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• W2076177946 abstract "Severe depletion of body protein stores can result from prolonged starvation or from hormonal and cytokine-mediated effects during critical illness. Recent advances in the understanding of cytokine actions have substantially refined the interpretation of the nutritional assessment of critically ill patients. In addition, the design of nutritional programs for hospitalized patients has changed considerably during the past decade. Although nutritional support of critically ill patients will not lead to positive nitrogen balance, nutrition can increase protein synthesis, enhance immune function, and beneficially modify the body's response to an illness. Severe depletion of body protein stores can result from prolonged starvation or from hormonal and cytokine-mediated effects during critical illness. Recent advances in the understanding of cytokine actions have substantially refined the interpretation of the nutritional assessment of critically ill patients. In addition, the design of nutritional programs for hospitalized patients has changed considerably during the past decade. Although nutritional support of critically ill patients will not lead to positive nitrogen balance, nutrition can increase protein synthesis, enhance immune function, and beneficially modify the body's response to an illness. Protein-calorie malnutrition is on a continuum with marasmus and the body's metabolic response to injury, inflammation, and infection at opposite ends of the spectrum (Table 1). Traditionally, malnutrition has often been equated with marasmus; however, the changes evoked by the hormonal and cytokine milieu of illness can also lead to the depletion of body protein stores. This review of these two states highlights the major differences in pathophysiologic features, clinical manifestations, effects on immune function, indications for initiation of nutritional intervention, and anticipated responses to such intervention.1Bistrian BR Nutritional assessment of the hospitalized patient: a practical approach.in: Wright RA Heymsfield S Nutritional Assessment. Blackwell Scientific Publications, Boston1984: 183-205Google Scholar, 2McMahon MM Bistrian BR The physiology of nutritional assessment and therapy in protein-calorie malnutrition.Dis Mon. 1990; 36: 375-417Abstract Full Text PDF Scopus (33) Google ScholarTable 1Clinical Expression of Protein-Calorie MalnutritionModified from McMahon M, Bistrian BR. Anthropometric assessment of nutritional status in hospitalized patients. In: Himes JH, editor. Anthropometric Assessment of Nutritional Status. New York: Wiley-Liss, 1991:365–381. By permission.AspectStarvation (marasmus)Metabolic response to injuryCauseInsufficient caloric intakeMetabolic stressHormonal and metabolic alterations HypoinsulinemiaDepression in metabolic rateCytokine response; increases in counter-regulatory hormones, aldosterone, and antidiuretic hormoneVisceral protein stores Normal serum albumin levelNo acute-phase protein response Low serum albumin levelAcute-phase protein responseImmune functionGenerally intactImpaired, if injury response is prolongedClinical manifestation and anthropometries Weight lossLow circumference of arm muscleMarkers of stress: fever, leukocytosis (± increase in band forms), hypoalbuminemia, increase in urea nitrogen excretionAnticipated response to appropriate nutritional therapy Restoration of lean tissuePositive nitrogen balance Lean tissue may or may not be restoredHypoalbuminemia persistsImmunocompetence returnsPrototypic disease statesAnorexia nervosa, malabsorption, or esophageal cancerClosed-head injury, burns, multiple trauma, or critical illness Open table in a new tab Starvation leads to a series of hormonal changes that allow the body to adapt to an insufficient diet.3Cahill Jr, GF Herrera MG Morgan AP Soeldner JS Steinke J Levy PL et al.Hormone-fuel interrelationships during fasting.J Clin Invest. 1966; 45: 1751-1769Crossref PubMed Scopus (715) Google Scholar, 4Cahill Jr, GF Starvation in man.Clin Endocrinol Metab. 