Determination of serum bile acids routinely may prevent delay in diagnosis of total parenteral nutrition-induced cholestasis.

BACKGROUND/PURPOSE: Early diagnosis of development of cholestasis is a current major problem for patients receiving total parenteral nutrition (TPN). Conventional tests for hepatic function such as serum transaminases and alkaline phosphatase do not often reflect simultaneously histopathologic changes of the liver. The aim of this study is to find out the relationships between conventional hepatic function tests, total serum bile acid concentrations (TSBA), and the histopathologic changes in the liver during TPN administration in rats. METHODS: Forty Albino rats were divided into four experimental groups, each consisting of 10 rats, as follows: control group (C), 0.9% saline for 14 days; T7 group, TPN for 7 days; T14 group, TPN for 14 days; T7O7 group, TPN for 7 days and then 0.9% saline for the next 7 days. All solutions were administered by infusion through intraperitoneal catheter in two equal doses. During the experiment, rats also maintained on rat chow and water ad libitum. Levels of serum glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, alkaline phosphatase, and TSBA were measured. Liver was evaluated histopathologically by light microscope and then Morphological Cholestasis Index (MCI) was calculated. RESULTS: Cholestasis was present in all experimental groups except control. Levels of transaminases and alkaline phosphatase were not correlated with the histopathologic changes (P > .05), but TSBA concentrations were correlated with MCI in all groups (P< .01). TSBA concentrations and MCI in all groups also were correlated with the duration of exposure with TPN (P< .01). CONCLUSIONS: Measurement of TSBA seems to be more sensitive in early diagnosis of TPN-induced cholestasis. Therefore, periodical determination of TSBA during TPN administration can be done routinely.

Aluminum in total parenteral nutrition solutions produces portal inflammation in rats.

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 microg/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.