Selenium in Intravenous Nutrition
2009; Elsevier BV; Volume: 137; Issue: 5 Linguagem: Inglês
10.1053/j.gastro.2009.07.071
ISSN1528-0012
Autores Tópico(s)Therapeutic Uses of Natural Elements
ResumoSelenium (Se) is an essential nutrient for human beings, with serious consequences resulting from clinical deficiency. It therefore should be provided intravenously to all patients who require parenteral nutrition (PN). Moreover, because the effects of suboptimal status are variable and unclear, this supplementation should be provided from the beginning of the course of PN. In most patients receiving PN at home or after surgery, 60–100 mcg/day will meet their requirements. Patients who commence PN already depleted in selenium may require more. Critically ill patients or those with severe burns may have higher requirements. There is good evidence that up to 400 mcg/day is beneficial in burn patients, but the evidence is inconclusive regarding the benefit of high-dose selenium in severe sepsis. Where increased Se provision is used, or in long-term PN, selenium status should be monitored by measurement of plasma Se together with a measure of systemic inflammatory response syndrome, such as C-reactive protein. There are many research issues, including which biochemical measurements best reflect tissue function, especially immune function in seriously ill patients, the clinical consequences of suboptimal biochemical Se status, whether high-dose Se improves outcome in critically ill patients, and whether extra Se always should be given with extra intakes of other antioxidants. Selenium (Se) is an essential nutrient for human beings, with serious consequences resulting from clinical deficiency. It therefore should be provided intravenously to all patients who require parenteral nutrition (PN). Moreover, because the effects of suboptimal status are variable and unclear, this supplementation should be provided from the beginning of the course of PN. In most patients receiving PN at home or after surgery, 60–100 mcg/day will meet their requirements. Patients who commence PN already depleted in selenium may require more. Critically ill patients or those with severe burns may have higher requirements. There is good evidence that up to 400 mcg/day is beneficial in burn patients, but the evidence is inconclusive regarding the benefit of high-dose selenium in severe sepsis. Where increased Se provision is used, or in long-term PN, selenium status should be monitored by measurement of plasma Se together with a measure of systemic inflammatory response syndrome, such as C-reactive protein. There are many research issues, including which biochemical measurements best reflect tissue function, especially immune function in seriously ill patients, the clinical consequences of suboptimal biochemical Se status, whether high-dose Se improves outcome in critically ill patients, and whether extra Se always should be given with extra intakes of other antioxidants. Selenium (Se) is required for synthesis of selenocysteine, now known as amino acid 21. The presence of a specific transfer RNA for incorporation of selenocysteine into mammalian proteins confirms the essential role it plays.1Kryukov G.V. Castellano S. Novoselov S.V. et al.Characterization of mammalian selenoproteomes.Science. 2003; 300: 1439-1443Crossref PubMed Scopus (1777) Google Scholar At least 25 selenoproteins exist in human tissues (Table 1). These fall into several classes, antioxidant enzymes (such as the glutathione peroxidases) and other putative antioxidant proteins (such as selenoprotein P and W), enzymes known to have other metabolic functions (eg, the iodothyronine deiodinases that regulate thyroid hormone metabolism and the thioredoxin reductases that regenerate reduced ascorbic acid), and many proteins for which the function is not yet known.2Beckett G.J. Arthur J.R. Selenium and endocrine systems.J Endocrinol. 