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PubMed2000

Leukocytosis in children with Escherichia coli O157:H7 enteritis developing the hemolytic-uremic syndrome.

BACKGROUND: Fewer than 10% of children with Escherichia coli O157:H7 enteritis develop hemolytic-uremic syndrome (HUS). OBJECTIVE: To determine whether circulating leukocytes are independent risk markers of developing HUS during E. coli O157:H7 enteritis. METHODS: We reviewed the charts of all children with culture-proved E. coli O157:H7 infections seen at Sainte-Justine Hospital between 1987 and 1997. Epidemiologic data, laboratory indices and circulating leukocytes counts were noted. HUS diagnosis was validated with independent HUS patient lists from the pediatric nephrology services of tertiary care hospitals in the Montreal metropolitan area. The date of onset of enteritis was determined by two independent observers. Leukocyte counts were compared among the following independent groups: (1) uncomplicated O157:H7 enteritis (Group 1); (2) O157:H7 enteritis with the subsequent development of HUS (Group 2); (3) HUS already present at the time of medical consultation (Group 3). RESULTS: There were 369 children with E. coli O157:H7 infection. A complete blood count was not performed in 114 (31%) patients. Observers disagreed on the date of onset of gastroenteritis in 34 (9%) children only (kappa 0.92). The study population thus included 221 patients: Group 1, n = 161; Group 2, n = 27; and Group 3, n = 33. Patients developing HUS (Group 2) presented greater total leukocyte (P < 0.008), polymorphonuclear (P < 0.008) and monocyte (P < 0.07) counts than those with an uncomplicated course (Group 1). Logistic regression analysis showed that young age [odds ratio (OR), 0.98; 95% confidence interval (CI), 0.96 to 0.99], duration of enteric prodrome < or =3 days (OR 4.8, 95% CI 1.13 to 20.7) and initial leukocytosis (OR 1.22, 95% CI, 1.11 to 1.35) were independent predictors of HUS. CONCLUSIONS: Based on the variables identified above, further studies are needed to determine whether the inflammatory response of the host represents only a marker of the severity of gastrointestinal infection or whether, alternatively, it is a pathophysiologic factor that leads to HUS.

Biomarkers↗
PubMed2000

Delivery of enteral nutrition.

There is increasing evidence that enteral feeding is superior to parenteral nutrition with regard to maintaining gut structure and function. Selection of the enteral access route depends on the type and anticipated duration of nutrient delivery. At present, enteral feeding devices can be divided into two major categories: those entering the gastrointestinal tract through the oral or nasal cavity (oroenteric or nasoenteric tubes) and those entering through the abdominal wall including gastrostomy, duodenostomy, or jejunostomy tubes. This article provides a review of methods to insert and confirm gastric and intestinal feeding tube placement. Care of the patient with an enteric tube will be described.

Acute Disease↗
PubMed2000

Infection control issues of enteral feeding systems.

Enteral feeding systems provide a mechanism for nutritional support for patients who may be unable to tolerate oral dietary sustenance. This review takes into account recent infection control issues relating to enteral feeding systems. The review is organized into the following areas of emphasis: infections associated with enteral tube feeding, the stability and contamination of enteral tube feeding, the risk:benefit analysis of enteral tube feeding, and the protective effects of enteral tube feeding.

Enteral Nutrition↗
PubMed2005

Bio-ecological control of acute pancreatitis: the role of enteral nutrition, pro and synbiotics.

PURPOSE OF REVIEW: Increasing knowledge, both experimental and clinical, supports the fact that early and aggressive enteral nutrition has the capacity to reduce superinflammation and prevent infections in severe acute pancreatitis. Clearly, the main role of enteral nutrition is to boost the immune system, and not, at least initially, to provide calories. Whereas enteral nutrition improves, parenteral nutrition reduces immune functions. RECENT FINDINGS: The content of enteral nutrition solutions is more important than the route of administration per se. Antioxidants, plant fibres and live lactic acid bacteria are especially important for boosting the immune system. Recent studies support the fact that enteral nutrition and the supply of fibres and live lactic acid bacteria may significantly reduce the rate of infections. So far none of the treatments has been able to reduce the incidence of the systemic inflammatory response syndrome and multiorgan dysfunction syndrome. A recent unpublished study indicates, however, that the systemic inflammatory response syndrome and multiorgan dysfunction syndrome can also be reduced if much higher doses of lactic acid bacteria and a combination of several bioactive lactic acid bacteria are used (synbiotics). SUMMARY: Immunosupporting enteral nutrition with synbiotics is an important tool to control superinflammation and infection, and might also reduce the multiorgan dysfunction syndrome and systemic inflammatory response syndrome. It is essential that it is supplied early, if possible in the emergency room. New autopositioning regurgitation-resistant feeding tubes are available to facilitate such a policy.

