Aluminum in parenteral products: medical perspective on large and small volume parenterals

Abstract

Bone abnormalities may complicate parenteral nutrition (PN) therapy given to patients. Bone disease, manifested by reduced bone formation and demineralization in adults, and poor mineralization in infants, is associated with bone aluminum accumulation at the mineralizing surface. Aluminum was first shown to contaminate casein hydrolysate, the PN protein source. Substitution of amino acid solutions, low in aluminum, reduced bone aluminum and improved bone formation in adults. Aluminum also accumulates ten-fold in the bones of premature infants receiving chronic PN. Present sources of aluminum in PN are calcium and phosphate salts, albumin, and heparin. Although increased bone aluminum in infants is not proven to cause disease, use of deferoxamine in one infant produced hypocalcemia. This suggested that chelation of bone aluminum by deferoxamine increased bone calcium uptake. Thus aluminum in bone may impair bone calcium uptake and may contribute to the pathogenesis of PN-related bone disease in infants. Another complication of PN therapy in infants is cholestatic liver disease, manifested by reduced bile flow, and, occasionally, gallstones. Aluminum has been found to accumulate in the livers of these infants, and there is experimental evidence that aluminum can reduce bile flow both in rats and in piglets. Aluminum contamination of PN solutions puts infants at increased risk for complications of PN therapy; amounts of aluminum in PN solutions should therefore be minimized.