Infant Parenteral Nutrition Remains a Significant Source for Aluminum Toxicity.

BACKGROUND: Aluminum toxicity is associated with anemia, impaired bone metabolism, neurologic defects, and parenteral nutrition (PN)-associated liver disease. This element is a ubiquitous contaminant of PN components, especially in infant formulations. We assessed the current levels of aluminum contamination in infant PN at a level III neonatal intensive care unit. MATERIALS AND METHODS: Thirty samples of PN prepared in the same hospital for infants aged <30 days (mean [SD] weight, 1.54 [0.71] kg) were collected from discarded solution. Each sample was analyzed for aluminum content via inductively coupled plasma mass spectrometry. The components of PN (from label) and measured aluminum content were then compared using linear regression and 1-way analysis of variance. RESULTS: The mean (SD) aluminum contamination of infant PN was 14.02 (6.51) mcg/kg/d. Only 3 samples were <5 mcg/kg/d. Aluminum levels and infant weight were not associated. Linear regression revealed a significant correlation between aluminum and both calcium gluconate ( P < .0001) and phosphate ( P = .05), with a trend between aluminum and potassium ( P = .07). CONCLUSIONS: Aluminum contamination in infant PN remains almost 3 times higher than the advised maximum exposure (<5 mcg/kg/d, Food and Drug Administration 2004). Unexpectedly, an association between infant weight and aluminum exposure was not apparent, likely due to the homogeneity of our population. Isolating the source of aluminum contamination is difficult, as multiple components appear to be involved. Calcium gluconate is likely still a major contributor, but further investigations into individual components are warranted to promote the reduction of aluminum in infant PN.

Reduced aluminum contamination decreases parenteral nutrition associated liver injury.

PURPOSE: Parenteral nutrition-associated cholestasis remains a significant problem, especially for the surgical neonates. Aluminum is a toxic element known to contaminate parenteral nutrition. We hypothesize that parenterally administered aluminum causes liver injury similar to that seen in parenteral nutrition-associated cholestasis. METHODS: Twenty 3- to 6-day-old domestic pigs were divided into 5 equal groups. A control group received daily intravenous 0.9% NaCl. Each subject in experimental groups received intravenous aluminum chloride at 1500 µg kg(-1) d(-1) for 1, 2, 3, or 4 weeks. At the end of the study, blood was sampled for direct bilirubin and total bile acid levels. Liver, bile, and urine were sampled for aluminum content. Liver tissue was imaged by transmission electron microscopy for ultrastructural changes. RESULTS: Transmission electron microscopy revealed marked blunting of bile canaliculi microvilli in all experimental subjects but not the controls. Serum total bile acids correlated with the duration of aluminum exposure. The hepatic aluminum concentration correlated with the duration of aluminum exposure. CONCLUSIONS: Parenterally infused aluminum resulted in liver injury as demonstrated by elevated bile acids and by blunting of the bile canaliculi microvilli. These findings are similar to those reported in early parenteral nutrition-associated liver disease.

Parenteral aluminum induces liver injury in a newborn piglet model.

PURPOSE: Parenteral nutrition-associated cholestasis remains a significant problem, especially for the surgical neonate. Aluminum is a toxic element known to contaminate parenteral nutrition. We hypothesize that parenterally administered aluminum causes liver injury similar to that seen in parenteral nutrition-associated cholestasis. METHODS: Twenty 3- to 6-day-old domestic pigs were divided into 5 equal groups. A control group received daily intravenous 0.9% sodium chloride. Each subject in experimental groups received intravenous aluminum chloride at 1500 µg/kg per day for 1, 2, 3, or 4 weeks. At the end of the study, blood was sampled for direct bilirubin and total bile acid levels. Liver, bile, and urine were sampled for aluminum content. Liver tissue was imaged by transmission electron microscopy for ultrastructural changes. RESULTS: Transmission electron microscopy revealed marked blunting of bile canaliculi microvilli in all experimental subjects but not the controls. Serum total bile acids correlated with the duration of aluminum exposure. The hepatic aluminum concentration correlated with the duration of aluminum exposure. CONCLUSIONS: Parenterally infused aluminum resulted in liver injury as demonstrated by elevated bile acids and by blunting of the bile canaliculi microvilli. These findings are similar to those reported in early parenteral nutrition-associated liver disease.

Effects of thickened beverages fortified with inulin on beverage acceptance, gastrointestinal function, and bone resorption in institutionalized adults.

OBJECTIVES: We wanted to develop thickened beverages that contain soluble fiber (inulin) with acceptable consistency, taste, and texture and to determine the effects of these beverages on bone resorption markers (to determine calcium retention), bowel frequency, and indicators of gastrointestinal function in institutionalized adults bound to wheelchairs. METHODS: A double-blind, 3-wk, cross-over study testing 13-g/d inulin-fortified versus isocaloric standard modified starch-thickened beverages was conducted in institutionalized adults who were bound to wheelchairs and had dysphagia or did not have dysphagia. Beverage acceptability, as assessed by discriminative and descriptive sensory testing, bowel frequency, fecal output, and laxative use, were determined by direct testing or by nursing charts. Bone resorption was measured by using the urinary excretion of fasting calcium and of cross-linked N-telopeptides of collagen. RESULTS: Sensory panelists were unable to detect a difference between beverages thickened with modified starch and those fortified with inulin. Few differences were found between the control and inulin-fortified beverages for sensory descriptors. No significant difference was found in frequency of bowel movements between treatments; however, weighted bowel movement frequency increased by 13% with inulin (P < 0.01), whereas enema and laxative administration decreased by 13% (P < 0.05). Bone resorption, as an indicator of calcium retention, remained unchanged. CONCLUSIONS: Inulin was incorporated into thickened beverages, with no decrease in acceptability; when consumed, perceived stool output increased in residents of long-term care facilities.

Parenteral nutrition-associated cholestasis in neonates: the role of aluminum.

Parenteral nutrition (PN) is an essential component in the care of premature and ill infants. The incidence of parenteral nutrition-associated cholestasis (PNAC) ranges from 7.4 to 84%. One substance in PN solutions that has been implicated in PNAC is aluminum. Aluminum loading in animals and humans causes hepatic accumulation and damage. The degree of aluminum contamination of PN solutions has decreased over time, but contamination still significantly exceeds levels that are safe for human neonates. Further study into the relationship between aluminum contamination in neonatal PN solutions and the development of PNAC is necessary.