2005; 184: 455-465Crossref PubMed Scopus (382) Google Scholar Although influencing function in all tissues, potentially of special importance clinically are the beneficial effects of Se on immune function and on reducing the risk of viral pathogenesis.3Rayman M.P. The argument for increasing selenium intake.Proc Nutr Soc. 2002; 61: 203-215Crossref PubMed Scopus (362) Google Scholar, 4Elsom R. Sanderson P. Hesketh J.E. et al.Functional markers of selenium status: UK Food Standards Agency workshop report.Br J Nutr. 2006; 96: 980-984Crossref PubMed Scopus (25) Google ScholarTable 1Mammalian Selenoproteins and Their FunctionsSelenoproteinProposed functionGlutathione peroxidases (GPXs)Antioxidants, remove hydroperoxides GPX1Antioxidant in cell cytosol, selenium store? GPX2Antioxidant in gastrointestinal tract GPX3Antioxidant in extracellular space and plasma GPX4Membrane antioxidant, structural protein in sperm, apoptosis? GPX6GPX1 homologue?Thioredoxin reductase (TRs)Multiple roles including dithiol-disulphide oxoreductaseDetoxifies peroxides, reduces thioredoxin (control of cell growth), maintains redox state of transcription factors TR1Mainly cytosolic, ubiquitous TR2Mitochondrial, ubiquitous TR3Expressed by testesIodothyronine deiodinasesProduction and regulation of active thyroid hormones Types D1 and D2Converts thyroxine (T4) to bioactive 3,5,3-tri-iodothyronine (T3) Types D1 and D3Converts thyroxine (T4) to bioinactive 3, 3, 5 reverse T3Selenoprotein PSelenium-transport protein, antioxidant on endotheliumSelenoprotein WAntioxidant in cardiac and skeletal muscle, and brain?Selenophosphate synthetase SPS2Synthesis of selenophosphate for selenocysteine and selenoprotein synthesis 15-kilodalton selenoproteinHigh levels in prostate H, I, K, M, N, O, R, S, T, VRole largely unknownAdapted from Beckett and Arthur2Beckett G.J. Arthur J.R. Selenium and endocrine systems.J Endocrinol. 2005; 184: 455-465Crossref PubMed Scopus (382) Google Scholar and Rayman.3Rayman M.P. The argument for increasing selenium intake.Proc Nutr Soc. 2002; 61: 203-215Crossref PubMed Scopus (362) Google Scholar Open table in a new tab Adapted from Beckett and Arthur2Beckett G.J. Arthur J.R. Selenium and endocrine systems.J Endocrinol. 2005; 184: 455-465Crossref PubMed Scopus (382) Google Scholar and Rayman.3Rayman M.P. The argument for increasing selenium intake.Proc Nutr Soc. 2002; 61: 203-215Crossref PubMed Scopus (362) Google Scholar The wide range of biochemical and physiologic functions inevitably has led to a variety of presentations of selenium deficiency. The earliest of these to be recognized was Keshan disease, a cardiomyopathy in selenium-poor parts of China, which was preventable by provision of oral selenium supplements.5Keshan Disease Research GroupObservations on effect of sodium selenite in prevention of Keshan disease.Chin Med J. 1979; 92: 471-476PubMed Google Scholar Since then there have been many case reports of Se deficiency during parenteral nutrition (PN), including fatal6Johnson R.A. Baker S.S. Fallon J.T. et al.An occidental case of cardiomyopathy and selenium deficiency.N Engl J Med. 1981; 304: 1210-1212Crossref PubMed Scopus (234) Google Scholar, 7Quercia R.A. Korn S. O'Neill D. et al.Selenium deficiency and fatal cardiomyopathy in a patient receiving long-term home parenteral nutrition.Clin Pharm. 1984; 3: 531-535PubMed Google Scholar or reversible8Reeves W.C. Marcuard S.P. Willis S.E. et al.Reversible cardiomyopathy due to selenium deficiency.JPEN J Parenter Enteral Nutr. 1989; 13: 663-665Crossref PubMed Scopus (65) Google Scholar cardiomyopathy, skeletal muscle myopathy,9van Rij A.M. Thomson C.D. McKenzie J.M. et al.Selenium deficiency in total parenteral nutrition.Am J Clin Nutr. 1979; 32: 2076-2085Crossref PubMed Scopus (301) Google Scholar, 10Brown M.R. Cohen H.J. Lyons J.M. et al.Proximal muscle weakness and selenium deficiency associated with long term parenteral nutrition.Am J Clin Nutr. 1986; 43: 549-554PubMed Google Scholar abnormalities in nails11Kien C.L. Ganther H.E. Manifestations of chronic selenium deficiency in a child receiving total parenteral nutrition.Am J Clin Nutr. 1983; 37: 319-328PubMed Google Scholar and hair,12Vinton N.E. Dahlstrom K.A. Strobel C.T. et al.Macrocytosis and pseudoalbinism: manifestations of selenium deficiency.J Pediatr. 1987; 111: 711-717Abstract Full Text PDF PubMed Scopus (95) Google Scholar and macrocytic anemia.12Vinton N.E. Dahlstrom K.A. Strobel C.T. et al.Macrocytosis and pseudoalbinism: manifestations of selenium deficiency.J Pediatr. 