Duodenal Disaccharidase Activities During and After Weaning off Parenteral Nutrition in Pediatric Intestinal Failure

Sanaksenaho, Galina; Mutanen, Annika; Koivusalo, Antti; Merras‐Salmio, Laura; Pakarinen, Mikko P.

doi:10.1097/mpg.0000000000001347

Cited by 4 publications

(3 citation statements)

References 47 publications

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“…an overabundance of LPS-producing Proteobacteria, while mucosal inflammation becomes increasingly prevalent. 14,20,21,42 Simultaneously, deprivation of enteral nutrients creates a proinflammatory state within the intestine increasing epithelial permeability and translocation of bacterial products. 11,15,21 PN-dependent SBS patients show increased intestinal permeability and increased plasma antibodies against LPS, suggesting continuous exposure to bowel-derived bacterial antigens.…”

Section: Discussionmentioning

confidence: 99%

Small bowel dilation in children with short bowel syndrome is associated with mucosal damage, bowel-derived bloodstream infections, and hepatic injury

Hukkinen

Mutanen

Pakarinen

2017

Surgery

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Section: Discussionmentioning

confidence: 99%

Small bowel dilation in children with short bowel syndrome is associated with mucosal damage, bowel-derived bloodstream infections, and hepatic injury

Hukkinen

Mutanen

Pakarinen

2017

Surgery

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“…Previous studies suggest that abnormal mucosal inflammation is frequent among PN‐dependent children with SBS . Most of our patients had received antimicrobial therapy prior to biopsy, which may have reduced mucosal inflammation so that significant differences were not found in the lamina propria–inflammation score or mRNA expression of proinflammatory cytokines.…”

Section: Discussionmentioning

confidence: 93%

Parenteral Nutrition–Dependent Children With Short‐Bowel Syndrome Lack Duodenal‐Adaptive Hyperplasia but Show Molecular Signs of Altered Mucosal Function

Sanaksenaho

Mutanen

Godbole

et al. 2020

J Parenter Enteral Nutr

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Background Although adaptive mucosal growth of the remaining small intestine is an essential compensatory mechanism to bowel resection in experimental short‐bowel syndrome (SBS), only scarce clinical data are available. We studied structural and molecular mechanisms of intestinal adaptation in children with SBS. Methods : Fourteen patients, who had been dependent on parenteral nutrition (PN) since neonatal period for a median (interquartile range)1.4 (0.7–6.5) years, were studied at the age of 1.5 (1.0–6.5) years. Median length of remaining small bowel was 33 (12–60) cm, and 6 patients had their ileocecal valve preserved. Six children without gastrointestinal disorders served as age‐matched and gender‐matched controls. All patients underwent duodenal biopsies. Mucosal microarchitecture, proliferation, apoptosis, inflammation, and epithelial‐barrier function were addressed using histology, immunohistochemistry, and quantitative real‐time polymerase chain reaction. Results : Villus height, crypt depth, enterocyte proliferation, and apoptosis were similar in patients and matched controls. Messenger RNA (mRNA) expression of numerous genes regulating gut epithelial‐barrier function (TGFB2, CAV1, CLDN1, MUC2, and NLRC4) was significantly altered. Of various nutrient transporters studied, only expression of SLC2A1 encoding facilitative glucose transporter GLUT1 was increased among patients, whereas RNA expression of genes encoding sodium‐dependent glucose, sterol, fatty‐acid, and peptide transport remained unchanged. Conclusion : Duodenal mucosal hyperplasia has a limited role in mediating physiological adaptation following intestinal resection among PN‐dependent children with SBS. Further clinical studies addressing functional significance of the observed alterations in mucosal RNA expression are warranted.

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“…When patients were weaned off PN, disaccharidase activities recovered to control levels. It should be noted that duodenal mucosal inflammation was present in a subgroup of PN-dependent patients in this study, and that activity of sucrase, maltase, and lactase was lower in this group than in those without inflammation [ 48 ]. As chronic inflammation is also a feature of EE, albeit likely in a considerably different microbiological environment to PN-dependent children, this has implications for disaccharidase activity in EE.…”

Section: Physiological Analysismentioning

confidence: 99%

Intestinal Biopsies for the Evaluation of Environmental Enteropathy and Environmental Enteric Dysfunction

Hodges

Tembo

Kelly

2021

The Journal of Infectious Diseases

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Environmental enteric dysfunction (EED) is a syndrome characterised by impairments of digestion and absorption and intestinal barrier failure in people living in insanitary or tropical environments. There is substantial evidence that it contributes to impaired linear growth of millions of children in low- and middle-income countries, to slowed neurocognitive development, and to diminished responses to oral vaccines. It represents the functional consequences of environmental enteropathy, an asymptomatic inflammatory disorder of the mucosa, and there is considerable overlap with the enteropathy observed in severe clinical malnutrition. The majority of studies of EED have employed functional tests based on lactulose permeation to define the presence of abnormal leak in the gut. However, where intestinal biopsies can safely be collected the opportunity then arises to study the underlying enteropathy in cellular and molecular detail, as well as to measure important functional elements such as enzyme expression. The purpose of this narrative review is to summarise the current understanding of environmental enteropathy (EE) obtained from small intestinal biopsies, and prospects for future work. We review histology, electron microscopy, transcription and protein expression, physiological measures, and the microbiome. We conclude that while non-invasive biomarkers of enteropathy and intestinal dysfunction permit large scale studies of unquestionable value, intestinal biopsies are still required to investigate pathophysiology in depth.

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Duodenal Disaccharidase Activities During and After Weaning off Parenteral Nutrition in Pediatric Intestinal Failure

Cited by 4 publications

References 47 publications

Small bowel dilation in children with short bowel syndrome is associated with mucosal damage, bowel-derived bloodstream infections, and hepatic injury

Small bowel dilation in children with short bowel syndrome is associated with mucosal damage, bowel-derived bloodstream infections, and hepatic injury

Parenteral Nutrition–Dependent Children With Short‐Bowel Syndrome Lack Duodenal‐Adaptive Hyperplasia but Show Molecular Signs of Altered Mucosal Function

Intestinal Biopsies for the Evaluation of Environmental Enteropathy and Environmental Enteric Dysfunction

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