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• W2124047443 abstract "Enteral nutrition (EN) by means of oral nutritional supplements (ONS) and tube feeding (TF) offers the possibility of increasing or ensuring nutrient intake in cases where normal food intake is inadequate.These guidelines are intended to give evidence-based recommendations for the use of ONS and TF in cancer patients. They were developed by an interdisciplinary expert group in accordance with officially accepted standards, are based on all relevant publications since 1985 and were discussed and accepted in a consensus conference.Undernutrition and cachexia occur frequently in cancer patients and are indicators of poor prognosis. EN should be started if undernutrition already exists or if food intake is markedly reduced for more than 7–10 days. Standard formulae are recommended for EN. Nutritional needs generally are comparable to non-cancer subjects. In cachectic patients metabolic modulators such as progestins, steroids and possibly eicosapentaenoic acid may help to improve nutritional status. EN is indicated preoperatively for 5–7 days in cancer patients undergoing major abdominal surgery. During radiotherapy of head/neck and gastrointestinal regions dietary counselling and ONS prevent weight loss and interruption of radiotherapy. Routine EN is not indicated during (high-dose) chemotherapy.The full version of this article is available at www.espen.org. Enteral nutrition (EN) by means of oral nutritional supplements (ONS) and tube feeding (TF) offers the possibility of increasing or ensuring nutrient intake in cases where normal food intake is inadequate. These guidelines are intended to give evidence-based recommendations for the use of ONS and TF in cancer patients. They were developed by an interdisciplinary expert group in accordance with officially accepted standards, are based on all relevant publications since 1985 and were discussed and accepted in a consensus conference. Undernutrition and cachexia occur frequently in cancer patients and are indicators of poor prognosis. EN should be started if undernutrition already exists or if food intake is markedly reduced for more than 7–10 days. Standard formulae are recommended for EN. Nutritional needs generally are comparable to non-cancer subjects. In cachectic patients metabolic modulators such as progestins, steroids and possibly eicosapentaenoic acid may help to improve nutritional status. EN is indicated preoperatively for 5–7 days in cancer patients undergoing major abdominal surgery. During radiotherapy of head/neck and gastrointestinal regions dietary counselling and ONS prevent weight loss and interruption of radiotherapy. Routine EN is not indicated during (high-dose) chemotherapy. The full version of this article is available at www.espen.org. Tabled 1Summary of statements: Non-surgical oncologySubjectRecommendationsGrade144Schütz T. Herbst B. Koller M. Methodology for the development of the ESPEN Guidelines on Enteral Nutrition.Clin Nutr. 2006; 25: 203-209Abstract Full Text Full Text PDF PubMed Scopus (23) Google ScholarNumberGeneralNutritional assessment of cancer patients should be performed frequently, and nutritional intervention initiated early when deficits are detected.C1.1There are no reliable data that show any effect of enteral nutrition on tumour growth. Such theoretical considerations should, therefore, have no influence on the decision to feed a cancer patient.C4.1Indication GeneralStart nutritional therapy if undernutrition already exists or if it is anticipated that the patient will be unable to eat for >7 days.C2.2Start enteral nutrition if an inadequate food intake (<60% of estimated energy expenditure for >10 days) is anticipated. It should substitute the difference between actual intake and calculated requirements.C2.2In weight losing patients due to insufficient nutritional intake enteral nutrition should be provided to improve or maintain nutritional status.B2.3 PerioperativePatients with severe nutritional risk benefit from nutritional support 10–14 d prior to major surgery even if surgery has to be delayed.A3.1 During radio- or radio-chemotherapyUse intensive dietary advice and oral nutritional supplements to increase dietary intake and