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Low melatonin production in infants with a life-threatening event

Published online by Cambridge University Press:  01 July 2000

Yakov Sivan
Affiliation:
Paediatric Intensive Care Unit, Dana Children's Hospital, Tel Aviv Medical Center, Tel Aviv, Israel.
Moshe Laudon
Affiliation:
Neurim Pharmaceuticals Ltd, Tel Aviv, Israel.
Jacob Kuint
Affiliation:
Neonatal Department, The Chaim Sheba Medical Center, Tel-Hashomer, Israel.
Nava Zisapel
Affiliation:
Department of Neurobiochemistry, Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel.
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Abstract

This study compares the urinary excretion of the main melatonin metabolite, 6-sulfatoxymelatonin (6SMT), in infants who have and have not experienced a life-threatening event (ALTE). 6SMT was assessed in the following groups of infants: 15 infants with ALTE for whom home monitoring had been recommended, 15 infants who had had an abrupt cyanotic apneic event but did not require mouth-to-mouth resuscitation, 15 siblings of those who had died from sudden infant death syndrome (SIDS), and 35 age-matched healthy comparison infants. All 80 infants were between 48 and 58 weeks of postconceptional age. On a double-blind basis, the total amount of 6SMT excreted over 24 hours and the diurnal rhythm in the rate of 6SMT excretion were assessed using urine samples taken from disposable diapers (nappies). The mean daily excretion of 6SMT was significantly lower in the ALTE (1588ng/24 hour) than in the comparison infants (3961ng/24 hour). No such difference was found between the infants with a cyanotic apneic event (3268ng/24 hour) and the SIDS siblings (2962ng/24 hour). The diurnal 6SMT rhythms in the ALTE infants were characterized by lower 24-hour mean and amplitude values, whereas the time of peak and nadir excretion rates (07:15 to 08:45 hours and 14:45 to 16:15 hours respectively) was similar in all four infant groups. Follow-up of the ALTE infants, performed 6 to 8 weeks later (59 to 66 weeks of postconceptional age), revealed that 6SMT excretion increased in all of them, suggesting a delayed ontogeny rather than permanent deficiency of melatonin production in ALTE.

Type
Original Articles
Copyright
© 2000 Mac Keith Press

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