Hepatic Abnormalities Associated with Aluminum Loading in Piglets

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Abstract
Cholestasis is a common complication of total parenteral nutrition (TPN) in infants. A contributing factor to the hepatic dysfunction may be a contaminant of the TPN solution, such as aluminum, that accumulates in liver and may act as a hepatotoxin. To study the hepatic effects of aluminum, growing piglets were given daily intravenous injections of aluminum, 1.5 mg/kg, for 50 days; pair‐fed controls were given heparinized saline. At sacrifice, liver and serum were obtained. Liver was analyzed for histopathology and for aluminum content and localization. The hepatocyte lysosomes of the experimental group showed aluminum peaks by x‐ray microanalysis, whereas the control group did not. No differences in ultrastructure were noted between the two groups when examined by electron microscopy. Mean serum total bile acid levels (27.8 ± 15.9 SD vs 6.3 ± 1.5 μmol/liter, p < 0.05), mean alkaline phosphatase (309 ± 108 vs 180 ± 27 lU/liter, p = NS), and mean hepatic copper content (24.8 ± 4.5 vs 14.4 ± μg/g dry weight, p < 0.01), were elevated in the aluminum‐loaded piglets, indicating that cholestasis may have been produced. Also, a small but significant reduction in serum levels of 25 hydroxyvitamin D was found in the aluminum‐loaded piglets, suggesting that vitamin D hydroxylation may be impaired. Inasmuch as lysosomal contents are excreted into the bile, aluminum accumulation in lysosomes may alter lysosomal function and possibly affect bile flow or content. (Journal of Parenteral and Enteral Nutrition 11:293–297, 1987)