Epidemiology of necrotizing enterocolitis

Am, Kosloske

doi:10.1111/j.1651-2227.1994.tb13232.x

Cited by 218 publications

(158 citation statements)

References 69 publications

(46 reference statements)

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“…Ninety percent of cases occur in preterm infants, with the greatest risk in the smaller, more premature infants (Lin et al 2008;Thompson and Bizzarro 2008;Schnabl et al 2008). Compared with an overall incidence rate of 1% to 7.7%, up to 7% to 14% of very-low-birth-weight infants (< 1,500 g) are diagnosed with NEC (Kosloske 1994;Neu 2005). NEC is characterized by disruption of mucosal integrity, feeding intolerance, bloody stools, cardiorespiratory compromise, and severe hemodynamic instability.…”

mentioning

confidence: 99%

“…The etiology and pathophysiology of NEC is not fully understood, in spite of extensive studies (Lin et al 2008;Thompson and Bizzarro 2008;Schnabl et al 2008). NEC is a devastating disease with a mortality rate of 10% to 50% (Kosloske 1994;Thompson and Bizzarro 2008;Schnabl et al 2008). Morbid sequelae among survivors include impaired growth, short bowel syndrome, prolonged neonatal hospitalization, and poor longterm neurodevelopment (Carter 2007;Schulzke et al 2007).…”

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confidence: 99%

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C5a, A Complement Activation Product, Is a Useful Marker in Predicting the Severity of Necrotizing Enterocolitis

Tayman

Tonbul

Kahveci³

et al. 2011

Tohoku J. Exp. Med.

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Necrotizing enterocolitis (NEC) is the most common neonatal gastrointestinal emergency, predominantly affecting low-birth weight, premature infants. Early clinical signs of NEC are nonspecific and the laboratory findings are not fully reliable. Its severe morbidities and rapid progression require the application of new biomarkers for early diagnosis and intervention. The complement activation product, C5a (anaphylatoxin) has been reported to be a contributing factor leading to mesenteric ischemia/reperfusion injury which is a predisposing factor in the pathogenesis of NEC. Therefore, our aim was to evaluate the efficacy of serial C5a measurements in the diagnosis and follow-up of NEC. Preterm infants, whose gestational age and weight matched each other, were grouped as controls (n = 23) and NEC (n = 22). Serum levels of C5a, serum amyloid-A (SAA), C-reactive protein (CRP), and interleukin-6 (IL-6) levels were measured on the third day of life for the control group and on the day of diagnosis (1 st day), 3 rd and 7 th days of the NEC group. C5a, SSA, CRP, and IL-6 levels were significantly higher in the NEC patients compared to the control group (P < 0.05) in the follow-up. Additionally, serum levels of C5a were found to be more accurate than the other parameters for the prediction of death and requirement for surgery at the time of diagnosis (P < 0.05). In conclusion, C5a may be useful as a new marker for both diagnosis and follow-up of infants with NEC in combination with clinical and radiographical findings.

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confidence: 99%

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confidence: 99%

C5a, A Complement Activation Product, Is a Useful Marker in Predicting the Severity of Necrotizing Enterocolitis

Tayman

Tonbul

Kahveci³

et al. 2011

Tohoku J. Exp. Med.

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“…Many risk factors have been identified as contributing to the pathogenesis of NEC, including prematurity, enteral feeding, hypothermia, bacterial colonization, and hypoxia [16][17][18][19][20][21][22][23]. Many believe NEC to be secondary to a deranged or uncontrolled inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

Unexpected Macrophage Activity Alters the Inflammatory Process in Necrotizing Enterocolitis

