ALUMINUM IN TOTAL PARENTERAL-NUTRITION SOLUTIONS PRODUCES PORTAL INFLAMMATION IN RATS

Background: Aluminum contaminates parenteral nutrition solutions and a ccumulates in bone and Liver of patients receiving total parenteral nu trition therapy. Although previous reports have shown that parenteral administration of aluminum in pharmacologic doses to rats results in t he production of elevated total serum bile acid concentrations alone o r in combination with decreased bile flow, they have failed to demonst rate any abnormalities in the histologic appearance of liver tissue. T he effects of aluminum in total parenteral nutrition and of aluminum c hloride on total serum bile acid concentrations, aluminum contents of the liver, and histopathologic changes in the liver were studied in ra ts. Methods: The aluminum concentrations in the aluminum chloride solu tion and total parenteral nutrition formula were equal (300 mu g/l). T hey were given intraperitoneally as follows: control group, 0.9% salin e for 14 days, T-7 group, total parenteral nutrition for 7 days: A(7) group, aluminum chloride for 7 days; A(14) group, aluminum chloride fo r 14 days; T(7)A(7) group, total parenteral nutrition for 7 days and a luminum chloride for the next 7 days; and T7O7 group, total parenteral nutrition for 7 days and 0.9% saline for the ne,ut 7 days. Volumes of 0.9% saline, aluminum chloride, and total parenteral nutrition given to rats were equal. During the experiment, mts were maintained on rat chow and water ad libitum. Serum glutamic oxaloacetic transaminase, se rum glutamic pyruvic transaminase, alkaline phosphatase, and bile acid concentrations and aluminum content of the liver were measured. The l iver was evaluated histopathologically by light microscope, and a morp hologic portal inflammation index was calculated. Results: Portal infl ammation was present in all groups except the control group. The morph ologic portal inflammation correlated with hepatic aluminum accumulati on in all groups and was the highest in the T(7)A(7) group. Levels of serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transa minase, and alkaline phosphatase did not correlate with the histopatho logic findings, but serum bile acid concentrations correlated with mor phologic portal inflammation and hepatic aluminum accumulation in all groups. Hepatic aluminum accumulation also correlated with the duratio n of exposure to total parenteral nutrition and aluminum chloride conc entration. Conclusion: Aluminum in contaminating doses, not in pharmac ologic doses, accumulates in the liver and can produce hepatobiliary d ysfunction characterized by portal inflammation detectable in histolog ic examination of liver tissue.