Growth retardation after dexamethasone administration: assessment by knemometry.

Gibson, Alan T.; Pearse, R G; Wales, J.

doi:10.1136/adc.69.5_spec_no.505

Cited by 122 publications

(69 citation statements)

References 35 publications

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“…In addition, mean concentrations of IGF-I were lower during both GR and CU phases for infants growth restricted in weight, length, or HC at birth compared with infants with appropriate growth. Postnatal treatment with dexamethasone has negative effects on longitudinal growth in preterm infants and has been associated with a decrease in IGF-I concentrations (21,22). In this study, intake of hydrocortisone or betamethasone was neither associated with decreased growth nor with reduced mean concentrations of IGF-I after adjustment for GA at birth.…”

Section: Discussionmentioning

confidence: 58%

Influence of Insulin-Like Growth Factor I and Nutrition During Phases of Postnatal Growth in Very Preterm Infants

et al. 2011

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Pronounced growth restriction (GR) occurs after very preterm birth. The interaction between IGF-I, nutritional intake, and growth was evaluated prospectively in 64 infants with a mean (SD) GA of 25.7 (1.9) wk. Blood sampling of IGF-I and measurements of weight, length, and head circumference were performed weekly until discharge. Daily calculation of nutritional intake was performed. Standard deviation scores (SDSs) for growth parameters defined two growth phases: GR phase (birth until lowest SDS) and catch-up (CU) phase (lowest SDS until 35 gestational weeks). IGF-I concentrations during the first postnatal weeks were low and increased at 30 wk GA, irrespective of GA at birth, coinciding with initiation of CU growth. Concentrations of IGF-I were positively associated with change in weight SDS during the GR phase, p ϭ 0.001 and CU phase, p ϭ 0.004 -0.027. Protein and energy intake were not associated with change in SDS weight during the GR phase as opposed to the CU phase (p Ͻ 0.001, respectively). Nutritional intake did not correlate to concentrations of IGF-I before 30 wk GA. IGF-I is associated with growth at an earlier postnatal age than nutrient intake and the effect of nutrition on levels of IGF-I may be restricted to the period of established CU growth. T he maximum growth rate of the fetus is reached in the middle of pregnancy, where it is approximately three times higher than at term (1). Fetal growth rate is to a large extent determined by placental capacity of delivering nutrients to the fetus, whereas genetic influence seems to play a less important role. Placental function depends on the maternal nutritional state and the intrauterine endocrine environment. At preterm birth, the fetal-placental interaction is interrupted, which has an impact on continued extrauterine growth capacity. Postnatal growth retardation occurs almost inevitably after preterm birth and has been associated with decreased brain volumes and impaired neurodevelopmental outcome (2,3). Although attempts are made to optimize postnatal nutritional intakes in preterm infants, these are still commonly suboptimal according to intrauterine requirements (4). Increased postnatal nutritional intake has been shown to improve growth rate in very LBW infants (5), although a recent study could not demonstrate any apparent effect of hyperalimentation on subsequent postnatal growth in very preterm infants (6).IGF-I is an important fetal growth factor, which is essential for the developing brain (7). Concentrations of fetal IGF-I are closely related to placental transfer of glucose where fetal glucose increases insulin secretion, which in turn stimulates fetal IGF-I production (8). Fetal levels of IGF-I may also be regulated by an interaction at the feto-maternal placental interface (9). The disruption of placental nutrient supply after birth is followed by a rapid decrease in postnatal levels of IGF-I, suggesting a low endogenous production (10). While term infants restore their IGF-I levels within the first postnatal weeks, very prete...

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Section: Discussionmentioning

confidence: 58%

Influence of Insulin-Like Growth Factor I and Nutrition During Phases of Postnatal Growth in Very Preterm Infants

et al. 2011

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“…Thus, a prolonged course of systemic corticoid has been associated with inadequate growth in ELW preterms during their first years of life. 34,35 Differences between the studies in terms of the definition and treatment of bronchopulmonary dysplasia, the period studied and the follow-up period together with small sample sizes involving very low weight and/or ELW preterms are all limiting factors that need to be considered when interpreting studies of the effects of dysplasia on premature children s growth. Further studies are needed to evaluate the impact of this disease on those ELW preterms that are surviving nowadays.…”

