Aluminum in Total Parenteral Nutrition Solutions Produces Portal Inflammation in Rats

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Abstract

Background:

Aluminum contaminates parenteral nutrition solutions and accumulates in bone and liver of patients receiving total parenteral nutrition therapy. Although previous reports have shown that parenteral administration of aluminum in pharmacologic doses to rats results in the production of elevated total serum bile acid concentrations alone or in combination with decreased bile flow, they have failed to demonstrate any abnormalities in the histologic appearance of liver tissue. The effects of aluminum in total parenteral nutrition and of aluminum chloride on total serum bile acid concentrations, aluminum contents of the liver, and histopathologic changes in the liver were studied in rats.

Methods:

The aluminum concentrations in the aluminum chloride solution and total parenteral nutrition formula were equal (300 μg/l). They were given intraperitoneally as follows: control group, 0.9% saline for 14 days; T7 group, total parenteral nutrition for 7 days; A7 group, aluminum chloride for 7 days; A14 group, aluminum chloride for 14 days; T7A7 group, total parenteral nutrition for 7 days and aluminum chloride for the next 7 days; and T7O7 group, total parenteral nutrition for 7 days and 0.9% saline for the next 7 days. Volumes of 0.9% saline, aluminum chloride, and total parenteral nutrition given to rats were equal. During the experiment, rats were maintained on rat chow and water ad libitum. Serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, alkaline phosphatase, and bile acid concentrations and aluminum content of the liver were measured. The liver was evaluated histopathologically by light microscope, and a morphologic portal inflammation index was calculated.

Results:

Portal inflammation was present in all groups except the control group. The morphologic portal inflammation correlated with hepatic aluminum accumulation in all groups and was the highest in the T7A7 group. Levels of serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, and alkaline phosphatase did not correlate with the histopathologic findings, but serum bile acid concentrations correlated with morphologic portal inflammation and hepatic aluminum accumulation in all groups. Hepatic aluminum accumulation also correlated with the duration of exposure to total parenteral nutrition and aluminum chloride concentration.

Conclusion:

Aluminum in contaminating doses, not in pharmacologic doses, accumulates in the liver and can produce hepatobiliary dysfunction characterized by portal inflammation detectable in histologic examination of liver tissue.

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