1976; 5: 397-415Abstract Full Text PDF PubMed Scopus (203) Google Scholar Hormonal alterations (that is, a decrease in plasma insulin and an increase in plasma cortisol and growth hormone) allow the body to mobilize and oxidize fat stores (approximately 160,000 kcal in a 70-kg subject), skeletal muscle stores (approximately 30,000 kcal), and glycogen stores (1,200 kcal) preferentially as sources of energy in order to preserve visceral protein. This preferential use of certain fuels is important because depletion of visceral protein stores is rapidly accompanied with functional changes. The decrease in energy intake during semistarvation is quickly followed by a lowering of the basal metabolic rate, which is modulated through changes in thyroid hormone metabolism5Portnay GI O'Brian JT Bush J Vagenakis AG Azizi F Arky RA et al.The effect of starvation on the concentration and binding of thyroxine and triiodothyronine in serum and on the response to TRH.J Clin Endocrinol Metab. 1974; 39: 191-194Crossref PubMed Scopus (191) Google Scholar and activities of the sympathetic nervous system. If the intake of calories and protein is severely depleted for a prolonged period, marasmus develops, and the principal losses are skeletal muscle and adipose tissue. Examples of conditions that can lead to marasmus include anorexia nervosa, malabsorption, and advanced esophageal or gastric cancer. In unstressed semistarvation, the plasma albumin level (a marker of visceral protein) should be in the normal or near-normal range. The body's adaptive response to starvation sharply contrasts with its response to injury—a dynamic process modulated by changes in the neuroendocrine and cytokine milieu. The hormonal response may include an increase in plasma concentration of catecholamines, aldosterone, antidiuretic hormone,6Moran Jr, WH Miltenberger FW Shuayb WA Zimmerman B The relationship of antidiuretic hormone secretion to surgical stress.Surgery. 1964; 56: 99-108Google Scholar and counterregulatory hormones. The increase in catecholamines may lead to an increase in basal metabolic rate. The elevation in plasma levels of aldosterone and antidiuretic hormone can impair excretion of water and lead to retention of sodium and water. The increase in counterregulatory hormones (that is, glucagon, epinephrine, cortisol, and growth hormone) can cause stress diabetes mellitus7Eigler N Saccà L Sherwin RS Synergistic interactions of physiologic increments of glucagon, epinephrine, and cortisol in the dog: a model for stress-induced hyperglycemia.J Clin Invest. 1979; 63: 114-123Crossref PubMed Scopus (181) Google Scholar, 8Shamoon H Hendler R Sherwin RS Synergistic interactions among antiinsulin hormones in the pathogenesis of stress hyperglycemia in humans.J Clin Endocrinol Metab. 1981; 52: 1235-1241Crossref PubMed Scopus (201) Google Scholar and a negative nitrogen balance. Cytokines, including the interleukins and tumor necrosis factor α (cachectin), are proteins synthesized and secreted by activated monocytes and phagocytes in response to an injury or inflammation stimulus.9Dinarello CA Interleukin-1 and the pathogenesis of the acute-phase response.N Engl J Med. 1984; 311: 1413-1418Crossref PubMed Scopus (922) Google Scholar, 10Dinarello CA Mier JW Lymphognes.N Engl J Med. 1987; 317: 940-945Crossref PubMed Scopus (459) Google Scholar Interleukin 1 activates lymphocytes and can replicate many of the acute-phase responses of the host to injury, including fever, anorexia,11Moldawer LL Andersson C Gelin J Lundholm KG Regulation of food intake and hepatic protein synthesis by recombinant-derived cytokines.Am J Physiol. 1988; 254: G450-G456PubMed Google Scholar increase in the blood leukocyte count with release of immature cells from the marrow, hypoalbuminemia, changes in the concentration of hepatic secretory proteins,12Wannemacher Jr, RW Pekarek RS Thompson WL Curnow RT Beall FA Zenser TV et al.A protein from polymorphonuclear leukocytes (LEM) which affects the rate of hepatic amino acid transport and synthesis of acute-phase globulins.Endocrinology. 1975; 96: 651-661Crossref PubMed Scopus (74) Google Scholar redistribution of trace minerals,13Klasing KC Effect of inflammatory agents and interleukin 1 on iron and zinc metabolism.Am J Physiol. 