Section: Important Conceptsmentioning

confidence: 99%

Crescimento e desenvolvimento a longo prazo do prematuro extremo

Rugolo¹

2005

J. Pediatr. (Rio J.)

134

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“…Very preterm infants developing BPD, with a persistent need for artificial ventilation and oxygenation, frequently show a very compromised growth in the neonatal period (1,2). Their growth will be further attenuated when DEXA treatment is given after conservative treatment, including increased ventilation settings and fluid restriction, has failed to wean them from the ventilator (3)(4)(5). The hormonal mechanisms underlying this early postnatal growth retardation and the role of glucocorticosteroids have not been elucidated.…”

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confidence: 99%

Effect of Dexamethasone Treatment on Serum GH, IGF-I, and the Binding Proteins IGFBP-1 and -3 in Ventilated Very Preterm Infants

Huysman

Hokken-Koelega

Hop³

et al. 2003

Pediatr Res

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Very preterm infants developing bronchopulmonary dysplasia frequently show a compromised growth in the neonatal period especially when steroids are given to facilitate weaning from the ventilator. The aim of this study was to evaluate the short-term effect of dexamethasone (DEXA) on the GH-IGF axis in ventilated very preterm infants developing bronchopulmonary dysplasia. We studied 10 very preterm artificially ventilated infants with bronchopulmonary dysplasia [median (range) gestational age 27.5 wk (25.9 -32.0 wk), median (range) birth weight 970 g (610 -2150 g)] immediately before and 2 d after the start of DEXA treatment. On both days of study, serum GH profiles were obtained, and serum IGF-I and IGF binding protein (IGFBP) -1 and -3 levels were measured. The ventilation score and the nutritional intake were calculated. Before the start of DEXA treatment, the median serum mean GH level was 12.0 g/L (6 -28.4 g/L), whereas 2 d after the start of DEXA treatment the median serum mean GH level declined significantly to a value of 4.4 g/L (1.7-11.9 g/L). During DEXA treatment, mean, baseline, and maximal GH levels (Pulsar analysis) were significantly lower compared with pretreatment levels (p Ͻ 0.01, p Ͻ 0.01, and p Ͻ 0.05, respectively). Serum IGF-I and IGFBP-3 levels did not decline during DEXA. Serum IGFBP-1 levels were significantly lower compared with pretreatment levels (p Ͻ 0.01). Serum GH levels during DEXA treatment were correlated with neither the time interval between the administration of DEXA and the second GH profile nor the cumulative DEXA dose administered. Ventilation score and nutritional intake did not significantly correlate with serum GH, IGF-I, or IGFBP-1 or -3 levels, either before or after the start of DEXA. Two days of DEXA treatment in very preterm ventilated infants has a suppressive effect on serum GH levels, without an acute decline in serum IGF-I levels. A concomitant decrease in serum IGFBP-1 levels was found. Very preterm infants developing BPD, with a persistent need for artificial ventilation and oxygenation, frequently show a very compromised growth in the neonatal period (1, 2). Their growth will be further attenuated when DEXA treatment is given after conservative treatment, including increased ventilation settings and fluid restriction, has failed to wean them from the ventilator (3-5). The hormonal mechanisms underlying this early postnatal growth retardation and the role of glucocorticosteroids have not been elucidated. DEXA has a catabolic effect by increasing protein breakdown and alters skeletal metabolism by inhibition of intestinal calcium absorption, stimulation of renal calcium excretion, and suppression of collagen turnover in preterm infants (6 -8).Glucocorticosteroids have been suggested to have a suppressive effect on the pituitary GH secretion with attenuation of the spontaneous GH secretion and decreased GH responses to various stimuli (9 -11). A direct antagonizing effect of DEXA on the epiphyseal cartilage to the action of GH has been reported, probably by inhi...

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Growth retardation after dexamethasone administration: assessment by knemometry.

Cited by 122 publications

References 35 publications

Influence of Insulin-Like Growth Factor I and Nutrition During Phases of Postnatal Growth in Very Preterm Infants

Influence of Insulin-Like Growth Factor I and Nutrition During Phases of Postnatal Growth in Very Preterm Infants

Crescimento e desenvolvimento a longo prazo do prematuro extremo

Effect of Dexamethasone Treatment on Serum GH, IGF-I, and the Binding Proteins IGFBP-1 and -3 in Ventilated Very Preterm Infants

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