Elsevier

Nutrition

Volume 14, Issue 1, January 1998, Pages 1-6
Nutrition

Gut Permeability, Intestinal Morphology, and Nutritional Depletion

https://doi.org/10.1016/S0899-9007(97)00385-7Get rights and content

Abstract

Nutritional depletion increases the risk for postoperative complications. The intestinal barrier may be important in the underlying pathophysiologic mechanism. In this study, 26 patients were evaluated to determine whether nutritional depletion was related to gut integrity and intestinal morphology. Nutritional depletion was estimated by calculating percentage ideal body weight (PIB) or percentage ideal fat free mass (PIFFM). To assess gut integrity, a lactulose/mannitol (L/M) test was performed. Duodenal biopsies were taken, and villous height, crypt depth, number of IgA-producing plasma cells, intraepithelial lymphocytes (IELs), and proliferating index were determined. The L/M ratio was increased, and villous height was decreased in depleted patients. Depletion was not associated with differences in the number of immune cells or proliferating index. The number of IgA-producing plasma cells was positively correlated with the L/M ratio. This study shows that nutritional depletion is associated with increased intestinal permeability and a decrease in villous height.

Introduction

The association between nutritional depletion, septic complications,1, 2and increased mortality rates[3]in postoperative patients is well established. The exact underlying mechanism is not known.

It has been hypothesized that the gut plays an important role in the development of complications in the postoperative patient.[4]An important function of the healthy gut is to prevent bacteria and endotoxins from reaching the portal circulation. This physiologic barrier is maintained by the mucous layer, the epithelial cells with their tight junctions, and the gut-associated lymphoid tissue (GALT). Impairment of one or several components of this intestinal barrier may result in bacterial translocation or endotoxemia.5, 6

Glutamine, a conditional essential amino acid, is used as fuel for rapidly dividing cells, for example, enterocytes and lymphocytes.7, 8A diminished glutamine supply during parenteral nutrition and enteral starvation results in morphologic changes and increased intestinal permeability.[9]Recently, we showed that nutritional depletion is associated with decreased concentrations of glutamine in the intestinal mucosa.[10]Nutritional depletion, via decreased glutamine supply, may impair intestinal barrier function.

In animal experiments, protein malnutrition results in an increased risk of endotoxin-related bacterial translocation and increased susceptibility to the lethal effects of endotoxins.11, 12The purpose of this study was to investigate the potential relationship between nutritional depletion, intestinal morphology, and permeability in humans.

Section snippets

Patients

Metabolically stable patients (temperature between 36.5 and 38°C, no intraabdominal abscesses, no signs of respiratory or cardiac failure) between 18 and 80 years of age admitted to the nutritional support team were eligible to enter the study. All patients were admitted because they were not allowed or were unable to receive enteral nutrition. The study was performed before parenteral nutrition was initiated. Patients with renal or liver failure, diabetes mellitus, ileus, or congenital

Patients

Intestinal biopsies were taken in 26 patients submitted to the care of the nutritional support team. Intestinal permeability was studied in 23 of these patients. Patients were treated for inflammatory bowel disease (IBD; n = 15), cancer (Ca; n = 6), and other diagnoses (NoCa/NoIBD) with subileus (n = 1), pancreatitis (n = 1), pyloric stenosis (n = 1), or fistula (n = 2). Patient data are summarized in Table I. Fourteen patients were considered nutritionally depleted because they had a PIFFM of

Discussion

This study was performed to assess the relationship between nutritional depletion, intestinal permeability, and morphology. The association between nutritional depletion and intestinal permeability in humans was first described by Maxton et al.[25]Starvation in obese patients and nutritional depletion in patients without gastrointestinal disease receiving enteral nutrition were associated with increased permeability. In our study, intestinal permeability and intestinal morphology were assessed

Acknowledgements

The authors thank Margriet Pijls, Anniek Moors, Janine Hoefnagels, and Margriet Rouflart for their help with this study.

References (46)

  • JA Windsor et al.

    Weight loss with physiologic impairmenta basic indicator of surgical risk

    Ann Surg

    (1987)
  • DW Wilmore et al.

    The guta central organ after surgical stress

    Surgery

    (1989)
  • CL Wells et al.

    Proposed mechanisms for the translocation of intestinal bacteria

    Rev Infect Dis

    (1989)
  • JW Alexander et al.

    The process of microbial translocation

    Ann Surg

    (1990)
  • EA Newsholme et al.

    Glutamine metabolism in lymphocytesits biochemical, physiological and clinical importance

    Q J Exp Physiol

    (1985)
  • EA Deitch et al.

    The gut as a portal of entry for bacteremiarole of protein malnutrition

    Ann Surg

    (1987)
  • EA Deitch et al.

    Protein malnutrition alone and in combination with endotoxin impairs systemic and gut-associated immunity

    J Parenter Enter Nutr

    (1992)
  • Metropolitan Life Insurance Company

    New weight standard for men and women. Bull Metro Life Ins Found

    (1983)
  • RL Shippee et al.

    Simultaneous determination of lactulose and mannitol in urine of burn patients by gas-liquid chromatography

    Clin Chem

    (1992)
  • T Eberts et al.

    A simplified colorimetric micromethod for xylose in serum or urine with phloroglucinol

    Clin Chem

    (1979)
  • CE Saraf et al.

    Proliferating cell nuclear antigen immunolocalization in gastro-intestinal epithelia

    Digestion

    (1991)
  • WA Aherne et al.

    Morphometry

    (1982)
  • HC Mitchison et al.

    A pilot study of fluticasone propionate in untreated coeliac disease

    Gut

    (1991)
  • Cited by (0)

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