1987; 111: 711-717Abstract Full Text PDF PubMed Scopus (95) Google Scholar An intriguing feature of these deficiency states is that only a small proportion of patients with very poor Se status develop clinical signs of deficiency, and it now is believed that some other agent or stressor is required to provoke symptoms.13Beck M.A. Levander O.A. Dietary oxidative stress and the potentiation of viral infection.Annu Rev Nutr. 1998; 18: 93-116Crossref PubMed Scopus (68) Google Scholar Selenium deficiency has been shown probably to cause mutation of benign Coxsackie virus to a virulent myocarditis-producing form.14Beck M.A. Levander O.A. Handy J. Selenium deficiency and viral infection.J Nutr. 2003; 133: 1463S-1467SPubMed Google Scholar Most of the deficiency states in clinical practice occur in relatively short-term, severe Se deficiency. There is also growing interest in the potential role of Se in many chronic diseases, and whether optimizing Se status in populations with subclinical Se deficiency (ie, poor status but no clinical signs of Se deficiency) may reduce the risk of certain cancers, heart disease, reproductive problems, and cognitive decline.15Rayman M.P. Food-chain selenium and human health: emphasis on intake.Br J Nutr. 2008; 100: 254-268PubMed Google Scholar This clearly is relevant to the large number of patients receiving long-term home PN. Despite early optimism that selenium supplements may reduce the incidence especially of prostate cancer,16Clark L.C. Combs Jr, G.F. Turnbull B.W. et al.Nutritional Prevention of Cancer Study GroupEffects of selenium supplementation for cancer prevention in patients with carcinoma of the skin A randomized controlled trial.JAMA. 1996; 276: 1957-1963Crossref PubMed Google Scholar the results of the recently published Selenium and Vitamin E Cancer Prevention Trial strongly suggest that selenium supplements, with or without added vitamin E, are ineffective in cancer prevention in an otherwise healthy population.17Lippman S.M. Klein E.A. Goodman P.J. et al.Effect of selenium and vitamin E on risk of prostate cancer and other cancers: the Selenium and Vitamin E Cancer Prevention Trial (SELECT).JAMA. 2009; 301: 39-51Crossref PubMed Scopus (1658) Google Scholar Nonetheless, further research is needed. A number of tests are available to assess Se status. Total plasma Se is the most widely used test of Se status. It reflects the amount of Se in plasma selenoproteins, the major components being selenoprotein P, which comprises more than 50% of the total, and extracellular glutathione peroxidase (GSHPx-3). At a concentration less than 7 μg/dL (0.8 μmol/L), the plasma concentration correlates with the dietary Se intake. At a concentration greater than 7 μg/dL, the tissue concentration of selenoproteins tends to plateau, and it is concluded that Se requirements largely have been met.18Food and Nutrition Board IoMDietary reference intakes for vitamin C, vitamin E, selenium, and carotenoids. National Academy Press, Washington, DC2000Google Scholar Plasma and indeed tissue measurements of Se need to be treated with some caution because organic Se in the form of selenomethionine may be incorporated nonspecifically into proteins in place of methionine, without reflecting a change in functional selenoproteins.19Thomson C.D. Assessment of requirements for selenium and adequacy of selenium status: a review.Eur J Clin Nutr. 2004; 58: 391-402Crossref PubMed Scopus (562) Google Scholar In patients receiving inorganic Se as part of PN this would not be an issue. In interpreting plasma Se concentrations in patients, it is important to note that trauma or systemic inflammatory response syndrome causes an obligatory decrease in Se level, and resolution of this leads to an increase in Se.20Nichol C. Herdman J. Sattar N. et al.Changes in the concentrations of plasma selenium and selenoproteins after minor elective surgery: further evidence for a negative acute phase response?.Clin Chem. 1998; 44: 1764-1766PubMed Google Scholar, 21Forceville X. Vitoux D. Gauzit R. et al.Selenium, systemic immune response syndrome, sepsis, and outcome in critically ill patients.Crit Care Med. 1998; 26: 1536-1544Crossref PubMed Scopus (286) Google Scholar This seems likely to be owing to transcapillary escape and redistribution of selenoproteins, similar to the effects of systemic inflammatory response syndrome on plasma albumin level.22Fleck A. Raines G. Hawker F. et al.Increased vascular permeability: a major cause of hypoalbuminaemia in disease and injury.Lancet. 