Necrotizing enterocolitis (NEC) represents a heterogeneous group of pathologic processes
in the intestines of neonates who are commonly premature with very low birth weights.
It is characterized by an intense inflammatory response and has mortality rates as high
as 20%–40% [
1
,
2
]. Despite the established relationship between necrotizing enterocolitis and a proinflammatory
cascade, the pathophysiology is still not completely understood. The involvement of
enteral feedings, compromised intestinal perfusion, and bacterial invasion are commonly
accepted factors [
[3]
]. There has been significant research into the pathophysiology of NEC; however, there
have been few major advances in its treatment. The mainstay of medical treatment continues
to be stabilization with bowel rest, gastrointestinal decompression, parenteral nutrition,
and antibiotics [
[4]
]. Further therapeutic strategies are much less well defined.To read this article in full you will need to make a payment
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References
- Necrotizing enterocolitis: research agenda for a disease of unknown etiology and pathogenesis.Pediatr Res. 1993; 34: 701
- Epidemiology of necrotizing enterocolitis temporal clustering in two neonatology practices.J Pediatr. 2009; 154: 656
- Epidemiology of necrotizing enterocolitis.Acta Paediatr Suppl. 1994; 396: 2
- Treatment and prevention of necrotizing enterocolitis.Semin Neonatol. 2003; 8: 449
- Induction of alkaline phosphatase in the inflamed intestine: a novel pharmacological target for inflammatory bowel disease.Biochem Pharmacol. 2004; 68: 2317
- Intestinal alkaline phosphatase detoxifies lipopolysaccharide and prevents inflammation in zebrafish in response to the gut microbiota.Cell Host Microbe. 2007; 2: 371
- Intestinal alkaline phosphatase prevents the systemic inflammatory response associated with necrotizing enterocolitis.J Surg Res. 2013; 180: 21
- Role of interleukin-10 in the pathogenesis of necrotizing enterocolitis.Am J Surg. 2012; 203: 428
- Intestinal alkaline phosphatase contributes to the reduction of severe intestinal epithelial damage.Eur J Pharmacol. 2010; 633: 71
- Transforming growth factor beta 1 null mutation in mice causes excessive inflammatory response and early death.Proc Natl Acad Sci U S A. 1993; 90: 770
Article info
Publication history
Published online: February 11, 2013
Accepted:
January 18,
2013
Received in revised form:
December 31,
2012
Received:
December 31,
2012
Identification
Copyright
© 2013 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