Raque¹,

Matheson²,

Connolly³

et al. 2017

J Cytokine Biol

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Objective: Macrophages play a role in clearing bacteria from the gut in the initial stages of necrotizing enterocolitis (NEC). Macrophage Inflammatory Protein-1α (MIP-1α), also known as CCL3, is a chemokine produced by macrophages that enhances the immune response. It acts as both a recruiter of immune cells and a coactivator of other macrophages. Interleukin-12 (IL-12) is a pro-inflammatory chemotactant produced by several types of phagocytic cells such as dendritic cells and neutrophils, but primarily by macrophages. We hypothesized that the pro-inflammatory state associated with NEC pathophysiology would induce increased expression of MIP-1α and IL-12 that would be detectable in serum and intestinal tissue.Methods: Timed pregnant Sprague-Dawley rats were randomized by litter. Controls were delivered vaginally and dam-fed. NEC pup groups were delivered 12 h prematurely via Cesarean section, formula fed, given a single oral dose of lipopolysaccharide, and subjected to intermittent cold and hypoxia as part of a proven NEC rat model protocol. Animals were sacrificed at 0, 12, 24, 48, 72, and 96 h of life and serum and intestinal tissue samples were collected. Samples were analysed via western blot using antibodies with affinity to MIP-1α and IL-12 respectively.Results: Serum and ileal levels of MIP-1 alpha were increased from 48 to 72 h in NEC animals when compared with controls. Serum and ileal IL-12 was downregulated in NEC groups at 12 and 24 h compared to controls. Conclusion:Macrophage function plays an important role in the first 48 h of NEC pathophysiology. Downregulation of IL-12 in the setting of increased MIP-1α expression may represent deranged or inhibited macrophage function in the context of NEC pathogenesis. Further work to elucidate the significance of these findings is warranted.

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“…The main component of the flora of these newborns is Bifidobacterium. Gestational age also affects the formation of the intestinal flora, preterm newborns in the neonatal intensive care unit have been observed to have a lower number of bacteria species, and the strains tended to be more virulent (24,25). Changes in the composition of intestinal microbiota occurs along the human intestinal tract and throughout the life of an individual, the composition of the flora however is quite stable during most of the individual's life (15).…”

Section: Normal Gut Microbiotamentioning

confidence: 99%

Translational research into gut microbiota: new horizons on obesity treatment: updated 2014

Tsukumo

Carvalho

Carvalho-Filho

et al. 2015

Arch. Endocrinol. Metab.

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Obesity is currently a pandemic of worldwide proportions affecting millions of people. Recent stu dies have proposed the hypothesis that mechanisms not directly related to the human genome could be involved in the genesis of obesity, due to the fact that, when a population undergoes the same nutritional stress, not all individuals present weight gain related to the diet or become hyperglycemic. The human intestine is colonized by millions of bacteria which form the intestinal flora, known as gut flora. Studies show that lean and overweight human may present a difference in the composition of their intestinal flora; these studies suggest that the intestinal flora could be involved in the development of obesity. Several mechanisms explain the correlation between intestinal flora and obesity. The intestinal flora would increase the energetic extraction of non-digestible polysaccharides. In addition, the lipopolysaccharide from intestinal flora bacteria could trigger a chronic sub-clinical inflammatory process, leading to obesity and diabetes. Another mechanism through which the intestinal flora could lead to obesity would be through the regulation of genes of the host involved in energy storage and expenditure. In the past five years data coming from different sources established causal effects between intestinal microbiota and obesity/insulin resistance, and it is clear that this area will open new avenues of therapeutic to obesity, insulin resistance and DM2. Arch Endocrinol Metab. 2015;59(2):154-60

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Epidemiology of necrotizing enterocolitis

Cited by 218 publications

References 69 publications

C5a, A Complement Activation Product, Is a Useful Marker in Predicting the Severity of Necrotizing Enterocolitis

C5a, A Complement Activation Product, Is a Useful Marker in Predicting the Severity of Necrotizing Enterocolitis

Unexpected Macrophage Activity Alters the Inflammatory Process in Necrotizing Enterocolitis

Translational research into gut microbiota: new horizons on obesity treatment: updated 2014

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