to prevent therapy-associated weight loss and interruption of radiation therapy.A3.2Routine enteral nutrition is not indicated during radiation therapy.C3.2 During chemotherapyRoutine enteral nutrition during chemotherapy has no effect on tumour response to chemotherapy or on chemotherapy-associated unwanted effects and, therefore, is not considered useful.C3.3 During stem cell transplantationThe routine use of enteral nutrition is not recommended.C3.4If oral intake is decreased parenteral nutrition may be preferred to tube feeding in certain situations (i.e. increased risk of haemorrhage and infections associated with enteral tube placement in immuno-compromised and thrombocytopenic patients).C3.4 In incurable patientsProvide enteral nutrition in order to minimise weight loss as long as the patient consents and the dying phase has not started.C3.6When the end of life is very close most patients only require minimal amounts of food and little water to reduce thirst and hunger.B3.6Small amounts of fluid may also help to avoid states of confusion induced by dehydratation.B3.6Subcutaneously infused fluids in hospital or at home may be helpful and also provide a vehicle for the administration of drugs.C3.6ApplicationPrefer the enteral route whenever feasible.A3.1Administer preoperative enteral nutrition preferably before admission to the hospital.C3.1RouteUse tube feeding if an obstructing head or neck or esophageal cancer interferes with swallowing or if severe local mucositis is expected.C3.2 During radio- or radio-chemotherapyTube feeding can either be delivered via transnasal or percutaneous routes.3.2Because of the radiation induced oral and esophageal mucositis a percutaneous gastrostomy (PEG) may be preferred.C3.2Type of formula GeneralUse standard formulae.C1.5Regarding ω-3 fatty acids, randomised clinical trial evidence is contradictory/controversial and at present it is not possible to reach any firm conclusion with regard to improved nutritional status/physical function.C2.5It is unlikely that ω-3 fatty acids prolong survival in advanced cancer.2.5 PerioperativeUse preoperative enteral nutrition preferably with immune modulating substrates (arginine, ω-3 fatty acids, nucleotides) for 5–7d in all patients undergoing major abdominal surgery independent of their nutritional status.A3.1 During stem cell transplantationEnteral administration of glutamine or eicosapentanoic acid is not recommended due to inconclusive data.C3.5Drug treatmentIn the presence of systemic inflammation pharmacological efforts are recommended in addition to nutritional interventions to modulate the inflammatory response.C2.3In cachectic patients steroids or progestins are recommended in order to enhance appetite, modulate metabolic derangements, and prevent impairment of quality of life.A2.4Administer steroids for short-term periods only weighing their benefits against their adverse side-effects.C2.4Consider the risk of thrombosis during progestin therapy.C2.4Grade: Grade of recommendation; Number: refers to statement number within the text. Open table in a new tab Grade: Grade of recommendation; Number: refers to statement number within the text. In the majority of tumour-bearing patients systemic proinflammatory processes are activated. Resulting metabolic derangements include insulin resistance, increased lipolysis and high normal or increased lipid oxidation with loss of body fat, increased protein turnover with loss of muscle mass and an increase in production of acute phase proteins. The systemic inflammatory reaction that develops with many cancers is an important cause of loss of appetite (anorexia) and weight. The syndrome of decreased appetite, weight loss, metabolic alterations and inflammatory state is referred to as cachexia, cancer cachexia or cancer anorexia–cachexia syndrome (CACS). These cytokine-induced metabolic alterations appear to prevent cachectic patients from regaining body cell mass (BCM) during nutritional support, are associated with a reduced life expectancy (III), and are not relieved by exogenous nutrients alone. Attempts to modulate these changes by other means should be integrated into the management of cancer patients (C). Nutritional assessment of cancer patients should be performed frequently, and nutritional intervention initiated early when deficits are detected (C). Comment: While undernutrition, both moderate and severe, is frequent in patients with malignant disease, many tumour-bearing patients display elevated inflammatory markers.1Moldawer L.L. Copeland E.M. Proinflammatory cytokines, nutritional support, and the cachexia syndrom.Cancer. 