Hypoglycaemia in newborn infants: Defining the features associated with adverse outcomes--a challenging remit. Commentary to Rozance PJ and Hay WW: Hypoglycaemia in newborn infants: Features associated with adverse outcomes (Biol Neonate 2006;90:74-86).

Abstract

may be defi ned. In order to do so they have conducted a rigorous critical appraisal of papers which have to date informed practice and dogma. As many others have concluded, they confi rm that there are no scientifi c fi ndings of suffi cient rigour to inform evidence-based guidelines and as others before them, they offer pragmatic guidance. Rozance and Hay review a wide range of published literature and emphasise the methodological weakness of many of the studies. In their excellent review of the descriptive papers of normal neonatal metabolic adaptation, they acknowledge the innate variation between babies in terms of the ability to mount protective responses (including ketone body production) and thus infants’ biological resistance to ‘hypoglycaemia’. The authors do stress that neonatal hyperinsulinism requires special attention, the signifi cant pathological mechanism being an inability to produce ketone bodies. They also consider how our own interventions, albeit well intended, may affect normal patterns of metabolic adaptation, for example the suppressive effect of formula feeding on ketogenesis. As for many other practising clinicians, Rozance and Hay acknowledge that clinical assessment of the baby, with laboratory measurements as part of this evaluation, invariably inform clinical management. That is, blood For many years, since the seminal works of the late and highly respected Marvin Cornblath, neonatologists and experts in metabolic medicine have been seeking to describe and defi ne the concept of neonatal hypoglycaemia, with some authors ready to stick their head above the parapet and pronounce upon that level of blood glucose which will result in brain injury and therefore must be avoided. Others, including an expert group led by Marvin Cornblath and the authors of this paper, remained circumspect, even after review of the available literature [1] . Some of these experts, recently faced again with the challenge to be more precise, have not changed their view [2–4] . In the current climate where the medical scientifi c community must meet the need to conduct high impact research exploring basic science, molecular genetics, and gene expression, we are far from fi nding scientifi c solutions to the neonatal hypoglycaemia dilemma. At the same time, although there are international epidemiological studies which are of a suffi ciently large scale to identify independent aetiological factors for some perinatal outcomes, there are no studies of the size or rigour to determine the independent effect of neonatal hypoglycaemia. The stated aim of Paul Rozance and Bill Hay was to determine whether the ‘damaging’ level of blood glucose Published online: March 9, 2006