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Effect of salt supplementation of newborn premature infants on neurodevelopmental outcome at 10–13 years of age
  1. E Sulyok
  1. Professor and Chairman, County Children’s Hospital, Institute of Health Promotion and Family Care, Faculty of Health Sciences, University of Pecs, H-7624 Pecs, PO Box 76, Hungary
    1. G Haycock1
    1. 1Blackheath, London SE3 9DE, UK; GHayc37893{at}aol.com

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      I read with interest the report by Al-Dahhan and colleagues1 on the beneficial effect of NaC1 supplementation of preterm infants during the neonatal period on their later neurodevelopmental outcome. They found better memory, learning, language, and educational performances at the age of 10–13 years in prematures who were given 4–5 mmol/day NaCl when compared with those not receiving NaCl supplement. In this regard it is relevant to mention our most recent findings describing a new aspect of the relation of neonatal sodium homoeostasis to central nervous system function. Namely, we showed that hyponatraemia is one of the most significant risk factors for development of sensorineural hearing impairment detected by transient evoked otoacoustic emission and confirmed by auditory brainstem response.2

      In addition, I consider their report raises an important ethical issue, in that I regard their selection of references as subjective and arbitrary. In particular, the work of our group in revealing some major features of sodium homoeostasis in premature infants has been ignored; for example, renal salt wasting, sodium depletion, and hyponatraemia,3–5 and the first introduction of NaCl supplementation in a dose of 3–5 mmol/kg/day to prevent sodium deprivation, to improve somatic stability, and to avoid untoward clinical consequences.6

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      Author’s reply

      Methinks Professor Sulyok doth protest too much. His early, pioneering work on electrolyte balance in the newborn is well known, and extensively cited in an earlier review of the subject co-authored by myself.1 In this, inter alia, his study of the effect of salt supplementation on the renin-angiotensin-aldosterone system2 is quoted in support of the hypothesis that hyponatraemia in premature infants is due to salt depletion rather than water retention. The reason these papers were not cited in the present paper is that they are not relevant to it. The paper is not a historical or general review of hyponatraemia in the newborn but the results of a study specifically designed to examine neurodevelopmental outcome in two particular groups of infants previously studied by ourselves.3–5 His recent study of hyponatraemia and sensorineural deafness in preterm infants6 had not been published when our paper was submitted to the Archives, although we would certainly have referred to it if it had been.

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