1997; 79: 1828-1839Crossref PubMed Scopus (146) Google Scholar, 2de Blaauw I. Deutz N.E.P. von Meyenfeldt M.F. Metabolic changes of cancer cachexia—second of two parts.Clin Nutr. 1997; 16: 223-228Abstract Full Text PDF PubMed Scopus (28) Google Scholar, 3de Blaauw I. Deutz N.E.P. von Meyenfeldt M.F. Metabolic changes in cancer cachexia—first of two parts.Clin Nutr. 1997; 16: 169-176Abstract Full Text PDF PubMed Scopus (36) Google Scholar, 4Barber M.D. The pathophysiology and treatment of cancer cachexia.Nutr Clin Pract. 2002; : 203-209Crossref PubMed Google Scholar The observed release of cytokines, catabolic hormones and further regulatory peptides appears to be the primary reaction of the cancer patient's host tissues.1Moldawer L.L. Copeland E.M. Proinflammatory cytokines, nutritional support, and the cachexia syndrom.Cancer. 1997; 79: 1828-1839Crossref PubMed Scopus (146) Google Scholar, 2de Blaauw I. Deutz N.E.P. von Meyenfeldt M.F. Metabolic changes of cancer cachexia—second of two parts.Clin Nutr. 1997; 16: 223-228Abstract Full Text PDF PubMed Scopus (28) Google Scholar, 3de Blaauw I. Deutz N.E.P. von Meyenfeldt M.F. Metabolic changes in cancer cachexia—first of two parts.Clin Nutr. 1997; 16: 169-176Abstract Full Text PDF PubMed Scopus (36) Google Scholar In addition, substances produced by tumour cells, such as tumour lipid mobilising factor (LMF) and proteolysis inducing factor (PIF), may add catabolic signals and further stimulate cytokine production and the acute phase response.5Tisdale M.J. Protein loss in cancer cachexia.Science. 2000; 289: 2293Crossref PubMed Scopus (70) Google Scholar, 6Tisdale M.J. Cachexia in cancer patients.Nat Rev Cancer. 2002; 2: 862-871Crossref PubMed Scopus (383) Google Scholar The systemic inflammatory reaction is assumed to be involved in causing loss of appetite7Inui A. Cancer anorexia–cachexia syndrome: are neuropeptides the key?.Cancer Res. 1999; 59: 4493-4501PubMed Google Scholar and body weight8von Meyenfeldt M.F. Nutritional support during treatment of biliopancreatic malignancy.Ann Oncol. 1999; 10: 273-277Crossref PubMed Google Scholar, 9Fearon K.C.H. Barber M.D. Falconer J.S. McMillan D.C. Ross J.A. Preston T. Pancreatic cancer as a model: inflammatory mediators, acute-phase response, and cancer cachexia.World J Surg. 1999; 23: 584-588Crossref PubMed Scopus (75) Google Scholar, 10Fordy C, Glover C, Henderson DC, Summerbell C, Wharton R, Allen-Mersh TG. Contribution of diet, tumour volume and patient-related factors to weight loss in patients with colorectal liver metastases. Br J Surg 1999; 639–44.Google Scholar, 11Simons J.P.F.H.A. Schols A.M. Buurman W.A. Wouters E.F. Weight loss and low body cell mass in males with lung cancer: relationship with systemic inflammation, acute-phase response, resting energy expenditure, and catabolic and anabolic hormones.Clin Sci. 1999; 97: 215-223Crossref PubMed Scopus (85) Google Scholar and may facilitate tumour progression.12Balkwill F. Mantovani A. Inflammation and cancer: back to Virchow?.Lancet. 2001; 357: 539-545Abstract Full Text Full Text PDF PubMed Scopus (2451) Google Scholar, 13Coussens L.M. Werb Z. Inflammation and cancer.Nature. 2002; 420: 860-867Crossref PubMed Scopus (4492) Google Scholar Cytokine-induced metabolic alterations also appear to prevent cachectic patients from regaining BCM during nutritional support14Espat N.J. Moldawer L.L. Copeland E.M. Cytokine-mediated alterations in host metabolism prevent nutritional repletion in cachectic cancer patients.J Surg Oncol. 1995; 58: 77-82Crossref PubMed Scopus (66) Google Scholar and are associated with a reduced life expectancy.4Barber M.D. The pathophysiology and treatment of cancer cachexia.Nutr Clin Pract. 2002; : 203-209Crossref PubMed Google Scholar, 6Tisdale M.J. Cachexia in cancer patients.Nat Rev Cancer. 2002; 2: 862-871Crossref PubMed Scopus (383) Google Scholar, 8von Meyenfeldt M.F. Nutritional support during treatment of biliopancreatic malignancy.Ann Oncol. 