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  1. JANET RENNIE, Deputy Editor

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Giant steps forward in neonatal hyperinsulinaemia

Few neonatologists can have failed to realise that progress in neonatal hyperinsulinaemia (HI) has been rapid since the genes associated with HI were first identified in 1994–95. All will appreciate the clarity and depth of the reviews published in this issue. Progress has been achieved as a result of effective collaboration between many laboratories, reflected in the authorship, and this research community deserve credit for working together in this way. Glaser et al (page F79) explain the pathways of insulin secretion and the possible genetic mutations in a way we can all understand, and teach us about a new genetic syndrome with hyperinsulinism and hyperammonaemia. Shepherd and colleagues in Sheffield (page F87) explain the physiology of insulin release with beautiful illustrations. Professor Aynsley-Green et al (page F98) translate the science into guidelines for management. They make strong recommendation for early transfer to a centre with experience so that the baby should have the best chance of early effective treatment, limiting the possibility of neural damage. Finally, Rahier et al (page F108) summarise the morphology of the pancreas in HI. This collection represents the state of the art in neonatal HI. The reviews need to be read slowly, carefully, and with concentration but the effort will be repaid by a vastly improved understanding of this complex condition.

Aussie neonatal units outperform Scottish equivalents

Tired of beating the UK at rugby and cricket the Australians are now apparently delivering better neonatal care (page F118). The risk adjusted mortality in neonatal intensive care units in Australia was significantly less than in similar units in Scotland in 1993–94. More infants survived without cerebral damage in Australia, and the differences remained robust after they were subjected to regression analysis. The authors speculate that the care model in Australia, involving more full time neonatologists and longer nurse training, with a staffing ratio of one nurse per ventilated baby may be the explanation. These data are thought provoking, particularly as they reflect similar differences in the outcome of paediatric intensive care, and will be of interest to many.

Deafness in ex-preterm infants may be due to a combination of risk factors

A team from Bristol has studied the factors underlying neonatal deafness in this high risk group using a case control methodology (pageF141). None of the usual culprits (aminoglycosides, bilirubin, frusemide) were implicated when examined by themselves, but when combined these factors differed significantly. A peak serum bilirubin of more than 200 μmol/l accompanied by netilmicin use or acidosis was associated with an increased chance of later deafness. Very few of the babies had a bilirubin of greater than 300, and only 15 deaf children were available to be studied, a reassuring number from a birth cohort of four years.

More news in neonatal neurology

Cioni and colleagues from Pisa demonstrated that visual function was a better predictor of adverse outcome in preterm babies that MRI scanning (page F134). Babies with poor visual acuity and/or eye movement patterns did badly in the long term.

 A group from the Hammersmith have followed up a cohort previously described in ADC—a group of term infants found to have abnormal cranial ultrasound scans on the postnatal wards (page F128). Abnormalities were surprisingly common and were found close to birth in 30%. The good news is that these changes do not usually matter and none of the infants had cerebral palsy when examined at 2 years. The only groups where there was a worry were those with periventricular white matter lesions (of whom half had locomotor delay) and asymmetrical ventriculomegaly (half with performance delay). Welcome reassurance for overworked neonatal ultrasonographers, and useful information to have to hand when the occasional term baby is found to have an ultrasound abnormality.