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Abstract

14 March 2001 Dear Editor REPLY Necrotizing enterocolitis (NEC) in full-term and preterm neonates are very different in some aspects such as aetiology and causation but can be quite similar in terms of management. This review article1 was written with the hope that we may learn from the experience gleaned from preterm infants and apply or modify that knowledge according to the differences already apparent in the full-term neonate. The reason why Drs Bolisetty and Lui had reported a very low incidence of NEC in their study2 could be because NEC is frequently not the first diagnosis to come to mind in a full-term infant who presents with an acute abdomen, especially if feeds had not been commenced (6/43 or 14% in the largest series of 43 full-term NEC neonates to date),3 and not because NEC is a rare event in Australia. Population-based studies on epidemiology and incidence are always fraught with problems such as non-recognition, misdiagnosis and therefore under-reporting and cannot be reasonably compared to figures derived from institution-based studies. 3–;6 The fact that a larger proportion of these full-term infants have congenital problems as compared to the preterm neonate who usually develops NEC secondary to prematurity-related complications remains undisputed as was clearly obvious in this review. Andrews et al.7 encountered two out of 10 full-term neonates (20%) who had Down syndrome with acyanotic heart defects in 1990, which was a similar observation noted by Polin et al. in 1976.5 Hypoglycaemia was noted in 20.9% of the 43 full-term neonates with NEC3 and was a statistically significant risk factor for NEC in infants weighing 2001–;2500 g at birth.8 Unfortunately, we do not know how many of these infants’ hypoglycaemia was secondary to an endocrine problem such as cortical adrenal hyperplasia or panhypopituitarism. Although it is true that the literature on T-cryptantigen screening was largely derived from the preterm population, the red cells of full-term neonates with NEC can be similarly activated. Novak et al.9 had found a significant decrease in mortality and need for surgery after prospectively testing for T antigen activation which was in contrast to the findings of Osborn et al.10 Considering that NEC in the full-term neonate can have a similarly aggressive onset culminating in death in some infants, the fact that mortality can ensue (albeit lower when compared to the preterm neonate) more than justifies the small efforts and/or expenditure involved in screening or just giving blood products with low titres of T or Tk antigens. Cytokine modulating therapy holds promise not just in the case of the preterm but also in the full-term neonate. Platelet-activating factor (PAF) may contribute to NEC. We know that PAF acetylhydrolase (PAF-AH) activity was not only significantly lower in both preterm milk of mothers who delivered between 26 and 32 weeks gestation and full-term breast milk, but also that PAF-AH activity decreases with advancing lactational age.11 The incidence of NEC may therefore be possibly reduced by either increasing plasma PAF-AH activity with steroids or adding recombinant enzymes to breast milk or infant formula.12 I would like to thank Drs Bolisetty and Lui for their comments. It is quite evident that there are wide gaps in our understanding of neonatal gastrointestinal physiology and pathophysiology. The aetiology and causation of NEC in some full-term neonates may be different when compared to the preterm neonate, but I would like to draw your attention to the fact that the aetiology may not be immediately obvious in up to 7% of these cases.2, 3 Considering the significant morbidity and potential mortality associated with NEC developing in full-term neonates, it would be presumptuous not to consider and explore ways to prevent or reduce the incidence, of this disease.