Acute Disease↗
PubMed2005

Enteric nervous system.

PURPOSE OF THE REVIEW: The purpose of this review is to provide a synopsis of how the field of enteric neurobiology has advanced during the past 2 years. RECENT FINDINGS: With more than 500 studies from which to choose, the authors have focused on several themes that illustrate recent progress. There has been an explosion of interest in the development of the enteric nervous system driven by the need to understand development abnormalities, particularly in Hirschsprung disease, and fueled by technical advances for investigating how neural crest-derived cells migrate, proliferate, and differentiate into enteric neurons and glia. The use of neural stem cells as a therapeutic strategy aimed at repopulating regions of bowel, where enteric neurones are reduced or absent, is on the horizon. Enteric reflexes involve interactions between sensory neurons, interneurons, and motor neurons. Recent findings suggest this distinction may be blurred, with neurons having multifunctional properties, perhaps because enteric neurons, unlike their central nervous system counterparts, are directly exposed to mechanical forces that they regulate. Another topic the authors have highlighted is pharmacology, with new tools for investigating ion channels, receptors, and transporters, leading to an expanding list of molecular mechanisms that regulate neuronal excitability. Long-term alterations in the expression of these molecules during disease or injury may underlie many gastrointestinal disorders that currently have unknown etiology. The authors finish with a look to the future and what may be the subject of this review next time. SUMMARY: Basic science information gathered during the past 2 years provides insight into pathophysiologic processes and will pave the wave for improved understanding of both organic and 'functional' gastrointestinal disorders.

Animals↗
PubMed1994

Interruption of enteral feedings in head injured patients.

This study was undertaken to determine differences between caloric intake and requirements of critically ill, enterally fed, neurosurgical and neurotrauma patients and to determine the nature and frequency of interruptions in enteral feedings in this same population. This descriptive, prospective study was conducted in a surgical intensive care unit (ICU) in a university teaching hospital. The sample consisted of 52 mechanically ventilated, critically ill patients with a mean age of 48.96 years who were receiving enteral nutrition for at least two days. Basal energy requirements, daily nutritional intake and enteral feeding interruption characteristics were recorded for a total of 586 study days. Underfeeding due to interruptions occurred in the majority of patients for the first eight days following initiation of enteral feeding. Reasons for underfeeding were interruptions of continuous tube feedings due to medication administration via the feeding tube (31%), feeding tube displacement (27%), surgery (12%), ileus (9%), radiologic studies (9%), airway management (8%), bedside procedures (3%) and agitation (1%). The frequency of these enteral feeding interruptions may indicate inadequate nutritional support, highlighting the importance of performing daily nutritional monitoring to prevent malnutrition.

Adolescent↗
PubMed1980

Enteric coated quinidine compared to sustained release preparations during repeated administration.

The concentration of quinidine in plasma was measured in 12 healthy subjects during multiple administration of an enteric coated tablet (Systodin) and two sustained release preparations (Kinidin Duretter and Kinilentin). In a second study, involving another 12 subjects, the enteric coated tablet and the most widely used sustained release preparation (Kinidin Duretter) were compared with plain uncoated quinidine sulphate tablets in order to calculate the relative bioavailability of the formulations used for maintenance therapy. The largest area under the plasma concentration-time curve (AUC12h) during a dosage interval (12 hours) was obtained with the plain tablets and with the enteric coated formulation. The variation of the plasma concentrations during the dosage interval was not larger with the enteric coated tablets than with the sustained release preparations. The time of appearance of peak concentration after administration was longer and more variable with the enteric coated tablets. In relation to the plain quinidine tablets, the bioavailability of Systodin and Kinidin Duretter was 96% and 84%, respectively. In 21 out of 24 crossover experiments with Kinidin Duretter and Systodin the AUC12h was larger with the latter formulation. Enteric coating appears to be a simple and reliable means of achieving delayed absorption and stable quinidine plasma levels during maintenance therapy.