1984; 247: R901-R904PubMed Google Scholar and, if infused with tumor necrosis factor, negative nitrogen balance.14Flores EA Bistrian BR Pomposelli JJ Dinarello CA Blackburn GL Istfan NW Infusion of tumor necrosis factor/cachectin promotes muscle catabolism in the rat: a synergistic effect with interleukin 1.J Clin Invest. 1989; 83: 1614-1622Crossref PubMed Scopus (353) Google Scholar Interleukin 6 seems the most efficient stimulator of the hepatic production of acute-phase proteins.15Marinkovic S Jahreis GP Wong GG Baumann H IL-6 modulates the synthesis of a specific set of acute phase plasma proteins in vivo.J Immunol. 1989; 142: 808-812PubMed Google Scholar Tumor necrosis factor, capable of inducing many of the same acute-phase changes, is a pivotal mediator of gram-negative sepsis.16Tracey KJ Beutler B Lowry SF Merry weather J Wolpe S Milsark IW et al.Shock and tissue injury induced by recombinant human cachectin.Science. 1986; 234: 470-474Crossref PubMed Scopus (2123) Google Scholar, 17Beutler B Milsark IW Cerami AC Passive immunization against cachectin/tumor necrosis factor protects mice from lethal effect of endotoxin.Science. 1985; 229: 869-871Crossref PubMed Scopus (1880) Google Scholar Although cytokines have many beneficial properties, including the stimulation of antimicrobial function, promotion of wound healing, and mobilization of substrate stores, excessive or prolonged release may lead to an exaggerated inflammatory response, a depletion of protein and energy stores, and adverse consequences. The serum albumin level reflects the synthesis, degradation, and clearance of albumin.18Rothschild MA Oratz M Schreiber SS Albumin synthesis (second of two parts).N Engl J Med. 1972; 286: 816-821Crossref PubMed Scopus (75) Google Scholar The balance between the production and catabolism of albumin and its equilibrium between the intravascular and interstitial compartments18Rothschild MA Oratz M Schreiber SS Albumin synthesis (second of two parts).N Engl J Med. 1972; 286: 816-821Crossref PubMed Scopus (75) Google Scholar determine the plasma concentration. The daily hepatic rate of synthesis is 120 to 270 mg/kg or approximately 15 g/day in a 70-kg subject. After synthesis, the albumin molecule is distributed—40% is in the intravascular space, and 60% is in the extravascular space. Approximately 10% of the pool undergoes catabolism daily in the intestinal tract and the vascular endothelium. Interleukin 1 and tumor necrosis factor share the ability to down-regulate the albumin gene and to decrease the rate of albumin messenger RNA translation.19Perlmutter DH Dinarello CA Punsal PI Colten HR Cachectin/tumor necrosis factor regulates hepatic acute-phase gene expression.J Clin Invest. 1986; 78: 1349-1354Crossref PubMed Scopus (443) Google Scholar This decrease in the production of albumin coupled with an increased catabolism and a shift of albumin from the intravascular to the extravascular space leads to the hypoalbuminemia of illness. Thus, in a stressed patient, hypoalbuminemia is an excellent marker for the injury response but an imperfect marker of nutritional status. Changes in trace minerals associated with the stress of illness often include a decrease in serum iron and zinc concentrations (within hours after infusion of cytokine) and an increase in serum copper. The mechanism of interleukin 1-induced hypoferremia has recently been described.20Goldblum SE Cohen DA Jay M McClain CJ Interleukin 1-induced depression of iron and zinc: role of granulocytes and lactoferrin.Am J Physiol. 1987; 252: E27-E32PubMed Google Scholar Interleukin 1 can cause exocytosis of intracellular granule contents, including the iron-binding protein lactoferrin. Lactoferrin is the carrier protein for the removal of iron from the intravascular space. The decrease in circulating zinc has been attributed to both increased urinary losses and accelerated flux of zinc from the plasma to the liver.20Goldblum SE Cohen DA Jay M McClain CJ Interleukin 1-induced depression of iron and zinc: role of granulocytes and lactoferrin.Am J Physiol. 