1985; 1: 781-784Abstract PubMed Scopus (630) Google Scholar Hence, as with other trace elements, caution must be used in interpreting a single plasma Se result in a patient with ongoing acute illness. Greater accuracy of interpretation can be achieved by measuring plasma C-reactive protein levels at the same time, and monitoring sequential Se concentrations relative to changes in C-reactive protein level.23Shenkin A. Trace elements and inflammatory response: implications for nutritional support.Nutrition. 1995; 11: 100-105PubMed Google Scholar, 24Galloway P. McMillan D.C. Sattar N. Effect of the inflammatory response on trace element and vitamin status.Ann Clin Biochem. 2000; 37: 289-297Crossref PubMed Scopus (148) Google Scholar Extracellular GSHPx-3 can be measured in plasma readily and accurately, and responds rapidly to changes in Se intake.25Cohen H.J. Chovaniec M.E. Mistretta D. et al.Selenium repletion and glutathione peroxidase—differential effects on plasma and red blood cell enzyme activity.Am J Clin Nutr. 1985; 41: 735-747Crossref PubMed Scopus (48) Google Scholar It therefore correlates closely to plasma Se concentration, although contributing less than 20% to the total plasma Se.26Burk R.F. Hill K.E. Motley A.K. Plasma selenium in specific and non-specific forms.Biofactors. 2001; 14: 107-114Crossref PubMed Scopus (141) Google Scholar GSHPx-1 measurement has been found to correlate more with selenium intake over a longer period relating to the life span of the erythrocyte.25Cohen H.J. Chovaniec M.E. Mistretta D. et al.Selenium repletion and glutathione peroxidase—differential effects on plasma and red blood cell enzyme activity.Am J Clin Nutr. 1985; 41: 735-747Crossref PubMed Scopus (48) Google Scholar It therefore reflects status over a longer term than plasma measurements. It is more difficult to measure accurately than plasma GSHPx-1. Selenoprotein P is the major selenoprotein in plasma and is optimized more slowly than GSHPx. It is probably a good marker of adequacy of Se intake,27Burk R.F. Hill K.E. Selenoprotein P: an extracellular protein with unique physical characteristics and a role in selenium homeostasis.Annu Rev Nutr. 2005; 25: 215-235Crossref PubMed Scopus (442) Google Scholar but assays are not widely available so it is not used in clinical practice. Because of limitations in the reliability of sampling and complexity of analysis, measurements of Se in hair and nails are confined to use in a research setting. Before its recognition as an essential element in nutrition, Se was noted for its toxic effects in areas of the world with high soil Se content.28Burk R.F. Norsworthy B.K. Selenium.in: Coates P.M. Moss J. Encyclopedia of dietary supplements. Marcel Dekker, New York2005: 645-652Google Scholar Although at physiologic concentrations Se has antioxidant activity, at very high concentrations it can function as a pro-oxidant and cause oxidative damage to cells and tissues.29Forceville X. Effects of high doses of selenium, as sodium selenite, in septic shock patients a placebo-controlled, randomized, double-blind, multi-center phase II study—selenium and sepsis.J Trace Elem Med Biol. 2007; 21: 62-65Crossref PubMed Scopus (56) Google Scholar High blood or plasma Se concentration is helpful in assessing potential toxicity, but the lack of relationship with intake at high levels limits the accuracy of such measurements in assessing total exposure. Inorganic selenium (eg, selenite) is more likely to cause toxicity than organic forms (eg, selenomethionine). However, in patients with clinical signs of chronic toxicity (hair loss and brittle nails), plasma concentration is likely to be very high, about 10 times the upper limit of normal.30Yang G. Zhou R. Further observations on the human maximum safe dietary selenium intake in a seleniferous area of China.J Trace Elem Electrolytes Health Dis. 1994; 8: 159-165PubMed Google Scholar If the plasma concentration is greater than 16 μg/dL (2 μmol/L) for a prolonged period as a result of high intake, this should be monitored and attenuated if possible. From studies in regions of selenosis, a