Nutrition
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Randomized Controlled Trial Clinical Trial
The use of an intravenous fish oil emulsion enriched with omega-3 fatty acids in patients with cystic fibrosis.
The effects of parenteral nutrition supplemented with a lipid emulsion enriched with the omega-3 fatty acids (FA), eicosapentaenoate (20:5n-3) and docosahexaenoate (22:6n-3), derived from fish oil were compared to a standard lipid emulsion containing omega-6 FA in patients with cystic fibrosis (CF). Patients were randomized to receive either Omegavenous 10%, which contains fish oil (IFO), or Liposyn III 10% (control) daily for 1 mo at a dose of 150 mg/kg. There were no observed allergic or toxic reactions, no abnormalities in liver function tests or coagulation parameters. ⋯ The effect of treatment on pulmonary function was also investigated. There were no significant changes in FVC, FEV1, PEFR, FEV1/ FVC, or FEF25-75 (absolute value or percentage) over the 4 weeks of study in the group receiving IFO or control. This preliminary investigation suggests that intravenous administration of fish oils enriched with long chain omega-3 FA to patients with CF is safe and bioavailable.
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Randomized Controlled Trial Clinical Trial
Effect of parenteral L-glutamine on muscle in the very severely ill.
Glutamine (Gln)-supplemented perioperative total parenteral nutrition (TPN) has been reported to reduce the loss of intramuscular glutamine following routine surgery. This study investigates whether glutamine-supplemented TPN can alter muscle biochemistry acutely in the very severely ill patient. Thirty-eight patients (age 19-77 yr; mean 55 yr), critically ill (APACHE II range 8-31; median 17) admitted to the intensive care unit (ICU) were recruited to receive either conventional TPN (CTPN) or an isonitrogenous, isoenergetic feed supplemented with 25 g crystalline L-glutamine per 24 h (GTPN) in a prospective, double blind, block-randomized study. ⋯ It also proved difficult in these very sick patients to correct a low plasma Gln with L-Gln-TPN during the initial phase of the severe illness. TPN supplementation with 25 g/24 h, L-glutamine appears inadequate in the acute period to counteract the muscle and plasma biochemical changes seen in these patients. It is unknown whether any larger dose could alter this state.
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Randomized Controlled Trial Comparative Study Clinical Trial
Hypermetabolism and increased peripheral release of amino acids after subarachnoidal hemorrhage and its operative treatment.
The metabolic response to surgery for acute subarachnoidal hemorrhage and its modification by amino acid infusions was studied. Thirty patients with acute subarachnoidal hemorrhage were randomly assigned to receive for 12 h either an infusion of glucose and a balanced amino acid solution (1.68 MJ = 400 kcal/d and 0.15 gN.kg-1.d-1; group AA) or a glucose and a solution containing 20% of total nitrogen as alanyl-glutamine (1.68 MJ = 400 kcal/d and 0.15 gN.kg-1.d-1; group ALAGLN). A separate control group received glucose alone (1.68 MJ = 400 kcal/d). ⋯ Also the release of alanine (ALAGLN: 35 +/- 24 mumol/min, AA: 34 +/- 24 mumol/min, and control: 30 +/- 18 mumol/min) and total amino acids (ALAGLN: 133 +/- 131 mumol/min, AA: 125 +/- 98 mumol/min, and control: 112 +/- 72 mumol/min) were similar in all groups. All groups were characterized by a pattern of preoperative hypermetabolism that persisted after the operation. The hypermetabolism was not related to increased peripheral oxygen consumption, since femoral oxygen consumption (VO2) represented only 3% of the whole body VO2-.
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The proportion of patients with total parenteral nutrition (TPN)-associated cholestasis (TPN-AC) who have necrotizing enterocolitis (NEC) has increased markedly in the past ten years. Little is known about how these diseases affect each other. We retrospectively studied 24 patients with NEC and bowel necrosis or perforation who required surgical intervention. ⋯ We conclude that NEC alone can cause functional cholestasis and histologic liver injury but does not cause the specific progressive damage caused by TPN. NEC may make the liver more susceptible to the effects of TPN. Partial enteral feeding does not halt or reverse this injury.