Necrotizing enterocolitis (NEC) is a severe neonatal disease affecting particularly preterm infants. Its exact pathogenesis still remains unknown. In this study, we have compared the prevalence of vascular obstructive lesions in placentae of premature newborns which developed NEC and of a control group. We further compared separately the findings of placentae of infants of less than 30 weeks of gestation, the age group in which NEC occurs most frequently. We found signs of fetal vascular obstructive lesions in 65% of the placentae of preterm patients developing NEC, compared to only 17% of the placentae of preterm patients in the control group. In the age groups below 30 weeks of gestation, 58.5% of placentae of later NEC patients presented such lesions compared to 24.5% in the control group. The significant difference between NEC and control group suggests a strong association between fetal vascular obstructive lesions and NEC. Therefore, we propose that fetal vascular obstructive lesions might be considered as a risk factor for the development of NEC in premature infants. 1. Introduction Necrotizing enterocolitis (NEC) is one of the most dreadful and unpredictable emergencies in premature infants [1, 2]. Its incidence is around 7% in very low-birth-weight infants (VLBW, birth weight <1500？g) [1, 3] and almost absent in full-term neonates [4]. The exact pathogenesis of NEC is still unknown. Many etiologic conditions have been described favorizing the development of NEC, such as gut immaturity, decreased gut motility, gastrointestinal bacterial colonization, and accelerated feeding [5–7]. Different authors suggested intestinal ischemia and hypoxia as important risk factors. The earlier proposed “diving reflex” in neonates suffering from severe hypoxic episodes with diversion of blood preferentially to heart, brain, and kidneys resulting in decreased perfusion of the intestinal tract could not explain all facets of the pathophysiology of NEC [8]. However, some pieces of evidence support the idea that hypoxic-ischemic events may play an important role in its etiology. (1) The ileocecal region which is often involved in NEC corresponds to an intestinal “watershed” area which might explain its susceptibility to hypoxic-ischemic events. (2) Reduced perfusion plays an important role in the pathophysiology of coagulation necrosis which represents one of the major histological findings of NEC [9]. (3) The rare condition of NEC in term infants is often associated with reduced intestinal perfusion secondary to congenital heart disease, patent ductus arteriosus,
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