2021
DOI: 10.1016/j.clnu.2020.07.029
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Abstract: Early oral feeding is the preferred mode of nutrition for surgical patients. Avoidance of any nutritional therapy bears the risk of underfeeding during the postoperative course after major surgery. Considering that malnutrition and underfeeding are risk factors for postoperative complications, early enteral feeding is especially relevant for any surgical patient at nutritional risk, especially for those undergoing upper gastrointestinal surgery. The focus of this guideline is to cover both nutritional aspects … Show more

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Cited by 24 publications
(20 citation statements)
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References 267 publications
(126 reference statements)
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“…The LBM loss in patients with LAHNSCC undergoing CCRT is mediated by elevated levels of reactive oxygen species and pro-inflammatory cytokines, activation of proteolysis machinery including ubiquitin-dependent, calcium-dependent, and autophage/lysosome systems, decreased mitochondrial biogenesis and mass, and alteration of lipid metabolism [ 26 , 27 ]. The above mechanisms are integrated into two essential clinical factors participating in LBM loss during CCRT: patient characteristics such as age [ 28 ], tumor features [ 29 ], comorbidity [ 30 ], performance status [ 31 ], lifestyle habits [ 32 , 33 , 34 ], pretreatment nutritional status [ 35 ]; treatment-related attributes including RT treatment (dose, fraction, and duration), chemotherapy regimen [ 26 , 36 , 37 ], daily calorie delivered over the treatment course [ 9 , 37 ], and CCRT-associated toxicities [ 38 , 39 ]. The multivariate analysis in the present study showed different factors contributing to LBM loss for the OCC and NOCC subgroups: age and mean daily calorie intake for the OCC; mean daily calorie intake, BMI, and grade ¾ mucositis toxicity for the NOCC.…”
Section: Discussionmentioning
confidence: 99%
“…The LBM loss in patients with LAHNSCC undergoing CCRT is mediated by elevated levels of reactive oxygen species and pro-inflammatory cytokines, activation of proteolysis machinery including ubiquitin-dependent, calcium-dependent, and autophage/lysosome systems, decreased mitochondrial biogenesis and mass, and alteration of lipid metabolism [ 26 , 27 ]. The above mechanisms are integrated into two essential clinical factors participating in LBM loss during CCRT: patient characteristics such as age [ 28 ], tumor features [ 29 ], comorbidity [ 30 ], performance status [ 31 ], lifestyle habits [ 32 , 33 , 34 ], pretreatment nutritional status [ 35 ]; treatment-related attributes including RT treatment (dose, fraction, and duration), chemotherapy regimen [ 26 , 36 , 37 ], daily calorie delivered over the treatment course [ 9 , 37 ], and CCRT-associated toxicities [ 38 , 39 ]. The multivariate analysis in the present study showed different factors contributing to LBM loss for the OCC and NOCC subgroups: age and mean daily calorie intake for the OCC; mean daily calorie intake, BMI, and grade ¾ mucositis toxicity for the NOCC.…”
Section: Discussionmentioning
confidence: 99%
“…Furthermore, hypothalamic inflammatory reactions drive the sympathetic nervous system and the hypothalamus–pituitary–adrenal axis to increase, respectively, systemic levels of epinephrine and glucocorticoids ( 4 , 6 , 22 ). These processes, uninterruptedly, stimulate muscle protein breakdown, inducing SMT atrophy ( 6 ). Thus, this reinforces our view that animals under CR have lost lean mass or have had a delay in their gain.…”
Section: Discussionmentioning
confidence: 99%
“…Proinflammatory mediators can alter the brain neurochemistry, influencing peripheral systems (20). Particularly in the hypothalamus, these signs are closely linked to alterations in BW and in muscle dysfunctions (5,6). Furthermore, hypothalamic inflammatory reactions drive the sympathetic nervous system and the hypothalamus-pituitary-adrenal axis to increase, respectively, systemic levels of epinephrine and glucocorticoids (4,6,22).…”
Section: Discussionmentioning
confidence: 99%
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“…Its overexpression led to weight loss, muscle atrophy, and sarcopenia [143], while its downregulation to muscle hypertrophy and a hypermuscular phenotype [144,145]. Because of its impact on muscle mass, several drugs that inhibit the myostatin signaling pathway have been evaluated in preclinical and clinical studies to treat a variety of musclewasting diseases [146]. Myostatin levels are significantly higher in ALS patients than in healthy individuals and they are positively correlated with the rate of muscle degeneration [147].…”
Section: Pharmacological Interventions To Increase Muscle Massmentioning
confidence: 99%