Small volumes of enteral feedings normalise immune function in infants receiving parenteral nutrition

被引:44
作者
Okada, Y
Klein, N
van Saene, HKF
Pierro, A
机构
[1] Inst Child Hlth, Paediat Surg Unit, London WC1N 1EH, England
[2] Inst Child Hlth, Immunol Unit, London WC1N 1EH, England
[3] UCL, Great Ormond St Hosp Children, Sch Med, London, England
[4] Royal Liverpool Childrens Hosp Alder Hey, Dept Clin Microbiol, Liverpool, Merseyside, England
关键词
parenteral nutrition; enteral feeding; bactericidal activity; tumour necrosis factor; coagulase-negative staphylococci;
D O I
10.1016/S0022-3468(98)90352-9
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Background/Purpose: Parenteral nutrition (PN) is associated with a risk of septicaemia. This may be caused by impairment of immune function related to PN. The authors investigated the effects of the addition of enteral feedings to PN on the immune status of human newborn infants. Methods: Ten surgical infants (age less than 6 months) requiring PN were studied in two consecutive phases: (A) after 31.1 +/- 6.0 days (mean +/- SEM) of PN with no enteral feeding (total PN); and (B) after 4.7 +/- 1.1 days from the addition of small volumes of enteral feeding to PN. Full blood count and liver function tests were not significantly different between phases A and B. A control group (n = 9) of infants receiving a normal enteral diet was also studied. Host bactericidal activity against coagulase-negative staphylococci (CNS) was measured by an in vitro whole blood model. Bacterial killing was measured after a 45-minute bacterial challenge using the Miles-Misra technique. Tumour necrosis factor-alpha (TNF-alpha) was measured by enzyme-linked immunosorbent assay (ELISA) after 2 hours of bacterial challenge. Results: The lowest level of CNS killing (37.7 +/- 5.2%), was observed in patients receiving total PN. This increased significantly after the addition of small enteral feeds (52.0 +/- 4.6%, P<.005) approaching the levels measured in controls (65.1 +/- 3.4%). TNF-alpha production was low during total PN (1467 +/- 297 pg/mL) and rose significantly after the addition of minimal enteral feeds (4,661 +/- 1,311 pg/mL, P <.05). The increase in CNS killing after the addition of small enteral feeds in patients on PN was significantly correlated with the duration of enteral feeding (r = 0.8, P =.006). Conclusions: These results indicate that the introduction of small volumes of enteral feed improve the impaired killing of CNS and the abnormal cytokine response observed during total PN. This implies that stimulation of the gastrointestinal tract may modulate immune function in neonates and prevent bacterial infection. Copyright (C) 1998 by W.B. Saunders Company.
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页码:16 / 19
页数:4
相关论文
共 20 条
[1]   THE EFFECT OF PARENTERAL-NUTRITION ON GASTROINTESTINAL IMMUNITY - THE IMPORTANCE OF ENTERAL STIMULATION [J].
ALVERDY, J ;
CHI, HS ;
SHELDON, GF .
ANNALS OF SURGERY, 1985, 202 (06) :681-684
[2]  
ALVERDY JC, 1988, SURGERY, V104, P185
[3]   THE GUT AS A PORTAL OF ENTRY FOR BACTEREMIA - ROLE OF PROTEIN-MALNUTRITION [J].
DEITCH, EA ;
WINTERTON, J ;
LI, M ;
BERG, R .
ANNALS OF SURGERY, 1987, 205 (06) :681-692
[4]   Reservoirs of coagulase negative staphylococci in preterm infants [J].
Eastick, K ;
Leeming, JP ;
Bennett, D ;
Millar, MR .
ARCHIVES OF DISEASE IN CHILDHOOD-FETAL AND NEONATAL EDITION, 1996, 74 (02) :F99-F104
[5]   OPSONIC DEFENSE TO STAPHYLOCOCCUS-EPIDERMIDIS IN THE PREMATURE NEONATE [J].
FLEER, A ;
GERARDS, LJ ;
AERTS, P ;
WESTERDAAL, NAC ;
SENDERS, RC ;
VANDIJK, H ;
VERHOEF, J .
JOURNAL OF INFECTIOUS DISEASES, 1985, 152 (05) :930-937
[6]  
FLETCHER JP, 1986, SURGERY, V100, P21
[7]  
ILLIG KA, 1992, SURGERY, V112, P631
[8]   WHOLE-BLOOD MODEL OF MENINGOCOCCAL BACTEREMIA - A METHOD FOR EXPLORING HOST BACTERIAL INTERACTIONS [J].
ISON, CA ;
HEYDERMAN, RS ;
KLEIN, NJ ;
PEAKMAN, M ;
LEVIN, M .
MICROBIAL PATHOGENESIS, 1995, 18 (02) :97-107
[9]  
Klein N. J., 1994, Immunology and Infectious Diseases (Oxford), V4, P33
[10]   The influence of capsulation and lipooligosaccharide structure on neutrophil adhesion molecule expression and endothelial injury by Neisseria meningitidis [J].
Klein, NJ ;
Ison, CA ;
Peakman, M ;
Levin, M ;
Hammerschmidt, S ;
Frosch, M ;
Heyderman, RS .
JOURNAL OF INFECTIOUS DISEASES, 1996, 173 (01) :172-179