Maternal Risk Factors
The current epidemiologic literature has identified potential
maternal risk factors and the later development of NEC in their offspring; however, these risk factors are not consistent across studies. Risk factors that may be important by reducing overall fetal mesenteric blood flow include preeclampsia/toxemia, maternal hemorrhage, and placental abruption. In the literature there is an emerging hypothesis of altered gastrointestinal susceptibility resulting from inflammatory stimuli and its associated modulation by maternal and fetal inflammatory responses. Maternal and fetal cytokine mediators have been detected in the amniotic fluid and fetal plasma in pregnancies complicated by chorioamnionitis, preterm labor, and prolonged premature rupture of membranes. Cytokine mediators released during the fetal inflammatory response may be responsible for initiating preterm delivery and for subsequent
neonatal morbidity, including NEC. Supporting evidence for the role of maternal/fetal
inflammation and the development of NEC include the findings of increased NEC with duration of ruptured membranes and maternal chorioamnionitis. IUGR and prematurity are the most common fetal complications of
lupus pregnancy. Maternal risk factors for threatened fetal growth and development are active SLE, impaired renal function, and presence of aPL. A retrospective review of 72 SLE pregnancies3 found that preterm deliveries, observed in 39% of their patients, were associated with aPL and higher prednisone dose.
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