Growth velocity is higher in late intra-uterine and early post-natal life than at any time thereafter, and accurate measurements are essential for appropriate monitoring. The accuracy with which such measurements are made and recorded is frequently questionable, however, and short- and medium-term changes in growth may be difficult to interpret in the light of normal variations in the pattern of growth. Infants who are small at birth must be accurately classified because intra-uterine growth retardation and small for gestational age have different implications for both causation and outcome. Prediction of expected growth on the basis of mid-parental height is essential but frequently omitted. Post-natal growth impairment is common in pre-term infants and is often rapid in onset. Poor growth may continue for many months, and catch-up may be incomplete. Early growth failure may have a significant influence on subsequent morbidity and mortality.

Measurement of newborn babies is widely regarded as being too inaccurate to justify its regular practice. It is common for infants to be weighed at birth and for no other measurements to be made. Although such assumptions are superficially correct, it is possible to train people to perform accurate measurements and for improved performance to be sustained. Accurate sequential measurements are possible and provide more information than single measurements. Detailed measurements show that postnatal growth may change rapidly and dramatically, particularly in preterm infants. Postnatal growth impairment is common in such infants and may be sustained. Limited evidence suggests that there may be a significant reduction in final stature. Preliminary data also suggest that many preterm infants may also show evidence of alterations in biochemical and physiological variables consistent with early programming and the potential for altered disease susceptibility in adult life.

There is considerable evidence to show that babies born prematurely have poor postnatal growth, and the more premature the baby, the greater the impairment is likely to be and the longer it will persist. Nutrition has been shown to play an important part in this, but adequate nutrition is difficult, if not impossible, to achieve in these infants. In the most immature infants, growth retardation may continue for many months and catch-up may be delayed and incomplete. Evidence from long-term studies suggests that preterm infants will be shorter and lighter than term controls and that reduced stature and head size may be linked with lower intelligence. Although there is evidence linking better growth to better neurodevelopmental outcome, with reports suggesting that this can be achieved with dietary manipulation, there are also data that suggest that there could be a link between increased postnatal growth and increased morbidity and mortality in later childhood and adult life. Here, we provide an overview of current understanding of growth impairment in infants born prematurely and the effects in later life.

Accurate measurements of both healthy and premature neonates are possible but rarely performed. Routine anthropometry is often not performed at all or with large measurement errors due to inadequate training of personnel or inappropriate equipment. Sick neonates are often considered unsuitable for anthropometry and growth is wrongly equated with weight gain. Gain in length may be disturbed by poor health and permanent extrauterine growth retardation and changes in body proportions induced in some survivors of neonatal intensive care. Drug treatments may have profound effects on length gain and the relationship of length to weight.

ABSTRACT:We determined the contributions of IGF-I, IGFBP-3 and leptin to growth in -extremely premature infants over the first two years. Weight (Wt), crown-to heel length (CHL), plasma IGF-I, IGFBP-3 and leptin were measured in infants (gestation 24 -33 wk) at birth (n ϭ 54), expected date of delivery (EDD) and 6, 12 and 24 mo post-EDD (n ϭ 29). Area under the curve (AUC) for hormone levels was calculated over 4 periods: birth-EDD, EDD-200 d, EDD-350 d and EDD-700 d. IGFBP-3, but not IGF-I or leptin, on day 1 correlated with birth Wt SD scores (SDS) (r ϭ 0.46, p ϭ 0.002) and CHL SDS (r ϭ 0.41, p ϭ 0.01). Wt SDS at EDD correlated with AUC IGF-I, IGFBP-3 and leptin (birth-EDD), but leptin was the best predictor in multiple regression(r ϭ 0.65, p Ͻ 0.0001). Wt at EDD ϩ 700 d correlated with AUC leptin (EDD-700 d) (r ϭ 0.62, p ϭ 0.002). CHL SDS at EDD correlated with AUC IGFBP-3 and leptin (birth-EDD), but IGFBP-3 was the best predictor (r ϭ 0.55, p Ͻ 0.0001). CHL at EDD ϩ 700 d correlated with AUC IGF-I and IGFBP-3 (EDD-700 d), but IGFBP-3 was the best predictor (r ϭ 0.47, p ϭ 0.01). Wt and CHL at birth were associated with IGFBP-3 levels in these infants. Wt at EDD and EDD ϩ 700 d was predicted by concurrent leptin output while linear growth at EDD and EDD ϩ P reterm birth interrupts the physiologic fetal phase of growth when growth velocity is highest. Infants born at gestational age (GA) Ͻ32 wk have a different pattern of postnatal growth than those born moderately premature (GA Ն32 wk) or at term (1,2) and often exhibit growth failure, particularly over the first months of life. Signs of catch-up growth in weight and length can be observed by expected date of delivery (EDD) in infants born at GA 29 -31 wk but are not seen until after one year corrected age for more premature infants Ͻ29 wk gestation (2). Growth restriction, especially if associated with later catch-up, is of particular concern in such infants owing to the association with cardiovascular disease in adulthood (3). Life-long programming of the insulin like growth factor-I (IGF-I) system by intrauterine and postnatal hormonal and nutritional environment has been suggested to be a key mediator of this association (4,5).Nutrition is a key regulator of pre-and early postnatal somatic growth. Other factors thought to be important include IGF-I, its principal binding protein insulin like growth factor binding protein-3 (IGFBP-3) and leptin. Leger et al. (6) examined growth hormone (GH), IGF-I and IGFBP-3 levels in relation to growth over the 1 st 24 mo in 254 growth retarded children (birth weight Ͻ3 rd percentile; 81 born at GA 29 -37 wk) and 84 appropriate-for-GA (AGA) controls (40 born at GA 29 -37 wk). The growth retarded infants had high GH but low IGF-I and IGFBP-3 levels at birth. However, these biologic parameters were not predictive of later growth or of short stature at 2 y of age, and levels over 24 mo did not correlate with weight or length gain. A number of studies have characterized longitudinal growth in very preterm children (7-9) and...