1999; 10: 273-277Crossref PubMed Google Scholar, 15Martin F. Santolaria F. Batista N. et al.Cytokine levels (IL-6 and IFN-gamma), acute phase response and nutritional status as prognostic factors in lung cancer.Cytokine. 1999; 11: 80-86Crossref PubMed Scopus (130) Google Scholar, 16O’Gorman P. McMillan D.C. McArdle C.S. Prognostic factors in advanced gastrointestinal cancer patients with weight loss.Nutr Cancer. 2000; 37: 36-40Crossref PubMed Google Scholar, 17Jamieson NB, Glen P, McMillan DC, et al. Systemic inflammatory response predicts outcome in patients undergoing resection for ductal adenocarcinoma head of pancreas. Br J Cancer 2004.Google Scholar Impaired glucose tolerance due to insulin resistance was an early finding in cancer patients.18Lundholm K. Holm G. Schersten T. Insulin resistance in patients with cancer.Cancer Res. 1978; 38: 4665-4670PubMed Google Scholar The relation of insulin to catabolic hormones is altered and an increased cortisol secretion as well as a reduced insulin:cortisol ratio are common.2de Blaauw I. Deutz N.E.P. von Meyenfeldt M.F. Metabolic changes of cancer cachexia—second of two parts.Clin Nutr. 1997; 16: 223-228Abstract Full Text PDF PubMed Scopus (28) Google Scholar, 19Starnes H.F. Warren R.S. Brennan M.F. Protein synthesis in hepatocytes isolated from patients with gastrointestinal malignancy.J Clin Invest. 2002; 80: 1384-1390Crossref Google Scholar As a result glucose turnover and gluconeogenesis are increased.3de Blaauw I. Deutz N.E.P. von Meyenfeldt M.F. Metabolic changes in cancer cachexia—first of two parts.Clin Nutr. 1997; 16: 169-176Abstract Full Text PDF PubMed Scopus (36) Google Scholar Weight loss in cancer patients is accompanied by a loss of fat as well as by enhanced plasma levels of triglycerides. Lipid oxidation can be normal or increased. What causes the alterations in lipid metabolism remains unclear.2de Blaauw I. Deutz N.E.P. von Meyenfeldt M.F. Metabolic changes of cancer cachexia—second of two parts.Clin Nutr. 1997; 16: 223-228Abstract Full Text PDF PubMed Scopus (28) Google Scholar However, increased lipolysis is frequently observed.20Shaw J.H.F. Wolfe R.R. Fatty acid and glycerol kinetics in septic patients and in patients with gastrointestinal cancer.Ann Surg. 1997; 205: 368-376Crossref Google Scholar, 21Zuijdgeest-van Leeuwen S.D. van den Berg J.W.O. Wattimena J.L.D. et al.Lipolysis and lipid oxidation in weight-losing cancer patients and healthy subjects.Metabolism. 2000; 49: 931-936Abstract Full Text PDF PubMed Scopus (39) Google Scholar Simultaneously, lipid oxidation is increased21Zuijdgeest-van Leeuwen S.D. van den Berg J.W.O. Wattimena J.L.D. et al.Lipolysis and lipid oxidation in weight-losing cancer patients and healthy subjects.Metabolism. 2000; 49: 931-936Abstract Full Text PDF PubMed Scopus (39) Google Scholar, 22Körber J. Pricelius S. Heidrich M. Müller M.J. Increased lipid utilization in weight losing and weight stable cancer patients with normal body weight.Eur J Clin Nutr. 1999; 53: 740-745Crossref PubMed Scopus (24) Google Scholar, 23Barber M.D. McMillan D.C. Preston T. Ross J.A. Fearon K.C.H. Metabolic response to feeding in weight-losing pancreatic cancer patients and its modulation by a fish-oil-enriched nutritional supllement.Clin Sci. 2000; 98: 389-399Crossref PubMed Google Scholar or in the high normal range,24Legaspi A. Jeevanandam M. Starnes Jr, H.F. Brennan M.F. Whole body lipid and energy metabolism in the cancer patient.Metabolism. 1987; 36: 958-963Abstract Full Text PDF PubMed Google Scholar while glucose oxidation is impaired. These observations may be taken to support recommendations to increase the fat/carbohydrate ratio in feeding cancer patients. The pro-inflammatory milieu5Tisdale M.J. Protein loss in cancer cachexia.Science. 2000; 289: 2293Crossref PubMed Scopus (70) Google Scholar, 25Cabal-Manzano R. Bhargava P. Torres-Duarte A. Marshall J. Bhargava P. Wainer I.W. Proteolysis-inducing factor is expressed in tumours of patients with gastrointestinal cancers and correlates with weight loss.Br J Cancer. 