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Response to aluminum in parenteral nutrition during infancy
Insights
Parenteral nutrition (PN) solutions contain aluminum (Al). Infants receiving PN showed increased urine Al and elevated serum Al, indicating incomplete aluminum elimination and potential bone deposition.
Area of Science:
- Neonatal Medicine
- Clinical Chemistry
- Toxicology
Background:
- Parenteral nutrition (PN) is essential for many infants but can be a source of aluminum (Al) exposure.
- Aluminum contamination in PN solutions is a concern, particularly for vulnerable infant populations.
Purpose of the Study:
- To assess aluminum (Al) loading and elimination in infants receiving parenteral nutrition (PN).
- To investigate the impact of different Al loads from PN solutions on infant Al levels.
Main Methods:
- Measured aluminum (Al) content in PN solutions administered to 20 infants (gestational age 29-41 weeks).
- Monitored urine Al/creatinine (Cr) ratios and serum Al concentrations during PN.
- Analyzed autopsy bone samples for Al deposition in two infants.
Main Results:
- Urine Al/Cr ratio significantly increased threefold during PN (P < 0.001), correlating with higher Al load.
- Serum Al concentrations were elevated compared to normal infants but did not significantly change during the study.
- Bone mineralization fronts stained positive for Al in infants with prolonged PN exposure, indicating deposition.
Conclusions:
- Parenteral nutrition solutions are a source of aluminum (Al) contamination.
- Infants exhibit incomplete renal elimination of Al, evidenced by elevated serum Al and bone deposition.
- Al loading and subsequent elimination do not significantly differ between preterm and term infants.
Abstract:
The response to aluminum loading from parenteral nutrition (PN) solutions was determined in 20 infants with gestational ages 29 to 41 weeks and birth weights 880 to 3630 gm. Mean duration of PN was 43 days (range 5 to 175 days). Ten infants received a high Al load (from an experimental high calcium- and phosphorus-containing PN solution, with a measured Al content of 306 +/- 26 micrograms/L (mean +/- SE), n = 11), for up to 6 weeks. Ten infants received a lower Al load (from standard Ca-P solutions, measured Al content 144 +/- 16 micrograms/L, n = 11). Five infants received PN with a low Al load for longer than 6 weeks. The mean urine Al/creatinine (Cr) ratio (micrograms/mg) increased threefold, from 0.3 +/- 0.09 to 0.97 +/- 0.17 during PN in the entire group (P less than 0.001), and was significantly higher in infants who received greater Al loading (P less than 0.001). There was no significant difference between preterm and term infants in the rate of change in urine Al/Cr during the study. Urine Al was calculated to account for less than 50% of Al load. During the study, serum Al concentrations ranged from 6 to 318 micrograms/L (median 37 micrograms/L, compared with the median 18 micrograms/L for normal infants and children). Serum Al concentrations were not significantly changed during the study, or between infants in high or lower Al loading groups. Vertebrae from autopsy of two infants who received the lower Al containing PN for 71 and 152 days, respectively, stained positive for Al at the bone mineralization front. Thus, currently used PN solutions are contaminated with Al, urine Al concentration is higher with higher Al loading, and is not different in term and preterm infants. We suggest that renal elimination of Al in infants is incomplete, as assessed by lower urine Al excretion versus load, elevated serum Al concentration, and bone deposition of Al.