1987; 252: E27-E32PubMed Google Scholar Cytokines increase the synthesis of metallothioneins—metal-binding proteins found in relatively high concentration in the liver—an outcome that offers a potential explanation for the loss of zinc from the plasma and for the accumulation of hepatic zinc. Thus, during illness, decreased plasma zinc and iron concentrations may reflect tissue sequestration rather than an actual deficiency. Serum copper levels may increase because of the cytokine-induced stimulation of production of ceruloplasmin, an acute-phase protein and the major copper-binding protein. Studies have shown that in patients experiencing pronounced stress, the capability of their mononuclear cells to produce interleukin 1 in vitro is impaired; however, short-term (1 to 7 days) parenteral nutrition increased the production.21Hoffman-Goetz L McFarlane D Bistrian BR Blackburn GL Febrile and plasma iron responses of rabbits injected with endogenous pyrogen from malnourished patients.Am J Clin Nutr. 1981; 34: 1109-1116PubMed Scopus (49) Google Scholar, 22Keenan RA Moldawer LL Yang RD Kawamura I Blackburn GL Bistrian BR An altered response by peripheral leukocytes to synthesize or release leukocyte endogenous mediator in critically ill, protein-malnourished patients.J Lab Clin Med. 1982; 100: 844-857PubMed Google Scholar Increased interleukin 1 levels were associated not only with improved nutritional support but also with improved survival.21Hoffman-Goetz L McFarlane D Bistrian BR Blackburn GL Febrile and plasma iron responses of rabbits injected with endogenous pyrogen from malnourished patients.Am J Clin Nutr. 1981; 34: 1109-1116PubMed Scopus (49) Google Scholar Serum interleukin 1 activity has been found to be significantly lower in nonsurviving patients with sepsis in an intensive-care unit than in surviving patients or in a control group.23Luger A Graf H Schwarz H-P Stummvoll H-K Luger TA Decreased serum interleukin 1 activity and monocyte interleukin 1 production in patients with fatal sepsis.Crit Care Med. 1986; 14: 458-461Crossref PubMed Scopus (94) Google Scholar In contrast, leukocyte production of interleukin 1 does not seem impaired during unstressed starvation.21Hoffman-Goetz L McFarlane D Bistrian BR Blackburn GL Febrile and plasma iron responses of rabbits injected with endogenous pyrogen from malnourished patients.Am J Clin Nutr. 1981; 34: 1109-1116PubMed Scopus (49) Google Scholar Cellular immune function may also be adversely affected during severe stress24Bistrian BR Blackburn GL Scrimshaw NS Flatt J-P Cellular immunity in semistarved states in hospitalized adults.Am J Clin Nutr. 1975; 28: 1148-1155PubMed Scopus (204) Google Scholar (and during unstressed starvation only if the current-to-ideal body weight ratio is less than 85%25Bistrian BR Sherman M Blackburn GL Marshall R Shaw C Cellular immunity in adult marasmus.Arch Intern Med. 1977; 137: 1408-1411Crossref PubMed Scopus (86) Google Scholar). Anergy can develop within 7 days after nutritional deprivation. The skin test response can be restored within 2 weeks after adequate nutrition if malnutrition is indeed the cause of the anergy. These examples illustrate the importance of adequate nutrition and nutritional status to the expression of the body's metabolic response to injury. In a broad sense, the nutritional assessment aims to identify malnourished patients, design the nutritional program, and assess the patient's response to nutritional support.1Bistrian BR Nutritional assessment of the hospitalized patient: a practical approach.in: Wright RA Heymsfield S Nutritional Assessment. Blackwell Scientific Publications, Boston1984: 183-205Google Scholar Interpretation of the nutritional assessment of critically ill patients is enhanced by an understanding of the hormonal and cytokine milieu of illness (Table 2). Of importance, anorexia is common in this group of patients. Infusions of interleukin 1, tumor necrosis factor, or endotoxin have been shown to cause a substantial decrease in food intake. As discussed earlier, hypoalbuminemia should be considered a marker of the injury response rather than of impaired nutrition. Hypoalbuminemia can affect interpretation of both plasma trace metal levels and pharmacokinetics. Zinc is 55% albumin-bound, calcium is 50%, and magnesium is 30%. As a result, an apparently low plasma calcium, magnesium, or zinc concentration may be “normal” because of a decreased plasma albumin level, and trace element supplementation may be unnecessary or inappropriate. Although algorithms have been developed to