title: Sleep, respiratory rate, and growth hormone in chronic neonatal lung disease.
abstract: This study assessed whether respiratory rates (RRs) correlate with urinary growth hormone (U-GH) excretion and sleep architecture in infants with chronic neonatal lung disease (CNLD) in early (1 month), middle (6 months), and late (10 months) infancy. Twenty-three preterm infants (CNLD=16, controls=7) were studied on 51 occasions. CNLD infants were stratified according to mean non-REM sleep respiratory rate (NREM RR) in early infancy into "High RR CNLD" infants (mean NREM RR >2 SD higher than controls) and "Normal RR CNLD" infants (mean NREM RR within 2 SD of controls' mean). "High RR CNLD" infants (RR >45) had a lower mean birthweight (P=0.015), current weight (P=0.042), current length (P=0.02), and growth velocity in early infancy (grams/week gained: P=0.042) than "Normal RR CNLD" and control infants. Mean (95% CI) U-GH excretion (ng U-GH/g urinary creatinine) was higher in "High RR CNLD" infants in air or their usual O2 (1,932 [459, 3,406]) than "Normal RR CNLD" (394 [147, 642]) and controls (320 [147, 492]) (P=0.024). With resolution of tachypnea by mid-infancy, hemoglobin oxygen saturation (SaO2) >93%, mean growth parameters and U-GH excretion for the "High RR CNLD" group were not significantly different from "Normal RR CNLD" and control groups. CNLD infants demonstrated increased sleep efficiency (P=0.016), whereas controls had similar sleep efficiency between early and middle infancy (P=0.452). Mean percent time in REM sleep (REM%) and slow wave sleep (SWS%) were not significantly different between early and middle infancy and did not vary in relation to respiratory rate. We conclude that tachypneic infants with CNLD have slower growth and elevated U-GH excretion in early infancy. With resolution of tachypnea, growth improved, U-GH excretion decreased, and sleep consolidation occurred. An elevated U-GH in tachypneic CNLD infants may reflect stress, compromised nutrition (GH resistance), or a feedback loop involving a direct effect of GH on lung growth and repair.
authors.affiliation: Royal Alexandra Hospital for Children, Sydney, Australia.
authors.forename: D
authors.initials: D
authors.lastname: Fitzgerald
authors.forename: P
authors.initials: P
authors.lastname: Van Asperen
authors.forename: P
authors.initials: P
authors.lastname: O'Leary
authors.forename: P
authors.initials: P
authors.lastname: Feddema
authors.forename: G
authors.initials: G
authors.lastname: Leslie
authors.forename: J
authors.initials: J
authors.lastname: Arnold
authors.forename: C
authors.initials: C
authors.lastname: Sullivan
mesh_terms: D001997:Bronchopulmonary Dysplasia / Q000503:physiopathology* / Q000652:urine; D016022:Case-Control Studies; D006130:Growth Disorders / Q000503:physiopathology* / Q000652:urine; D019382:Human Growth Hormone / Q000652:urine*; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008137:Longitudinal Studies; D017286:Polysomnography; D012119:Respiration; D012890:Sleep / Q000502:physiology*; D014939:Work of Breathing
chemical_list: D019382:Human Growth Hormone