Adult↗
PubMed1991

Aspirin-induced gastric mucosal damage: prevention by enteric-coating and relation to prostaglandin synthesis.

1. Gastric damage induced by low-dose aspirin and the protective effect of enteric-coating was assessed in healthy volunteers in a double-blind placebo-controlled cross-over trial using Latin square design. Each was administered placebo, plain aspirin 300 mg daily, plain aspirin 600 mg four times daily, enteric-coated aspirin 300 mg daily, or enteric-coated aspirin 600 mg four times daily for 5 days. Gastric damage was assessed endoscopically, and gastric mucosal bleeding measured. 2. Aspirin 300 mg daily and 600 mg four times daily caused significant increases in gastric injury compared with placebo. Gastric mucosal bleeding was significantly more with the high dose, with a trend towards increased gastric erosions, compared with the low dose. 3. Enteric-coating of aspirin eliminated the injury caused by low dose aspirin and substantially reduced that caused by the higher dose. 4. All dosages and formulations caused similar inhibition of gastric mucosal prostaglandin E2 synthesis. 5. Serum thromboxane levels were suppressed equally with plain and enteric-coated aspirin. 6. In this short-term study in healthy volunteers, gastric toxicity from aspirin was largely topical, independent of inhibition of prostaglandin synthesis, and could be virtually eliminated by the use of an enteric-coated preparation.

Adult↗
PubMed1977

The effects of enteric coating of aspirin tablets on occult gastrointestinal blood loss.

The effect of enteric coating of aspirin tablets on the gastrointestinal blood loss associated with high dose aspirin therapy was investigated in 12 patients with rheumatoid arthritis. Occult blood loss was measured after labelling the patients' red blood cells with Cr51. Three salicylate preparations were used: enteric coated tablets of aspirin ("Rhusal", G.P. Laboratories, 7 x 650 mg per day), uncoated tablet cores of aspirin from the same batch (7 x 650 mg per day) and enteric coated tablets of sodium salicylate (7 x 600 mg and 1 x 300 mg per day). Daily blood loss during a salicylate-free period was (0.7 +/- 0.15 ml, mean +/- SE). Blood loss was significantly increased during dosage with all three salicylate preparations. Daily blood loss during dosage with the uncoated tablets of aspirin (5.3 +/- 0.3 ml) was significantly greater than during dosage with the enteric coated tablets of aspirin (2.3 +/- 0.3 ml) and enteric coated tablets of sodium salicylate (2.1 +/- 0.4 ml). The bioavailability of the salicylate preparations was studied in seven of the 12 patients. Mean plasma salicylate concentration two hours after the second daily dose during dosage with the enteric coated tablets of aspirin was 118 +/- 15 microgram/ml compared to 131 +/- 16 microgram/ml during dosage with the uncoated tablets. Urinary recoveries of the daily dosage of aspirin in the two formulations were also similar.

Aged↗
PubMed2004

Enteral nutrition in patients with acute renal failure.

BACKGROUND: Systematic studies on safety and efficacy of enteral nutrition in patients with acute renal failure (ARF) are lacking. METHODS: We studied enteral nutrition-related complications and adequacy of nutrient administration during 2525 days of artificial nutrition in 247 consecutive patients fed exclusively by the enteral route: 65 had normal renal function, 68 had ARF not requiring renal replacement therapy, and 114 required renal replacement therapy. RESULTS: No difference was found in gastrointestinal or mechanical complications between ARF patients and patients with normal renal function, except for high gastric residual volumes, which occurred in 3.1% of patients with normal renal function, 7.3% of patients with ARF not requiring renal replacement therapy, 13.2% of patients with ARF on renal replacement therapy (P= 0.02 for trend), and for nasogastric tube obstruction: 0.0%, 5.9%, 14%, respectively (P < 0.001). Gastrointestinal complications were the most frequent cause of suboptimal delivery; the ratio of administered to prescribed daily volume was well above 90% in all the three groups. Definitive withdrawal of enteral nutrition due to complications was documented in 6.1%, 13.2%. and 14.9% of patients, respectively (P= 0.09 for trend). At regimen, mean delivered nonprotein calories were 19.8 kcal/kg (SD 4.6), 22.6 kcal/kg (8.4), 23.4 kcal/kg (6.5); protein intake was 0.92 g/kg (0.21), 0.87 g/kg (0.25), and 0.92 g/kg (0.21), the latter value being below that currently recommended for ARF patients on renal replacement therapy. Median fluid intake with enteral nutrition was 1440 mL (range 720 to 1960), 1200 (720 to 2400), and 960 (360 to 1920). CONCLUSION: Enteral nutrition is a safe and effective nutritional technique to deliver artificial nutrition in ARF patients. Parenteral amino acid supplementation may be required, especially in patients with ARF needing renal replacement therapy.