correct the plasma calcium level for the albumin level, use of these algorithms has been shown to be inaccurate in stressed patients. Albumin, a major plasma protein, is responsible for the binding of acidic drugs. The activity of drugs that have a high affinity for albumin and a narrow therapeutic index (for example, phenytoin) may be affected by a change in the plasma albumin.26Koch-Weser J Sellers EM Binding of drugs to serum albumin (first of two parts).N Engl J Med. 1976; 294: 311-316Crossref PubMed Scopus (298) Google Scholar Changes in the serum albumin can alter the pharmacokinetics of these drugs by increasing the amount of free, active drug. The percentage of free to bound drug may be disproportionately increased, an outcome that leads to a normal total plasma level of the drug but an increased free level.27Driscoll DF McMahon M Blackburn GL Bistrian BR Phenytoin toxicity in a critically ill, hypoalbuminemic patient with normal serum drug concentrations.Crit Care Med. 1988; 16: 1248-1249Crossref PubMed Scopus (22) Google Scholar Unexplained hyperglycemia may be a harbinger of infection due to cytokine and hormonal effects on carbohydrate metabolism. Finally, although weight is often a useful anthropometric marker, its interpretation becomes difficult during illness. Many critically ill patients have increased total body water or salt due to the underlying illness (for example, malnutrition or cardiac, hepatic, or renal disease), the treatment modalities (for example, crystalloid or colloid infusion), or the hormonal milieu of critical illness and refeeding. Therefore, daily changes in weight generally reflect fluid balance.Table 2Influence of Cytokines on Interpretation of Nutritional AssessmentAnorexiaHypoalbuminemia; synthesis of acute-phase proteinsRedistribution of plasma trace metalsMarkers of stress Fever Leukocytosis ± increase in band formsAltered intermediary metabolism, including stress diabetes mellitus and negative nitrogen balance Open table in a new tab The decision of when to initiate nutritional support in a specific patient depends in part on the timing and the amount of unintentional recent (previous 3- to 6-month interval) weight change; the fluid status of the patient must be considered. In general, a recent weight loss in excess of 10% of the usual weight necessitates a thorough nutritional assessment. A recent weight loss of 10 to 20% of the usual weight represents moderate protein-calorie malnutrition, and a loss of more than 20% indicates severe protein-calorie malnutrition.1Bistrian BR Nutritional assessment of the hospitalized patient: a practical approach.in: Wright RA Heymsfield S Nutritional Assessment. Blackwell Scientific Publications, Boston1984: 183-205Google Scholar, 2McMahon MM Bistrian BR The physiology of nutritional assessment and therapy in protein-calorie malnutrition.Dis Mon. 1990; 36: 375-417Abstract Full Text PDF Scopus (33) Google Scholar The metabolic response to injury has a more serious effect on a malnourished person than on a nourished person. The greater the decrease in body protein stores, the greater the risk from recent starvation because body protein stores must compensate for the deficit when the diet is inadequate. Protein-calorie malnutrition can adversely affect the structure and function of many organs, including the lungs,28Arora NS Rochester DF Respiratory muscle strength and maximal voluntary ventilation in undernourished patients.Am Rev Respir Dis. 1982; 126: 5-8PubMed Google Scholar heart,29Heymsfield SB Bethel RA Ansley JD Gibbs DM Felner JM Nutter DO Cardiac abnormalities in cachectic patients before and during nutritional repletion.Am Heart J. 1978; 95: 584-594Abstract Full Text PDF PubMed Scopus (142) Google Scholar gastrointestinal tract,30James WPT Effects of protein-calorie malnutrition on intestinal absorption.Ann N Y Acad Sci. 1971; 176: 244-261Crossref Scopus (36) Google Scholar and musculoskeletal system,31Jeejeebhoy KN Muscle function and nutrition.Gut. 1986; 27: 25-39Crossref PubMed Scopus (55) Google Scholar as well as wound healing32Haydock DA Hill GL Improved wound healing response in surgical patients receiving intravenous nutrition.Br J Surg. 1987; 74: 320-323Crossref PubMed Scopus (106) Google