no-observed-adverse-effect-level of 800 μg/day was identified, including an uncertainty factor of 2 in the calculations leads to a tolerable upper intake level of 400 μg/day,18Food and Nutrition Board IoMDietary reference intakes for vitamin C, vitamin E, selenium, and carotenoids. National Academy Press, Washington, DC2000Google Scholar which is the highest level of daily intake likely to pose no risk of adverse health effects. Establishing the dietary requirement for Se has been a controversial process, mainly because of the different approaches used, with the aim either of preventing clinical deficiency symptoms or of optimizing biochemical function.19Thomson C.D. Assessment of requirements for selenium and adequacy of selenium status: a review.Eur J Clin Nutr. 2004; 58: 391-402Crossref PubMed Scopus (562) Google Scholar The minimum amount thought to be necessary for good health initially was set at 20 μg/day, this being the intake in adults in areas where Keshan disease does not occur in children.18Food and Nutrition Board IoMDietary reference intakes for vitamin C, vitamin E, selenium, and carotenoids. National Academy Press, Washington, DC2000Google Scholar However, a more physiologic approach is to determine the amount necessary to optimize function of the various selenoproteins.18Food and Nutrition Board IoMDietary reference intakes for vitamin C, vitamin E, selenium, and carotenoids. National Academy Press, Washington, DC2000Google Scholar, 19Thomson C.D. Assessment of requirements for selenium and adequacy of selenium status: a review.Eur J Clin Nutr. 2004; 58: 391-402Crossref PubMed Scopus (562) Google Scholar A New Zealand study suggested that to optimize plasma GSHPx requires an average intake of 68 μg/day, and allowing for dietary variation this led to an upper estimated requirement of 90 μg/day.31Duffield A.J. Thomson C.D. Hill K.E. et al.An estimation of selenium requirements for New Zealanders.Am J Clin Nutr. 1999; 70: 896-903PubMed Google Scholar A similar Chinese study suggested 52 μg/day.32Yang G.Q. Zhu L.Z. Liu L.Z. et al.Human selenium requirements in China.in: Combs G.F. Spallholtz J.E. Levander O.A. Selenium in biology and medicine. Nostrand Reinhold, New York1987: 587-607Google Scholar Interpretation of these studies is complex,19Thomson C.D. Assessment of requirements for selenium and adequacy of selenium status: a review.Eur J Clin Nutr. 2004; 58: 391-402Crossref PubMed Scopus (562) Google Scholar but taken overall the data from these studies led to the US recommendation of 55 μg/day.18Food and Nutrition Board IoMDietary reference intakes for vitamin C, vitamin E, selenium, and carotenoids. National Academy Press, Washington, DC2000Google Scholar A more recent report from Australia and New Zealand recommends a dietary intake of 70 μg/day in men and 60 μg/day in women.33National Health and Medical Research CouncilNutrient reference values for Australia and New Zealand, including recommended dietary intakes. Ministry of Health, Canberra, Australia2006Google Scholar There is uncertainty whether an intake that achieves 66% of maximal activity of plasma GSHPx, the approach taken by the World Health Organization (WHO)/Food and Agriculture Organization (FAO),34WHO/FAO/IAEATrace elements in human nutrition and health. World Health Organisation, Geneva1996Google Scholar is sufficient to achieve optimal health. These amounts more readily are achieved in the typical diet in many countries. However, there is a lack of logic in this approach if the objective is to optimize function.19Thomson C.D. Assessment of requirements for selenium and adequacy of selenium status: a review.Eur J Clin Nutr. 2004; 58: 391-402Crossref PubMed Scopus (562) Google Scholar There is also the question of optimizing all other selenoproteins, but the current data suggest that an intake that achieves a plasma Se concentration of 8.0–9.5 μg/dL (1.0–1.2 μmol/L) will maximize the activities of most selenoproteins.19Thomson C.D. Assessment of requirements for selenium and adequacy of selenium status: a review.Eur J Clin Nutr. 2004; 58: 391-402Crossref PubMed Scopus (562) Google Scholar It is clear that a wide range of dietary intakes can meet the requirements in different individuals and in different countries, possibly by adaptation