APACHE↗
PubMed1999

Palliative transhepatic biliary drainage and enteral nutrition.

Simultaneous intestinal and biliary obstruction is a rare but agonizing complication of metastatic abdominal cancer. Although endoscopic procedures exist that relieve jaundice or restore enteral nutrition, they can be impossible to perform for technical or anatomical reasons. We propose a palliative approach for these patients that includes transcutaneous common bile duct drainage, progressive dilation of the transhepatic channel over 1 wk, and, finally, insertion of a permanent silicon catheter that drains bile into the duodenum and is combined with an enteral feeding line. We report three patients whose metastatic abdominal tumors had led to simultaneous jaundice and gastric outlet obstruction, neither of which could be treated endoscopically. In all patients, the transcutaneous bile drainage catheter combined with the enteral feeding line was inserted and tumor symptoms resolved rapidly. As a result, the patients chose to return to home care with enteral nutrition and pain medication. The creation of a transhepatic access for simultaneous enteral bile drainage and nutrition is a technically simple procedure that causes little discomfort to a terminally ill patient. It relieves the symptoms of tumor obstruction, and the option of enteral nutrition and medication can obviate the need for intravenous infusions.

Aged↗
PubMed1986

Gut hormones and 'minimal enteral feeding'.

Previously we have identified multiple surges in plasma concentrations of gut hormones postnatally in enterally fed term and preterm infants. In this study on 104 preterm infants we have shown that such surges are induced after ingestion of very small quantities of human milk. Whereas 6-day-old exclusively parenterally fed infants showed no postnatal elevation in enteroglucagon, gastrin, GIP, motilin and neurotensin, infants recovering from hyaline membrane disease who had received restricted enteral nutrition had similar hormone surges to those seen in well infants on full enteral feeds. Significant elevations in enteroglucagon, gastrin and GIP occurred after a cumulative mean enteral feed volume since birth of only 24 ml (12 ml/kg body weight) had been consumed and after a mean total intake of 96 ml (50 ml/kg) the response was maximal. Greater feed volumes were required to produce a neurotensin or motilin surge, but even these volumes were substantially lower than those required for full enteral feeding. In view of the proposed roles of gut hormones in the adaptation to extrauterine nutrition these data have implications for mammalian biology and raise the possibility that 'minimal enteral feeding' might have a clinical therapeutic role in infants undergoing prolonged parenteral nutrition.

Enteral Nutrition↗
PubMed2004

Enteric neural crest-derived cells and neural stem cells: biology and therapeutic potential.

The enteric nervous system arises from two regions of the neural crest; the vagal neural crest which gives rise to the vast majority of enteric neurones throughout the gastrointestinal tract, and the sacral neural crest which contributes a smaller number of cells that are mainly distributed within the hindgut. The migration of vagal neural crest cells into, and along the gut is promoted by GDNF, which is expressed by the gut mesenchyme and is the ligand for the Ret/GFRalpha1 signalling complex present on migrating vagal-derived crest cells. Sacral neural crest cells enter the gut after it has been colonized by vagal neural crest cells, but the molecular control of sacral neural crest cell development has yet to be elucidated. Under the influence of both intrinsic and extrinsic cues, neural crest cells differentiate into glia and different types of enteric neurones at different developmental stages. Recently, the potential for neural stem cells to form an enteric nervous system has been examined, with the ultimate aim of using neural stem cells as a therapeutic strategy for some gut disorders where enteric neurones are reduced or absent.

Animals↗
PubMed1991

Enteral feeding as sole treatment for Crohn's disease: controlled trial of whole protein v amino acid based feed and a case study of dietary challenge.