2001; 84: 1599-1601Crossref PubMed Scopus (57) Google Scholar induces skeletal muscle proteolysis3de Blaauw I. Deutz N.E.P. von Meyenfeldt M.F. Metabolic changes in cancer cachexia—first of two parts.Clin Nutr. 1997; 16: 169-176Abstract Full Text PDF PubMed Scopus (36) Google Scholar, 26Jeevanandam M. Horowitz G.D. Lowry S.F. Brennan M.F. Cancer cachexia and protein metabolism.Lancet. 1984; 1: 1424-1426Google Scholar resulting in a loss of muscle mass and simultaneously leads to an increased production of acute phase proteins. The ATP- and ubiquitin-dependent proteasome proteolytic system is activated at an early stage.27Williams A. Sun X. Fischer J.F. Hasselgren P.O. The expression of genes in the ubiquitin-proteasome proteolytic pathway is increased in skeletal muscle from patients with cancer.Surgery. 1999; 126: 744-750Abstract Full Text Full Text PDF PubMed Scopus (136) Google Scholar, 28Bossola M. Muscaritoli M. Costelli P. et al.Increased muscle ubiquitin mRNA levels in gastric cancer patients.Am J Physiol Regulatory Integrative Comp Phsyiol. 2001; 280: R1518-R1523PubMed Google Scholar Thus, cachexia should be no longer considered a late stage phenomenon. Rather, since the metabolic and molecular mechanisms ultimately leading to the phenotypic pattern of the anorexia–cachexia syndrome are already operating early during tumour growth and development, cachexia should be seen as a partially preventable phenomenon, the onset of which could be at least delayed by means of early pharmacological and nutritional intervention.29Muscaritoli M. Bossola M. Bellantone R. Rossi F.F. Therapy of muscle wasting in cancer: what is the future?.Curr Opin Clin Nutr Metab Care. 2004; 7: 459-466Crossref PubMed Scopus (29) Google Scholar 1.2. Does cancer influence nutritional status? Yes. Weight loss is frequently the first symptom occurring in cancer patients. Depending on tumour entity, weight loss is reported in 30 to more than 80% of patients and is severe (>10% of initial weight) in some 15% (IIb). Comment: Weight loss preceding tumour diagnosis has been reported by many groups to occur in 31–87% of the patients, depending on the tumour entity30DeWys W.D. Begg C. Lavin P.T. et al.Prognostic effect of weight loss prior to chemotherapy in cancer patients.Am J Med. 1980; 69: 491-497Abstract Full Text PDF PubMed Scopus (849) Google Scholar, 31Chute C.G. Greenberg E.R. Baron J. Korson R. Baker J. Yates J. Presenting conditions of 1539 population-based lung cancer patients by cell type and stage in New Hampshire and Vermont.Cancer. 1985; 56: 2107-2111Crossref PubMed Scopus (64) Google Scholar, 32Wigmore S.J. Plester C.E. Richardson R.A. Fearon K.C.H. Changes in nutritional status associated with unresectable pancreatic cancer.Br J Cancer. 1997; 75: 106-109Crossref PubMed Google Scholar, 33Andreyev H.J.N. Norman A.R. Oates J. Cunningham D. Why do patients with weight loss have a worse outcome when undergoing chemotherapy for gastrointestinal malignancies?.Eur J Cancer. 1998; 34: 503-509Abstract Full Text Full Text PDF PubMed Scopus (266) Google Scholar (III). A severe involuntary weight loss of more than 10% of initial weight over the previous 6 months has already occurred in 15% of all patients at the time of diagnosis.30DeWys W.D. Begg C. Lavin P.T. et al.Prognostic effect of weight loss prior to chemotherapy in cancer patients.Am J Med. 1980; 69: 491-497Abstract Full Text PDF PubMed Scopus (849) Google Scholar Eighty-five per cent of patients with pancreatic or stomach cancer have lost weight at the time of diagnosis, and in 30% the loss was severe.30DeWys W.D. Begg C. Lavin P.T. et al.Prognostic effect of weight loss prior to chemotherapy in cancer patients.Am J Med. 1980; 69: 491-497Abstract Full Text PDF PubMed Scopus (849) Google Scholar Both frequency and severity of weight loss are correlated with tumour stage34Bozzetti F. Migliavacca S. Scotti A. et al.Impact of cancer, type, site, stage and treatment on the nutritional status of patients.Ann Surg. 1982; 196: 170-179Crossref PubMed Google Scholar (III). Quite often, when toxicity of treatment outweighs tumour response, cancer therapies are associated with anorexia and further weight loss35Costa G. Donaldson S.S. Current concepts in cancer.N Engl J Med. 1979; 300: 1471-1473Crossref PubMed Google Scholar, 36McAnena O.J. Daly J.M. Impact of antitumor therapy on nutrition.Surg Clin North Am. 1986; 66: 1213-1228PubMed Google Scholar (IV). 