to a low intake. Moreover, factors that increase oxidative stress such as smoking or high polyunsaturated fat intake will increase Se requirement. Most dietary selenium is in the form of selenomethionine and selenocysteine, about 90% of which is absorbed. Inorganic Se as selenite or selenate is absorbed more variably, to levels of 50%–90%.19Thomson C.D. Assessment of requirements for selenium and adequacy of selenium status: a review.Eur J Clin Nutr. 2004; 58: 391-402Crossref PubMed Scopus (562) Google Scholar The form most widely used in PN is selenite, which readily can be incorporated directly into selenocysteine. Although selenomethionine also can be used intravenously,35van Rij A.M. McKenzie J.M. Thomson C.D. et al.Selenium supplementation in total parenteral nutrition.JPEN J Parenter Enteral Nutr. 1981; 5: 120-124Crossref PubMed Scopus (37) Google Scholar it first may be incorporated nonspecifically into other tissue or plasma proteins, and needs to be converted to selenocysteine before selenoproteins can be synthesized. Excess selenium in the diet largely is excreted via the kidney.18Food and Nutrition Board IoMDietary reference intakes for vitamin C, vitamin E, selenium, and carotenoids. National Academy Press, Washington, DC2000Google Scholar Defining the requirement in PN is a complex task. First, as noted earlier, there is substantial individual variation in requirements for Se in health,4Elsom R. Sanderson P. Hesketh J.E. et al.Functional markers of selenium status: UK Food Standards Agency workshop report.Br J Nutr. 2006; 96: 980-984Crossref PubMed Scopus (25) Google Scholar so supply in PN must at least meet the dietary Reference Nutrient Intake, which as summarized earlier is probably in the range of 55–70 μg/day. Some patients may have basal requirements similar to an oral diet in health if they are well and on home PN. However, many will have an increased requirement if they have ongoing or intercurrent disease or are postsurgical because of the increased metabolic and antioxidant needs. Some seriously ill patients will have a very much higher requirement, both to meet the demands of oxidative stress and to replace increased losses. Definitive dose-ranging studies in these different conditions have not been undertaken, and intakes usually have been selected on a theoretical basis, and then assessed by monitoring the status of patients to determine if supply is adequate. Most of the studies to evaluate Se requirements during PN have been in patients receiving long-term PN at home because this is the group in which biochemical and clinical evidence of Se deficiency largely has been observed. A summary of studies is given in Table 2. Taken overall the following conclusions can be reached.Table 2Studies on Selenium Supplementation in Home PNStudyNumber of patientsIntake Se μg/dDuration of Intravenous NutritionResultsNotesLane et al,58Lane H.W. Lotspeich C.A. Moore C.E. et al.The effect of selenium supplementation on selenium status of patients receiving chronic total parenteral nutrition.JPEN J Parenter Enteral Nutr. 1987; 11: 177-182PubMed Google Scholar 1987780 followed by 1601 month each levelPlasma Se increased but not normalizedShort-term studyMalone et al,36Malone M. Shenkin A. Fell G.S. et al.Evaluation of a trace element preparation in patients receiving home intravenous nutrition.Clin Nutr. 1989; 8: 307-312Abstract Full Text PDF PubMed Scopus (12) Google Scholar 198914323–13 mo8/14 low plasma Se at end of study periodMansell et al,37Mansell P.I. Allison S.P. Vardey H. et al.Clinical effects and adequacy of a new all-in-one dextrose-electrolyte-trace element preparation in patients on prolonged TPN.Clin Nutr. 1989; 8: 313-319Abstract Full Text PDF PubMed Scopus (4) Google Scholar 1989114013–280 dMaintained but did not correct Se statusRannem et al,59Rannem T. Ladefoged K. Hylander E. et al.The effect of selenium supplementation on skeletal and cardiac muscle in selenium-depleted patients.JPEN J Parenter Enteral Nutr. 1995; 19: 351-355Crossref PubMed Scopus (20) Google Scholar 19939200 followed by 1004 and 8 moPlasma Se level higher than healthy controlsGiven as bolus IV injectionForbes and Forbes,38Forbes G.M. Forbes A. Micronutrient status in patients receiving home parenteral nutrition.Nutrition. 