A controlled trial was performed to compare enteral feeding with either an amino acid based feed or a whole protein feed as sole treatment for active Crohn's disease. Twenty four patients were studied (nine with ileal, 11 with ileocolonic, and four with colonic disease). Both feeds proved effective; nine of 13 patients randomised to receive the amino acid based feed were in clinical remission within three weeks as defined by a simple activity index compared with eight of 11 treated with the whole protein feed. Patients in clinical remission were then crossed over onto the other feed. None of the six patients who were changed to the whole protein feed relapsed over the subsequent three week period compared with three of seven patients who were changed to the amino acid based feed. In responders the median serum C reactive protein concentration fell from 21 mg/l (range 9-82) on entry to 6 mg/l (range 3-19) at six weeks. Seven patients relapsed within eight months of starting solid food (mean 3.7 months), while nine were still in remission (follow up period 3-9 months, median six months). Detailed studies of staged reintroduction of food and permitted food additives were carried out over a four year period in a patient with extensive stricturing small bowel Crohn's disease who had been brought into remission by open treatment with enteral feeding. Carrageenan, other permitted emulsifiers, bread, meat, potatoes, oranges, refined sugar, dairy produce, flour, and rice were all reintroduced without any objective ill effect, but green vegetables provoked a clinical and biochemical relapse within one week of introduction. Remission was rapidly achieved by switching back to the enteral feed but reintroduction of the low residue diet that had been previously tolerated produced a brisk relapse. Clinical and biochemical remission was again achieved by a return to the enteral feed but relapse again occurred with reintroduction of the low residue diet. These studies confirm the therapeutic effect of enteral feeding in Crohn's disease. This effect does not seem to be due to avoidance of whole protein, but the very low residue of chemically defined enteral feeds may be important, particularly in patients with intestinal strictures.

Adult↗
PubMed1996

Supplementary enteral nutrition maintains remission in paediatric Crohn's disease.

BACKGROUND: Liquid diets given enterally combined with "bowel rest' are efficacious in the treatment of active Crohn's disease, but rapid recrudescence of gastrointestinal symptoms after resumption of a normal diet is common. AIMS: This study examined whether continuation of enteral nutrition as a nocturnal supplement to an ad libitum daytime intake of a normal diet increased the length of remission of Crohn's disease in children. PATIENTS AND METHODS: Children and adolescents with active Crohn's disease treated successfully with exclusive enteral nutrition were classified retrospectively according to whether they continued supplementary enteral nutrition or not. Time to relapse and linear growth were compared between the two cohorts. RESULTS: Between January 1986 and December 1992, 65 patients aged 7-17 years (mean (SD) 13.6 (2.1) years) (36 males, 29 females) with Crohn's disease in exacerbation were treated for > or = four weeks by bowel rest and nasogastric tube feeding of an oligopeptide or amino acid based formula. At first follow up visit, remission (fall in Paediatric Crohn's Disease Activity Index, PCDAI to < or = 20) was achieved in 47 of 65 (72%) patients. Subsequently, 20 of these 47 (43%) relapsed by six months and 28 of 47 (60%) by 12 months. Patients who continued nasogastric supplementary feeding (n = 28) after resumption of an otherwise normal diet remained well longer than those who discontinued nocturnal supplements completely (n = 19) (p < 0.02). Furthermore, continued use of nasogastric supplements before completion of puberty was associated with improved linear growth. CONCLUSION: After successful treatment of active Crohn's disease by exclusive enteral nutrition, supplementary enteral nutrition without restriction of normal diet is associated with prolongation of remission and improved linear growth in children and adolescents.

Adolescent↗
PubMed1997

Energy expenditure and body composition in children with Crohn's disease: effect of enteral nutrition and treatment with prednisolone.

BACKGROUND: Malnutrition and growth retardation are common complications of Crohn's disease in children. The contribution of resting energy expenditure (REE) to malnutrition is unclear. AIMS: To characterise the REE and body composition in children with Crohn's disease and compare them with normal controls and patients with anorexia nervosa; to compare the effects of prednisolone and enteral nutrition on energy expenditure and body composition. SUBJECTS: Twenty four children with Crohn's disease, 19 malnourished females with anorexia nervosa, and 22 healthy control subjects were studied. METHODS: In children with Crohn's disease measurements were done when the disease was acute and repeated at one and three months after treatment with either prednisolone or enteral nutrition. Resting energy expenditure was measured by indirect calorimetry and body composition by anthropometry, bioelectrical impedance analysis, total body potassium, H218O, and bromide space studies. RESULTS: Body weight and ideal body weight were significantly lower in patients with Crohn's disease than in healthy controls. Lean tissue was depleted and there was an increase in extracellular water. Per unit of lean body mass, there was no difference between REE in patients with Crohn's disease and controls, whereas patients with anorexia nervosa had significantly reduced REE. With enteral nutrition all body compartments and REE increased significantly (p < 0.001). In a subgroup of age-matched men there was a significant increase in height after three months of enteral nutrition compared with prednisolone (p < 0.01). Those treated with steroids did not show a significant change in height but did show an increase in all body compartments. However, intracellular water as well as lean body mass accretion were significantly higher in the enteral nutrition group than in the prednisolone group. CONCLUSIONS: Despite being malnourished, children with Crohn's disease fail to adapt their REE per unit of lean body mass. This might be a factor contributing to their malnutrition. Lean tissue accretion is higher in patients treated with enteral nutrition than in those treated with prednisolone.