1.3. Does nutritional status influence the clinical course and the prognosis? An impaired nutritional status is associated with reduced quality of life, lower activity level, increased treatment-related adverse reactions, reduced tumour response to treatment and reduced survival (IIb). However, a cause–effect relationship has not yet been established. Comment: Longitudinal studies have demonstrated that the prognosis for cancer patients with weight loss is worse than that for weight-stable patients. There are more pronounced treatment-related adverse reactions,33Andreyev H.J.N. Norman A.R. Oates J. Cunningham D. Why do patients with weight loss have a worse outcome when undergoing chemotherapy for gastrointestinal malignancies?.Eur J Cancer. 1998; 34: 503-509Abstract Full Text Full Text PDF PubMed Scopus (266) Google Scholar the response to cancer treatment is impaired,30DeWys W.D. Begg C. Lavin P.T. et al.Prognostic effect of weight loss prior to chemotherapy in cancer patients.Am J Med. 1980; 69: 491-497Abstract Full Text PDF PubMed Scopus (849) Google Scholar, 33Andreyev H.J.N. Norman A.R. Oates J. Cunningham D. Why do patients with weight loss have a worse outcome when undergoing chemotherapy for gastrointestinal malignancies?.Eur J Cancer. 1998; 34: 503-509Abstract Full Text Full Text PDF PubMed Scopus (266) Google Scholar, 37van Eys J. Effect of nutritional status on response to therapy.Cancer Res. 1982; 42: 747-753Google Scholar and there is reduced activity level,30DeWys W.D. Begg C. Lavin P.T. et al.Prognostic effect of weight loss prior to chemotherapy in cancer patients.Am J Med. 1980; 69: 491-497Abstract Full Text PDF PubMed Scopus (849) Google Scholar, 33Andreyev H.J.N. Norman A.R. Oates J. Cunningham D. Why do patients with weight loss have a worse outcome when undergoing chemotherapy for gastrointestinal malignancies?.Eur J Cancer. 1998; 34: 503-509Abstract Full Text Full Text PDF PubMed Scopus (266) Google Scholar subjective quality of life33Andreyev H.J.N. Norman A.R. Oates J. Cunningham D. Why do patients with weight loss have a worse outcome when undergoing chemotherapy for gastrointestinal malignancies?.Eur J Cancer. 1998; 34: 503-509Abstract Full Text Full Text PDF PubMed Scopus (266) Google Scholar, 38Ollenschläger G. Thomas W. Konkol K. Diehl V. Roth E. Nutritional behaviour and quality of life during oncological polychemotherapy: results of a prospective study on the efficacy of oral nutrition therapy in patients with acute leukaemia.Eur J Clin Invest. 1992; 22: 5-23Crossref Google Scholar and survival30DeWys W.D. Begg C. Lavin P.T. et al.Prognostic effect of weight loss prior to chemotherapy in cancer patients.Am J Med. 1980; 69: 491-497Abstract Full Text PDF PubMed Scopus (849) Google Scholar, 33Andreyev H.J.N. Norman A.R. Oates J. Cunningham D. Why do patients with weight loss have a worse outcome when undergoing chemotherapy for gastrointestinal malignancies?.Eur J Cancer. 1998; 34: 503-509Abstract Full Text Full Text PDF PubMed Scopus (266) Google Scholar, 37van Eys J. Effect of nutritional status on response to therapy.Cancer Res. 1982; 42: 747-753Google Scholar, 38Ollenschläger G. Thomas W. Konkol K. Diehl V. Roth E. Nutritional behaviour and quality of life during oncological polychemotherapy: results of a prospective study on the efficacy of oral nutrition therapy in patients with acute leukaemia.Eur J Clin Invest. 1992; 22: 5-23Crossref Google Scholar, 39Tubiana M. Attié E. Flamant R. Gérard-Marchant R. Hayat M. Prognostic factors in 454 cases of Hodgkin's disease.Cancer Res. 1971; 31: 1801-1810PubMed Google Scholar, 40Swenerton K.D. Legha S.S. Smith T. et al.Prognostic factors in metastatic breast cancer treated with combination chemotherapy.Cancer Res. 1979; 39: 1552-1562PubMed Google Scholar, 41Pedersen H. Hansen H.S. Cederqvist C. Lober J. The prognostic significance of weight loss and its integration in stage-grouping of oesophageal cancer.Acta Chir Scand. 1982; 148: 363-366PubMed Google Scholar, 42Fein R. Kelsen D.P. Geller N. Bains M. McCormack P. Brennan M.F. Adenocarcinoma of the esophagus and gastroesophageal junction.Cancer. 