Is the elimination of endotoxin and cytokines with continuous lavage an alternative procedure in necrotizing enterocolitis?

Birk, Dieter; Berger, D.; Limmer, J.; Beger, H G

doi:10.1111/j.1651-2227.1994.tb13237.x

Cited by 14 publications

(11 citation statements)

References 12 publications

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“…The available clinical and animal studies suggest that the major etiologic factors include (1) intestinal mucosal injury, (2) presence of bacteria, (3) presence of bacterial substrate (e.g., feedings), and (4) immunologic immaturity of the preterm intestinal tract [3, 8, 10, 111. The histologic findings of coagulation necrosis, acute and chronic inflammation, ulceration, and hemorrhage are pathologic hallmarks of the disease [ 121. Several inflammatory cytokines that mediate inflammatory cell recruitment and activation and amplify the immune response in local host defense [ 13-1 51 have been implicated in NEC, including tumor necrosis-factor-a (TNF-a), interleukin-6 (IL-6), and IL-1p [16][17][18]. In most of the prior studies, cytokines were measured in plasma [16,171 or ascites fluid [18] rather than in affected intestinal tissue.…”

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confidence: 99%

Inflammatory Cytokine mRNAs in Surgical Specimens of Necrotizing Enterocolitis and Normal Newborn Intestine

Viscardi

Lyon

Sun

et al. 1997

Pediatric Pathology & Laboratory Medicine

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Coagulation necrosis, inflammation, and hemorrhage are pathologic hallmarks of necrotizing enterocolitis (NEC). Because cytokines are peptides that mediate inflammatory cell recruitment and amplify the immune response, several of the inflammatory cytokines have been implicated in NEC. We hypothesized that mRNA levels for the interrelated cytokines interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), IL-6, and the neutrophil chemotactic factor IL-8 would be increased in NEC and would be associated with the presence of inflammation. In this study, we determined the relative levels and localization of mRNA for these cytokines in surgical pathology archival intestinal tissue from 29 premature infants with acute NEC and 15 control infants with congenital intestinal malformations using a novel quantitative in situ hybridization technique. Compared with controls, there were higher IL-1 beta mRNA levels in full-thickness sections and higher TNF-alpha mRNA levels in full-thickness and mucosa sections of acute NEC samples, suggesting a potential role for these cytokines in the pathogenesis of local inflammation in NEC. IL-6 and IL-8 mRNA levels were similar in samples of control and acute NEC cases. Analysis of covariance including all subjects showed that the presence of acute inflammation was associated with increased IL-1 beta mRNA levels in mucosa (P = .035) and increased IL-8 in full-thickness sections (P = .005) and mucosa (P = .01). In four of five NEC cases in which intestinal specimens were available from reanastomosis surgery, cytokine mRNA levels decreased to low or undetectable levels. These data suggest that the inflammatory cytokines are involved in neutrophil recruitment and augmentation of the inflammatory response in neonatal intestine.

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confidence: 99%

Inflammatory Cytokine mRNAs in Surgical Specimens of Necrotizing Enterocolitis and Normal Newborn Intestine

Viscardi

Lyon

Sun

et al. 1997

Pediatric Pathology & Laboratory Medicine

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“…Epidemiological studies showed that prematurity, infection, early enteral feeding, and hypoxia are risk factors for NEC [3,4]. Although the definitive pathogenesis of the disease is not completely understood, a final common pathway of NEC was found to be the endogenous production of mediators and a systemic inflammatory reaction similar to that in sepsis and adult respiratory distress syndrome [4][5][6]. Concentrations of various mediators were found to be increased in plasma of human neonates with NEC [3][4][5][7][8][9][10].…”

Section: Introductionmentioning

confidence: 84%

Effect of C1-Inhibitor in a Rat Model of Necrotizing Enterocolitis

Sonntag

Wagner²,

Liu³

et al. 1999

Neonatology

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Our aim was to investigate the effect of C1-inhibitor (C1-INH) in a rat model of necrotizing enterocolitis (NEC). Twenty-four anesthetized and artificially ventilated rats received 0.1 mg/kg endotoxin. Fifteen minutes later, the animals in the study group (n = 12) were treated with 200 IU/kg C1-INH whereas the control animals (n = 12) received normal saline. In all animals, FiO₂ was reduced after 90 min from 0.21 to 0.05 and ventilation continued until 180 min or death. All animals developed shock symptoms. Drop in mean arterial blood pressure was more pronounced and survival time was shorter in the control group. Whereas the C1-INH activity increased in the study group, it decreased in the control group. The extent of macroscopic intestinal lesions did not differ between the groups. In conclusion, C1-INH did not prevent shock, but mitigated and delayed its course.

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“…In patients with NEC undergoing surgical intervention, IL-1 concentrations are elevated in peritoneal uid (52). Serum concentrations of IL-1 and IL-1ra are also elevated in more severe cases of NEC, implying that there is an association between NEC and this proinammatory cytokine (53).…”

Section: Interleukin-1mentioning

confidence: 99%

Enteral administration of hematopoietic growth factors in the neonatal intensive care unit

Calhoun¹

2002

Acta Paediatrica

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Calhoun DA. Enteral administration of hematopoietic growth factors in the neonatal intensive care unit. Acta Paediatr 2002; Suppl 438: 43-53. Stockholm. ISSN 0803-5326 By 20 wk of gestation, the human fetal gastrointestinal (GI) tract morphologically resembles that of the term infant, but functional development is limited before 26 wk. By 30 wk of gestation, the fetus has the capacity for limited digestion and enteral absorption. GI growth and development continue postnatally. Trophic factors, including nutrients, peptides, hormones and growth factors, are recognized as having important in uences on the morphology and histology of the developing GI tract. Other trophic factors are important in adaptation and repair following injury. Many such factors are provided in utero via amniotic uid swallowing and later by human colostrum and milk.Conclusion: This review discusses cytokines with known GI trophic effects, either in vitro or in vivo, and focuses on those cytokines that have been used in the neonatal intensive care unit.

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Is the elimination of endotoxin and cytokines with continuous lavage an alternative procedure in necrotizing enterocolitis?

Cited by 14 publications

References 12 publications

Inflammatory Cytokine mRNAs in Surgical Specimens of Necrotizing Enterocolitis and Normal Newborn Intestine

Inflammatory Cytokine mRNAs in Surgical Specimens of Necrotizing Enterocolitis and Normal Newborn Intestine

Effect of C1-Inhibitor in a Rat Model of Necrotizing Enterocolitis

Enteral administration of hematopoietic growth factors in the neonatal intensive care unit

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