normal changes in milk carotenoid concentrations in healthy, well-nourished women during the first month of lactation. OBJECTIVES: This study investigated milk carotenoid concentrations during days 4-32 postpartum and assessed the effects of maternal beta-carotene supplementation. DESIGN: Subjects (n = 21; aged 19-39 y) were randomly assigned to receive beta-carotene (30 mg/d) or placebo from days 4 to 32 postpartum. Each subject provided 8 diet records and 8 milk samples during the study. Diet records were analyzed for energy, macronutrients, vitamins A and E, and carotenoids. Milk samples were analyzed with HPLC for concentrations of carotenoids, retinol, and alpha-tocopherol. Data were analyzed by using repeated-measures analysis and orthogonal contrasts. RESULTS: No significant differences in average dietary intakes, body mass index, age, or parity were found between groups at baseline or after supplementation. Milk carotenoid concentrations decreased over time (P < 0.01), as did retinol and alpha-tocopherol concentrations (P < 0.003). Concentrations of most carotenoids decreased to those reported for mature milk by day 32 postpartum. Milk lutein concentrations remained elevated throughout the study compared with values reported for mature milk, whereas plasma lutein concentrations decreased significantly over time. beta-carotene supplementation did not significantly change the milk concentrations of beta-carotene, the other carotenoids, retinol, or alpha-tocopherol. CONCLUSIONS: The lack of increase in milk beta-carotene despite supplementation suggests that transitional milk may be already nearly saturated with beta-carotene. The elevated milk lutein concentration and simultaneous decrease in plasma lutein suggest that lutein metabolism may be altered during early lactation.

Magnesium, calcium, zinc, and nitrogen loss in trauma patients during continuous renal replacement therapy.

BACKGROUND: Whether standard nutrition support is sufficient to compensate for mineral loss during continuous renal replacement therapy (CRRT) is not known. METHODS: Adult men with traumatic injuries were recruited; one-half of recruits required CRRT for acute renal failure. All urine and effluent (from CRRT) were collected for 72 hours. Urine, effluent, and dialysate were analyzed for magnesium, calcium, and zinc using atomic absorption spectrometry. Urea nitrogen in blood, urine, and effluent were determined by measuring conductivity changes after the addition of urease. Blood was analyzed for magnesium and calcium as part of routine care. Intake was calculated from orders and intake records. RESULTS: Patients receiving CRRT (n = 6) lost 23.9+/-3.1 mmol/d (mean +/- SEM) of magnesium and 69.8+/-2.7 mmol/d of calcium compared with 10.2+/-1.2 mmol/d and 2.9+/-2.5 mmol/d, respectively, lost in patients not in acute renal failure (n = 6; p < .01). Zinc intake was significantly greater than loss in both groups (p < .03). Urea nitrogen excretion did not differ between groups. Serum magnesium was 0.75+/-0.04 mmol/L for CRRT patients, significantly lower than the 0.90+/-0.03 mmol/L for control patients (p < .01). Total blood calcium was below normal in both groups; ionized calcium was below normal in CRRT patients. CONCLUSIONS: CRRT caused significant loss of magnesium and calcium, necessitating administration of more magnesium and calcium than was provided in standard parenteral nutrition formulas. However, additional zinc was not required. CRRT removed amounts of urea nitrogen similar to amounts removed by normally functioning kidneys.