Scholar and immune function.33Scrimshaw NS Taylor CE Gordon JE Interactions of Nutrition and Infection. World Health Organization, Geneva1968Google Scholar In addition to the magnitude of recent weight loss, the adequacy of recent food intake,34Windsor JA Knight GS Hill GL Wound healing response in surgical patients: recent food intake is more important than nutritional status.Br J Surg. 1988; 75: 135-137Crossref PubMed Scopus (116) Google Scholar the presence or absence of clinical markers of stress, and the anticipated time that the patient will be unable to eat determine the need for nutritional intervention (Table 3). In general, a recent weight loss of less than 10% of the usual weight is well tolerated. For a well-nourished and unstressed patient (afebrile and normal leukocyte count and differential) or a mildly stressed patient who is expected to be eating during the next week, provision of fluid and electrolytes should be sufficient. Generally, nutritional intervention should begin early for those who have recently lost more than 10% of their usual weight and are moderately or severely stressed. Nutritional support should be promptly provided for severely stressed patients because the stress response generally exceeds 1 week.Table 3Indications for Initiation of Nutritional SupportModified from McMahon and Bistrian.2McMahon MM Bistrian BR The physiology of nutritional assessment and therapy in protein-calorie malnutrition.Dis Mon. 1990; 36: 375-417Abstract Full Text PDF Scopus (33) Google Scholar By permission of Mosby-Year Book, Inc.Recent weight loss (%)Degree of stressIntervention<10Mild or moderateFluid and electrolytes (up to 7–10 days)10–20MildFluid and electrolytes (up to 7–10 days)Moderate or severeNutrition>20AnyNutritionAnySevere*Examples include closed-head injury, multiple trauma, severe burn, or critical illness.Nutrition* Examples include closed-head injury, multiple trauma, severe burn, or critical illness. Open table in a new tab The importance of a functional assessment of protein-calorie malnutrition is now recognized.35Windsor JA Hill GL Weight loss with physiologic impairment: a basic indicator of surgical risk.Ann Surg. 1988; 207: 290-296Crossref PubMed Scopus (305) Google Scholar, 36Windsor JA Hill GL Risk factors for postoperative pneumonia: the importance of protein depletion.Ann Surg. 1988; 208: 209-214Crossref PubMed Scopus (226) Google Scholar After major gastrointestinal surgical procedures, patients with both recent weight loss of 10% and physiologic impairment in two or more areas (that is, activity level, wound healing, or psychologic, respiratory, or skeletal muscle function) had a significantly higher incidence of major complications and a longer hospital stay than did patients with recent weight loss but no evidence of physiologic impairment.35Windsor JA Hill GL Weight loss with physiologic impairment: a basic indicator of surgical risk.Ann Surg. 1988; 207: 290-296Crossref PubMed Scopus (305) Google Scholar, 36Windsor JA Hill GL Risk factors for postoperative pneumonia: the importance of protein depletion.Ann Surg. 1988; 208: 209-214Crossref PubMed Scopus (226) Google Scholar Although the amount of weight loss was similar at baseline in the two groups, the group with evidence of physiologic dysfunction had decreased body protein stores as measured by in vivo neutron activation analysis. If the gastrointestinal tract is functional, the enteral, rather than the parenteral, route is preferred for the delivery of nutrients. Advantages of enteral nutrition include lower cost, avoidance of central catheter-related complications, more physiologic route, and a trophic effect on gastrointestinal cells. Starvation dramatically affects the morphologic features and function of the intestinal mucosa.37Clarke RM The effect of growth and of fasting on the number of villi and crypts in the small intestine of the albino rat.J Anat. 1972; 112: 27-33PubMed Google Scholar, 38Goodlad RA Wright NA The effects of starvation and refeeding on intestinal cell proliferation in the mouse.Virchows Arch [Cell Pathol]. 1984; 45: 63-73Crossref Scopus (62) Google Scholar, 39Hagemann RF Stragand JJ Fasting and refeeding: cell kinetic response of jejunum, ileum and colon.Cell Tissue Kinet. 