Outcomes analysis for 50 liver transplant recipients: the Vanderbilt experience.

Healthcare reform has mandated scrutiny of the fiscal aspects of patient care as well as medical outcomes. Therefore, we reviewed our experience with 50 liver transplant recipients from a multidisciplinary collaborative transplant team. From February 1991 to July 1994, of 175 patients referred, 75 were formally evaluated for transplantation; 56 (76%) of these patients were accepted for transplantation; 50 patients underwent 53 transplants. Operative mortality of 6 per cent, retransplantation rate of 6 per cent, 6-month actuarial survival of 88 per cent, 1-year survival of 86 per cent, and the 2 and 3-year survival of 83 per cent were unchanged over time. Quality of life evaluated by the Karnofsky Performance Status was a mean of 55 pretransplant, 72 at 3 months, 79 at 6 months, 84 at 1 year, 88 at 2 years, and 95 at 3 years, demonstrating improved general health and functional rehabilitation after transplantation. Psychosocial Adjustment to Illness Scale scores demonstrated significant improvement following transplantation, improving most dramatically in the vocation environment, domestic environment, and sexual relationship domains. Postoperative length of stay has declined with an average of 28 days in 1991, 22 days in 1992, 19 days in 1993, and 14 days in 1994. Average total hospital, organ procurement, and physician charges for the transplantation hospitalization was $165,000. Average 91-92 hospital charges were $154,000 and were reduced in 93-95 to $103,000 (P < .05). We found that charges and length of stay decreased over time, while the outcome and quality of patient care was maintained. We believe the collaborative practice, case management, and revised patient care protocols are responsible.

Selenoprotein P concentration in plasma is an index of selenium status in selenium-deficient and selenium-supplemented Chinese subjects.

Selenoprotein P, a selenium-rich plasma protein, is an index of selenium status in rats. Antibodies against human selenoprotein P were raised to study the protein and to develop a radioimmunoassay for it. A single collection of plasma from a healthy person in the United States contained 1.84 mumol selenium/L and was defined as containing 1 Unit (U) selenoprotein P/L. Removal of selenoprotein P from the reference plasma by an antibody column indicated that 0.81 mumol selenium/L, or 44% of the plasma selenium, was present as selenoprotein P. Work by others had determined that glutathione peroxidase accounted for 12% of plasma selenium. Stored plasma samples from selenium-deficient (Dechang County) and selenium-supplemented (Mianning County) populations in China were assayed for selenoprotein P. Boys aged 8-12 y had selenoprotein P concentrations of 0.10 +/- 0.04 U/L (n = 22) in Dechang and 0.39 +/- 0.17 U/L (n = 17) in Mianning. Supplementation with 100 micrograms selenium as selenate per day for 14 d raised those levels to 0.51 +/- 0.13 U/L in Dechang and to 0.76 +/- 0.27 U/L in Mianning. Similar results were obtained in men, and plasma selenium concentrations correlated with selenoprotein P concentrations. A study comparing indices of selenium status was conducted in the two counties. Selenoprotein P concentration in Dechang subjects (n = 79) was 36% of that in Mianning subjects (n = 117). For plasma glutathione peroxidase activity the value was 54%; for plasma selenium, 47%; and for whole blood selenium, 64%. We conclude that selenoprotein P is the major selenoprotein in human plasma and that its concentration is an index of selenium nutritional status that appears to be as sensitive as other indices in common use.

Pathogenesis of diquat-induced liver necrosis in selenium-deficient rats: assessment of the roles of lipid peroxidation and selenoprotein P.

A dose of diquat below the amount injurious to selenium-replete animals causes lipid peroxidation and massive liver necrosis in selenium-deficient rats. The current study was undertaken to characterize the lipid peroxidation with respect to the liver injury and to correlate the presence of several selenoproteins with the protective effect of selenium. Lipid peroxidation was assessed by measurement of F2 isoprostanes. Diquat caused an increase in liver and plasma F2 isoprotanes. A gradient of these compounds was detected across the liver in some animals, indicating that this organ was a source of some of the plasma F2 isoprostanes. A time-course experiment showed that liver F2 isoprostane concentration increased before plasma alanine transaminase (ALT) levels rose. Selenium-deficient rats were injected with selenium doses from 2 to 50 micrograms/kg and studied 12 hours later. A dose of 10 micrograms/kg or more prevented diquat-induced lipid peroxidation and liver injury. This dose increased plasma selenoprotein P substantially, and a dose-response was present. Liver cellular and plasma glutathione peroxidase activities remained below 2% of their values in control rats for all selenium doses. In selenium-deficient rats given diquat, hepatic lipid peroxidation precedes hepatic necrosis and could therefore be an important mechanism of the necrosis. Selenoprotein P levels were increased by selenium injections, which protected against diquat injury, but glutathione peroxidase activity was not increased. This is consistent with selenoprotein P being the mediator of the selenium effect.