The Absorption and Excretion of Tocopherol

The plasma tocopherol level is often low in cirrhosis (1, 2). Whether such low values reflect alterations in the absorption, utilization or excretion of tocopherol related to liver damage, or are the result of a decreased dietary intake is not known. Previous attempts to investigate tocopherol metabolism in liver disease have been limited to tests of tocopherol tolerance based on plasma curves (1, 2) and have shed little light on the problem, largely because tolerance tests cannot be interpreted in terms of absorption and utilization without parallel studies of excretion and storage. The present report is concerned with the results of such studies in Laennec's cirrhosis. These have been made possible by the recent development of analytical methods for the determination of tocopherol in excreta. In a preliminary investigation (1) of a group of subjects with a variety of liver diseases, including Laennec's cirrhosis, it was found that the plasma tocopherol level was significantly lower than in young healthy adults, but that it did not differ significantly from that of randomly-selected, hospitalized convalescent controls without evidence of liver disease. Moreover, there was no correlation between the plasma level and the degree of hepatic dysfunction, suggesting that low levels might be related to extrahepatic factors. Oral tocopherol tolerance tests were carried out to exclude impairment of absorption as one of these factors. These revealed relative flat plasma curves, but the lack of any correlation between the height of the curve and the original plasma level did not appear to be consistent with the interpretation that low plasma concentrations were the result of impaired absorption. Attempts to investigate tocopherol utilization by means of parenteral tolerance tests 1 Supported by research grants from Hoffmann-La Roche, Inc., Nutley, N. J., and the National Institutes of Health, U. S. Public Health Service. 2 Present address: Pack Medical Group, New York, N. Y. were unsuccessful, because none of the available preparations of tocopherol could be used intravenously, and none was freely absorbed from muscle. No definite conclusions could be drawn from these observations, but it was suggested that the low plasma levels seen in some subjects with liver disease might be the result of a reduced dietary intake of tocopherol. The present study was limited to Laennec's cirrhosis, since there was reason to believe that alterations in tocopherol metabolism might differ in the various hepatic disease groups previously investigated. The results indicate that there is no impairment of tocopherol absorption or storage in the cirrhotic, and suggest that low plasma tocopherol levels are probably indicative of depleted tissue stores related to a deficient dietary intake.