1985; 56: 2512-2518Crossref PubMed Scopus (49) Google Scholar, 43van Bokhorst-de van der Schueren M.A.E. van Leeuwen P.A.M. Kuik D.J. et al.The impact of nutritional status on the prognoses of patients with advanced head and neck cancer.Cancer. 1999; 86: 519-527Crossref PubMed Scopus (133) Google Scholar (IIb; III). Next to sepsis, cachexia is one of the commonest causes of death in cancer, ranging from 5% to 25%44Klastersky J. Daneau D. Verhest A. Causes of death in patients with cancer.Eur J Cancer. 1972; 8: 149-154Abstract Full Text PDF PubMed Google Scholar, 45Inagaki J. Rodriguez V. Bodey G.P. Proceedings: causes of death in cancer patients.Cancer. 1974; 33: 568-573Crossref PubMed Google Scholar, 46Ambrus J.L. Ambrus C.M. Mink I.B. Pickren J.W. Causes of death in cancer patients.J Med. 1975; 6: 61-64PubMed Google Scholar, 47Warren S. The immediate causes of death in cancer.Am J Med Sci. 1932; 184: 610-615Crossref Google Scholar (III). In a recent trial total body nitrogen was found to be the most powerful predictor of neutropenia after chemotherapy in breast cancer patients48Aslani A. Smith R.C. Allen B.J. Paviakis N. Levi J.A. The predictive value of body protein for chemotherapy-induced toxicity.Cancer. 2000; 88: 796-803Crossref PubMed Scopus (50) Google Scholar (III). Undernutrition, therefore, appears to be a marker of disease severity and poor prognosis, although it has not been established, whether undernutrition per se has a direct influence on prognosis, independently of the underlying disease. 1.4. Does cancer influence energy expenditure? Cancer itself does not have a consistent effect on resting energy expenditure. Oncological treatment, however, may modulate energy expenditure (III). Comment: Resting energy expenditure (REE) can be unchanged, increased or decreased in relation to the predicted energy expenditure. The energy requirements of cancer patients should therefore be assumed to be normal unless there are specific data showing otherwise. In about 25% of patients with active cancer, REE measured by the gold standard method, indirect calorimetry, is more than 10% higher, and in another 25% it is more than 10% lower than predicted energy expenditure. The extent or direction of the error cannot be predicted for individual cases49Knox L.S. Crosby L.O. Feurer I.D. Buzby G.P. Miller C.L. Mullen J.L. Energy expenditure in malnourished cancer patients.Ann Surg. 1983; 197: 152-161Crossref PubMed Google Scholar, 50Dempsey D.T. Feurer I.D. Knox L.S. Crosby L.O. Buzby G.P. Mullen J.L. Energy expenditure in malnourished gastrointestinal cancer patients.Cancer. 1984; 53: 1265-1273Crossref PubMed Google Scholar (III). The mean value in a group of cancer patients did not differ from the mean value of healthy subjects50Dempsey D.T. Feurer I.D. Knox L.S. Crosby L.O. Buzby G.P. Mullen J.L. Energy expenditure in malnourished gastrointestinal cancer patients.Cancer. 1984; 53: 1265-1273Crossref PubMed Google Scholar, 51Dempsey D.T. Knox L.S. Mullen J.L. Miller C.L. Feurer I.D. Buzby G.P. Energy expenditure in malnourished patients with colorectal cancer.Arch Surg. 1986; 121: 789-795Crossref PubMed Google Scholar (III). Studies in subjects with different types of tumour reported normal REE in patients with gastric or colorectal cancers52Hansell D.T. Davies J.W. Burns H.J. Effects of hepatic metastases on resting energy expenditure in patients with colorectal cancer.Br J Surg. 1986; 73: 659-662Crossref PubMed Google Scholar, 53Fredrix E.W. Soeters P.B. Wouters E.F. Deerenberg I.M. von Meyenfeldt M.F. Saris W.H. Effect of different tumor types on resting energy expenditure.Cancer Res. 1991; 51: 6138-6141PubMed Google Scholar (III) and higher than expected REE in subjects with pancreatic or lung cancers53Fredrix E.W. Soeters P.B. Wouters E.F. Deerenberg I.M. von Meyenfeldt M.F. Saris W.H. Effect of different tumor types on resting energy expenditure.Cancer Res. 1991; 51: 6138-6141PubMed Google Scholar, 54Moses A.W. Slater C. Preston T. Barber M.D. Fearon K.C. Reduced total energy expenditure and physical activity in cachectic patients with pancreatic cancer can be modulated by an energy and protein dense oral supplement enriched with n-3 fatty acids.Br J Cancer. 2004; 90: 996-1002Crossref PubMed Scopus (159) Google Scholar, 55Gibney E. Elia M. Jebb S.A. Murgatroyd P. Jennings G. T" @default.