1997; 13: 941-944Abstract Full Text PDF PubMed Scopus (61) Google Scholar 1997326364 mo (range, 1–175 mo)5/32 low plasma Se at end of studyReimund et al,60Reimund J.M. Arondel Y. Duclos B. et al.Vitamins and trace elements in home parenteral nutrition patients.J Nutr Health Aging. 2000; 4: 13-18PubMed Google Scholar 20002243, women; 66, men18 mo (range, 1–132 mo)Plasma Se below reference in many patientsRange, 20–120 μg/dayHoward et al,39Howard L. Ashley C. Lyon D. et al.Autopsy tissue trace elements in 8 long-term parenteral nutrition patients who received the current U.S. Food and Drug Administration formulation.JPEN J Parenter Enteral Nutr. 2007; 31: 388-396Crossref PubMed Scopus (64) Google Scholar 200788514 y (range, 2–21 y)Normal tissue content of Se in heart and liver, some low results in skeletal muscle and kidney Open table in a new tab An intake of 30–50 μg/day meets the ongoing requirements of some patients, probably those with basal requirements, but it is inadequate to correct Se depletion.36Malone M. Shenkin A. Fell G.S. et al.Evaluation of a trace element preparation in patients receiving home intravenous nutrition.Clin Nutr. 1989; 8: 307-312Abstract Full Text PDF PubMed Scopus (12) Google Scholar, 37Mansell P.I. Allison S.P. Vardey H. et al.Clinical effects and adequacy of a new all-in-one dextrose-electrolyte-trace element preparation in patients on prolonged TPN.Clin Nutr. 1989; 8: 313-319Abstract Full Text PDF PubMed Scopus (4) Google Scholar An intake of 63 μg/day is adequate for the majority of home patients, but about 15% have a higher requirement than this.38Forbes G.M. Forbes A. Micronutrient status in patients receiving home parenteral nutrition.Nutrition. 1997; 13: 941-944Abstract Full Text PDF PubMed Scopus (61) Google Scholar An intake of 85 μg/day seems to be sufficient to maintain tissue concentrations in most patients, although some may have even higher requirements.39Howard L. Ashley C. Lyon D. et al.Autopsy tissue trace elements in 8 long-term parenteral nutrition patients who received the current U.S. Food and Drug Administration formulation.JPEN J Parenter Enteral Nutr. 2007; 31: 388-396Crossref PubMed Scopus (64) Google Scholar There is substantial variability in requirements, possibly related to the ongoing disease process. It also should be noted that not all patients in these studies received the supplements every day; therefore, the average daily intravenous (IV) intake was somewhat less. On the other hand, most patients had some oral intake, although absorption from the oral diet is uncertain. It therefore can be concluded that the IV requirement for most patients on home PN is in the range of 60–100 μg/day, although some patients may require more if they are depleted on commencing home PN. There have been few reports of Se status during typical postsurgery PN. Two reports suggested that 32 μg/day was adequate to maintain Se status over short PN feeding periods,40Smith A.D.S. Shenkin A. Fell G.S. et al.Trace element supplementation in surgical patients receiving parenteral nutrition.JPEN J Parenter Enteral Nutr. 1982; 6: 334Google Scholar, 41Shenkin A. Fraser W.D. McLelland A.J. et al.Maintenance of vitamin and trace element status in intravenous nutrition using a complete nutritive mixture.JPEN J Parenter Enteral Nutr. 1987; 11: 238-242Crossref PubMed Scopus (25) Google Scholar and more variable amounts prevented the decrease in Se usually found after surgery.42Alfieri M.A. Leung F.Y. Grace D.M. Selenium and zinc levels in surgical patients receiving total parenteral nutrition.Biol Trace Elem Res. 1998; 61: 33-39Crossref PubMed Scopus (15) Google Scholar, 43Winnefeld K. Dawczynski H. Schirrmeister W. et al.Selenium in serum and whole blood in patients with surgical interventions.Biol Trace Elem Res. 1995; 50: 149-155Crossref PubMed Scopus (21) Google Scholar Such patients are likely to have requirements higher than basal, to meet the increased oxidative stress of hypermetabolism. They also may have increased losses via fistulae or aspirates. It can be concluded that requirements are at least as high as those on home PN (60–100 μg/day), with some having a greater requirement. Patients in intensive care, especially i
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