A 17-year-old woman with phenytoin-induced hepatotoxicity was compared with 23 other cases from the literature. Hepatic injury caused by phenytoin is rare but important because of its significant morbidity and mortality. A typical multisystem clinical pattern precedes the manifestations of hepatic dysfunction. Pathologic findings indicate a mixed hepatocellular damage of cholestasis and necrosis. Pathogenic mechanisms are unexplained, but a delayed hypersensitivity reaction appears likely.
A study of the level and availability of trace elements in commercial and compounded hyperalimentation solutions was performed. Analyses of the zinc, copper, and manganese content of Aminosol®, Amigen®, Cutter Protein Hydrolysate®, and FreAmine II® were carried out using atomic absorption spectrophotometry. Zinc was found to be present in the highest concentrations in the solutions and copper in the lowest. Although the concentrations of a particular element varied between batches of a given solution, there was a greater variation in concentrations between the different nitrogen sources. No loss of trace elements by precipitation or absorption occurred following their addition to a compounded hyperalimentation solution. A suggested trace element solution for supplementation to a compounded TPN preparation is presented.
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