Adolescent↗
PubMed2006

Role of enteric glia in intestinal physiology: effects of the gliotoxin fluorocitrate on motor and secretory function.

The role of enteric glia in gastrointestinal physiology remains largely unexplored. We examined the actions of the gliotoxin fluorocitrate (FC) on intestinal motility, secretion, and inflammation after assessing its efficacy and specificity in vitro. FC (100 microM) caused a significant decrease in the phosphorylation of the glucose analog 2-[N-(7-nitrobenz-2-oxa-1,3-diaz-4-yl)amino]-2-deoxyglucose in enteric glial cultures and a reduction in glial uptake of the fluorescent dipeptide Ala-Lys-7-amino-4-methylcoumarin-3-acetic acid in both the ileum and colon. Dipeptide uptake by resident murine macrophages or guinea pig myenteric neurons was unaffected by FC. Incubation of isolated guinea pig ileal segments with FC caused a specific and significant increase in glial expression of the phosphorylated form of ERK-1/2. Disruption of enteric glial function with FC in mice reduced small intestinal motility in vitro, including a significant decrease in basal tone and the amplitude of contractility in response to electrical field stimulation. Mice treated with 10 or 20 micromol/kg FC twice daily for 7 days demonstrated a concentration-dependent decrease in small intestinal transit. In contrast, no changes in colonic transit or ion transport in vitro were observed. There were no changes in glial or neuronal morphology, any signs of inflammation in the FC-treated mice, or any change in the number of myenteric nitric oxide synthase-expressing neurons. We conclude that FC treatment causes enteric glial dysfunction, without causing intestinal inflammation. Our data suggest that enteric glia are involved in the modulation of enteric neural circuits underlying the regulation of intestinal motility.

4-Chloro-7-nitrobenzofurazan↗
PubMed2003

Platelet-activating factor concentration in the stool of human newborns: effects of enteral feeding and neonatal necrotizing enterocolitis.

Epidemiologic studies have identified enteral feedings as a risk factor for necrotizing enterocolitis (NEC). Enteral feedings provide the substrate for colonization of the newborn gut with gram-negative bacteria with endotoxin production, which may trigger the production of endogenous inflammatory mediators, including platelet-activating factor (PAF). In this prospective study, we examined the effect of enteral feeding on PAF concentration in the stool of preterm and full-term human newborns. The concentration of PAF levels in stool was measured at the following times: at passage of first meconium, within 24 h prior to the onset of feedings, at the 3rd and 14th day of feeding and at any time confirmed NEC developed. Stool samples also were analyzed for levels of acetylhydrolase, the PAF breakdown enzyme. Stool PAF concentration rose significantly following the start of enteral feedings. The mean PAF concentration for day 14 samples was significantly higher than the mean concentration of meconium samples (4.90 +/- 1.03 vs. 1.81 +/- 0.38 ng/g, p < 0.05) and day 0 samples (4.90 +/- 1.03 vs. 1.79 +/- 0.39 ng/g, p < 0.05). For the 7 patients diagnosed with definite NEC, the mean stool PAF concentration was 12.42 +/- 0.77 ng/g, significantly elevated compared to the mean PAF levels in stool from healthy infants at all sampling times (p < 0.01). There was no significant change in acetylhydrolase activity at any of the sampling times. Stool PAF concentration increases with the provision of enteral feedings and rises further with the development of NEC. Since stool acetylhydrolase activity remained unchanged, we speculate the increase of PAF in stool likely represents increased PAF production at the local level following the provision of enteral feedings or the development of neonatal necrotizing enterocolitis.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