1977; 10: 3-14PubMed Google Scholar Villus height and production of epithelial cells in the crypts decrease, and the mass of mucosa is substantially decreased. Soon after refeeding, markers of crypt cell proliferation are increased. Enteral nutrition can stimulate mucosal growth through direct and indirect effects. Direct effects occur by contact of the nutrients with the villus, local presence of nutrients, and stimulation of gastric, biliary, and pancreatic secretions. Indirect effects are mediated by enhanced secretion of gastrointestinal hormones, stimulation of the autonomic nervous system, and augmented blood flow. Mucosal atrophy of cells occurs in the absence of enteral nutrition, during starvation,40Steiner M Bourges HR Freedman LS Gray SJ Effect of starvation on the tissue composition of the small intestine in the rat.Am J Physiol. 1968; 215: 75-77PubMed Google Scholar during parenteral nutrition and bowel rest,41Levine GM Deren JJ Steiger E Zinno R Role of oral intake in maintenance of gut mass and disaccharide activity.Gastroenterology. 1974; 67: 975-982PubMed Google Scholar or in defunctionalized intestinal segments.42Gleeson MH Dowling RH Peters TJ Biochemical changes in intestinal mucosa after experimental small bowel by-pass in the rat.Clin Sci. 1972; 43: 743-757PubMed Google Scholar The intestinal barrier is dependent on intraluminal factors, epithelial cell and tight junction integrity, and local and systemic immune function.43Rolandelli RH DePaula JA Guenter P Rombeau JL Critical illness and sepsis.in: Rombeau JL Caldwell MD Clinical Nutrition: Enteral and Tube Feeding. 2nd ed. Saunders, Philadelphia1990: 288-305Google Scholar, 44O'Dwyer ST Smith RJ Kripke SA Settle RG Rombeau JL New fuels for the gut.in: Rombeau JL Caldwell MD Clinical Nutrition: Enteral and Tube Feeding. 2nd ed. Saunders, Philadelphia1990: 540-555Google Scholar, 45Wilmore DW Smith RJ O'Dwyer ST Jacobs DO Ziegler TR Wang X-D The gut: a central organ after surgical stress.Surgery. 1988; 104: 917-923PubMed Google Scholar Key intraluminal factors include chemical barriers (for example, gastric acid, pepsin, bile, secretory IgA, and indigenous gut flora) and mechanical barriers (for example, migrating motor complex and intestinal mucin). Mucosal integrity necessitates the preservation of tight junctions between mucosal cells. Throughout much of the enteric tract, a single simple columnar cell separates its sterile interior from the gut lumen, which hosts many bacteria. The presence of nutrients in the gut lumen fosters rapid turnover of the enterocytes. Both local gastrointestinal immune defense and systemic immune defense are important. Although not always appreciated, the gut is one of the largest immune organs in the body.46Langkamp-Henken B Glezer JA Kudsk KA Immunologic structure and function of the gastrointestinal tract.Nutr Clin Pract. 1992; 7: 100-108Crossref PubMed Scopus (64) Google Scholar In certain circumstances (that is, bacterial translocation), the gut can serve as a reservoir for bacteria that can cause systemic infection. Bacterial translocation refers to the passage of viable indigenous bacteria from the gastrointestinal tract through the epithelial mucosa47Berg RD Garlington AW Translocation of certain indigenous bacteria from the gastrointestinal tract to the mesenteric lymph nodes and other organs in a gnotobiotic mouse model.Infect Immun. 1979; 23: 403-411PubMed Google Scholar into the lymph as well as the portal and systemic blood. Promoters of the translocation of bacteria or endotoxin (or both) include disruption of the normal gut microflora that results in bacterial overgrowth,48Deitch EA Maejima K Berg R Effect of oral antibiotics and bacterial overgrowth on the translocation of the GI tract microflora in burned rats.J Trauma. 1985; 25: 385-391Crossref PubMed Scopus (251) Google Scholar impaired host immune defense,49Deitch EA Winterton J Berg R Thermal injury promotes bacterial translocation from the gastrointestinal tract in mice with impaired T-cell-mediated immunity.Arch Surg. 1986; 121: 97-100Crossref PubMed Scopus (114) Google Scholar and physical disruption of the gut mucosa50Fong Y Marano MA Barber A He W Moldawer LL Bushman ED et al.Total parenteral" @default.