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• W2124047443 title "ESPEN Guidelines on Enteral Nutrition: Non-surgical oncology" @default.
• W2124047443 cites W115239203 @default.
• W2124047443 cites W1507798652 @default.
• W2124047443 cites W1571192964 @default.
• W2124047443 cites W1579998928 @default.
• W2124047443 cites W174800916 @default.
• W2124047443 cites W1757058093 @default.
• W2124047443 cites W1844670809 @default.
• W2124047443 cites W1918057844 @default.
• W2124047443 cites W1922471005 @default.
• W2124047443 cites W1965037168 @default.
• W2124047443 cites W1965429735 @default.
• W2124047443 cites W1967521667 @default.
• W2124047443 cites W1967784390 @default.
• W2124047443 cites W1972184261 @default.
• W2124047443 cites W1974744320 @default.
• W2124047443 cites W1978092220 @default.
• W2124047443 cites W1979599244 @default.
• W2124047443 cites W1979666460 @default.
• W2124047443 cites W1980983039 @default.
• W2124047443 cites W1985933936 @default.
• W2124047443 cites W1987288378 @default.
• W2124047443 cites W1991006545 @default.
• W2124047443 cites W1992809077 @default.
• W2124047443 cites W1994233879 @default.
• W2124047443 cites W1997155298 @default.
• W2124047443 cites W2000417148 @default.
• W2124047443 cites W2001403065 @default.
• W2124047443 cites W2001606267 @default.
• W2124047443 cites W2001885251 @default.
• W2124047443 cites W2003567705 @default.
• W2124047443 cites W2003779506 @default.
• W2124047443 cites W2004918651 @default.
• W2124047443 cites W2004997237 @default.
• W2124047443 cites W2008046885 @default.
• W2124047443 cites W2008780953 @default.
• W2124047443 cites W2008869575 @default.
• W2124047443 cites W2009784013 @default.
• W2124047443 cites W2011226735 @default.
• W2124047443 cites W2014090617 @default.
• W2124047443 cites W2015563479 @default.
• W2124047443 cites W2027858518 @default.
• W2124047443 cites W2028429494 @default.
• W2124047443 cites W2030994139 @default.
• W2124047443 cites W2034271440 @default.
• W2124047443 cites W2034557970 @default.
• W2124047443 cites W2034681353 @default.
• W2124047443 cites W2036179489 @default.
• W2124047443 cites W2037470757 @default.
• W2124047443 cites W2038500596 @default.
• W2124047443 cites W2040101947 @default.
• W2124047443 cites W2041301317 @default.
• W2124047443 cites W2043658135 @default.
• W2124047443 cites W2046220472 @default.
• W2124047443 cites W2047258940 @default.
• W2124047443 cites W2047427543 @default.
• W2124047443 cites W2047971264 @default.
• W2124047443 cites W2050638087 @default.
• W2124047443 cites W2054300553 @default.
• W2124047443 cites W2056670090 @default.
• W2124047443 cites W2057348394 @default.
• W2124047443 cites W2057783569 @default.
• W2124047443 cites W2059227921 @default.
• W2124047443 cites W2060078508 @default.
• W2124047443 cites W2061465717 @default.
• W2124047443 cites W2066620273 @default.
• W2124047443 cites W2067042175 @default.
• W2124047443 cites W2068008235 @default.
• W2124047443 cites W2074564761 @default.
• W2124047443 cites W2075978435 @default.
• W2124047443 cites W2077962133 @default.
• W2124047443 cites W2078608486 @default.
• W2124047443 cites W2079633493 @default.
• W2124047443 cites W2081341811 @default.
• W2124047443 cites W2081578487 @default.
• W2124047443 cites W2083307422 @default.
• W2124047443 cites W2085133875 @default.
• W2124047443 cites W2086687462 @default.

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