IMR Press / FBL / Volume 11 / Issue 1 / DOI: 10.2741/1819

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


Genetic basis for necrotizing enterocolitis - risk factors and their relations to genetic polymorphisms

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1 First Department of Pediatrics, Semmelweis University, Budapest, First Department of Pediatrics, Budapest Bokay u. 53, H1083 Hungary
2 Research Laboratory of Pediatrics and Nephrology, Hungarian Academy of Sciences and Semmelweis University, Budapest Bokay u. 53, H-1083 Hungary
Front. Biosci. (Landmark Ed) 2006, 11(1), 570–580;
Published: 1 January 2006

Necrotizing enterocolitis (NEC) is a common, life-threatening neonatal gastrointestinal disease; it affects approximately 11% of extremely premature neonates. The etiology of NEC is multifactorial. Risk factors may roughly be grouped into four main categories: prematurity; transient ischemia of the intestine; local/systemic inflammation predisposing the bowel to injury, and therapeutic interventions. Recent studies have shown that carrier state of genetic polymorphisms may be associated with perinatal morbidity, including NEC. In perinatal disorders, the significance of genetic variants of cytokines, the renin-angiotensin-aldosterone system, and surfactant proteins have been investigated most widely. Positive findings indicate the implication of genetic polymorphisms of proinflammatory cytokines in premature birth; angiotensin converting enzyme in perinatal adaptation and angiotensin type 1 receptor in the closure of ductus arteriosus; surfactant proteins A and B in respiratory distress syndrome; interleukin (IL)-6 in sepsis, and IL-4-receptor α chain and IL-18 in NEC. This review provides an insight into the genetics of NEC and summarizes genetic data in light of pathologic processes leading to NEC.

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