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• W2076177946 cites W1526023472 @default.
• W2076177946 cites W1570782716 @default.
• W2076177946 cites W1614524975 @default.
• W2076177946 cites W1839111542 @default.
• W2076177946 cites W1860323961 @default.
• W2076177946 cites W1905885715 @default.
• W2076177946 cites W1937079800 @default.
• W2076177946 cites W1964891036 @default.
• W2076177946 cites W1965952579 @default.
• W2076177946 cites W1968713831 @default.
• W2076177946 cites W1970910808 @default.
• W2076177946 cites W1972163315 @default.
• W2076177946 cites W1974548695 @default.
• W2076177946 cites W1983207116 @default.
• W2076177946 cites W1985138005 @default.
• W2076177946 cites W1987122163 @default.
• W2076177946 cites W1987711508 @default.
• W2076177946 cites W1992966972 @default.
• W2076177946 cites W1999246265 @default.
• W2076177946 cites W2019669277 @default.
• W2076177946 cites W2025109953 @default.
• W2076177946 cites W2035424185 @default.
• W2076177946 cites W2035495484 @default.
• W2076177946 cites W2038323300 @default.
• W2076177946 cites W2039111148 @default.
• W2076177946 cites W2039766330 @default.
• W2076177946 cites W2041811148 @default.
• W2076177946 cites W2044599257 @default.
• W2076177946 cites W2048452629 @default.
• W2076177946 cites W2050994709 @default.
• W2076177946 cites W2053277538 @default.
• W2076177946 cites W2054976074 @default.
• W2076177946 cites W2055392678 @default.
• W2076177946 cites W2056587425 @default.
• W2076177946 cites W2058435277 @default.
• W2076177946 cites W2061631206 @default.
• W2076177946 cites W2063859567 @default.
• W2076177946 cites W2067090040 @default.
• W2076177946 cites W2069791682 @default.
• W2076177946 cites W2070069097 @default.
• W2076177946 cites W2072486140 @default.
• W2076177946 cites W2072711448 @default.
• W2076177946 cites W2074126390 @default.
• W2076177946 cites W2075064717 @default.
• W2076177946 cites W2077634049 @default.
• W2076177946 cites W2078389625 @default.
• W2076177946 cites W2078792792 @default.
• W2076177946 cites W2079333603 @default.
• W2076177946 cites W2079577855 @default.
• W2076177946 cites W2083634842 @default.
• W2076177946 cites W2088295190 @default.
• W2076177946 cites W2089548237 @default.
• W2076177946 cites W2092852042 @default.
• W2076177946 cites W2092860487 @default.
• W2076177946 cites W2095088339 @default.
• W2076177946 cites W2097716400 @default.
• W2076177946 cites W2122016427 @default.
• W2076177946 cites W2125884465 @default.
• W2076177946 cites W2132033716 @default.
• W2076177946 cites W2156549131 @default.
• W2076177946 cites W2161674805 @default.
• W2076177946 cites W2171532347 @default.
• W2076177946 cites W2198664016 @default.
• W2076177946 cites W2327007297 @default.
• W2076177946 cites W2346761245 @default.
• W2076177946 cites W2400507537 @default.
• W2076177946 cites W2417924319 @default.
• W2076177946 cites W4229921485 @default.
• W2076177946 cites W4230495280 @default.
• W2076177946 cites W4232576781 @default.
• W2076177946 cites W4293242440 @default.
• W2076177946 cites W86248671 @default.
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