Management strategies in the care of the ill elderly: a case study review.
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Biomedical subjects
Publications and source records attributed to M K Brown.
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Previous studies with methyl ethyl ketone peroxide (MEKP), a radical generator, showed depletion of plasma vitamin E and liver glutathione (GSH) levels prior to a decrease of liver vitamin E levels. Since hepatic pools of this vitamin may serve to maintain circulating levels of vitamin E under conditions of oxidative challenge, we have evaluated the similarity of response after treatment with 1,2-dibromoethane (DBE), a compound that is not known to generate oxyradicals or to induce lipid peroxidation in vivo. Treatment of normal rats with DBE caused a depletion in hepatic vitamin E levels 1 day after treatment; however, in contrast to our prior findings with MEKP this depletion after DBE treatment was observed in tandem with elevations in the plasma content of vitamin E. Liver vitamin E depletion was neither dependent upon a sustained liver GSH depletion nor upon hepatocellular death. Mobilization and export of hepatic vitamin E did not result in an immediate whole body redistribution of this vitamin in that pulmonary and renal levels of vitamin E remained normal under conditions of liver vitamin E depletion. Moreover, the stimulus that resulted in exportation of liver vitamin E was maintained by daily treatments with DBE. DBE caused a substantial elevation above control values in liver GSH content and these elevations were also maintained by daily DBE treatments. In experiments to assess the influence of prandial replacement of vitamin E on the extent of depletion in response to DBE treatment, rats were fed a vitamin E-deficient diet for 2 days prior to treatment. This short pulse of a vitamin E-deficient diet delayed (to 2 days) both the elevation in liver GSH content and the depletion of liver vitamin E and hastened (to 1 day) the elevation in plasma vitamin E concentration. These observations suggest the presence of at least two pools of liver vitamin E and that one of these pools, which comprises at least 30% of the total hepatic vitamin E content, is able to be mobilized and exported in response to chemical challenge. The stimulus that resulted in liver vitamin E exportation in response to DBE treatment seems to result from wholly intrahepatic processes and may not be a direct response to lipid peroxidation. Moreover, the similarity between the time-course and the extent of hepatic vitamin E depletion observed after treatment with either MEKP or DBE suggests a similarity in physiochemical processes that function to mobilize hepatic vitamin E stores.
A radial immunodiffusion technique for detecting faecal haemoglobin and the Hemoccult II kit used with and without rehydration of the faecal sample were compared in a screening programme for bowel cancer, in which 1328 subjects took part. A positive result was obtained in 170 (13%) subjects. Nineteen of the 153 subjects investigated were found to have colorectal carcinomas and 52 had polyps (40 with adenomas). Radial immunodiffusion and Hemoccult II with and without rehydration detected bleeding in, respectively, all 19, 15, and 11 subjects with colorectal carcinoma. Hemoccult II with and without rehydration detected only seven and six, respectively, of 11 Duke's stage A carcinomas, whereas all 11 were detected with the immunological test. Hemoccult II with and without rehydration and radial immunodiffusion detected bleeding from adenomas in, respectively, 22, 14, and 34 of the 40 subjects. False positive results occurred in 55 out of 1302 subjects by Hemoccult II with rehydration, in 28 out of 1304 by Hemoccult II without rehydration, and in 50 out of 1304 by the immunological technique; true positive results were defined as bleeding from carcinomas and adenomas. Immunological detection of occult blood in faecal samples seems to show more adenomas and carcinomas (particularly early lesions) than the Hemoccult II kit and has a rate of false positive results that is acceptably low.
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