Growth of Extremely Preterm Survivors From Birth to 18 Years of Age Compared With Term Controls

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Growth of Extremely Preterm Survivors From Birth to

18 Years of Age Compared With Term Controls

WHAT’S KNOWN ON THIS SUBJECT: Children born at very low birth weights have signiﬁcant catch-up weight gain but

differences in height remain. Their BMI, however, tends not to be higher than expected. Data are lacking regarding representative cohorts, deﬁned by gestation and compared with

contemporaneous controls.

WHAT THIS STUDY ADDS: In a geographic cohort of extremely preterm participants followed until age 18, compared with term controls, weight differences diminish over time, and height differences persist. BMI at age 18 is similar. Height at age 2 is a better predictor ofﬁnal height than midparental height.

abstract

OBJECTIVES: To determine changes in height, weight, and BMI of extremely preterm (EPT; gestational age,28 completed weeks) sur-vivors from birth to 18 years of age, compared with term controls. METHODS:Birth, discharge, and follow-up at ages 2, 5, 8, and 18 years of consecutive EPT survivors and contemporaneous term controls born in 1991–1992 in Victoria, Australia. Weight, height, and BMI were converted to z scores and compared between groups. Height z scores at age 2 and midparental heightz scores were examined as predictors of heightzscore at age 18 years.

RESULTS:Follow-up rates were.90% until 18 years, when 166 (74%) of 225 EPT subjects and 153 (60%) of 253 controls were assessed. EPT subjects had lower weight z scores than controls at birth, with

a much greater difference at discharge, which reduced

progressively until age 18 years. EPT children were shorter than controls at all ages, and this difference did not alter greatly over time. BMIzscores were lower in EPT children at younger ages, but by age 18 were similar between groups. Height at age 2 was a better predictor of height at age 18 in EPT participants, compared with midparental height.

CONCLUSIONS:EPT survivors were substantially lighter than term con-trols from birth to late adolescence, although the gap in weight steadily decreased over time from a peak at the time of discharge. The height disadvantage in EPT children compared with controls remained con-stant over time and BMI scores were similar at age 18 years.Pediatrics 2013;131:e439–e445

AUTHORS:Gehan Roberts, MPH, PhD, FRACP,a,b,c_Jeanie

Cheong, MD, FRACP,a,c,d_{Gillian Opie, FRACP,}e_Elizabeth

Carse, FRACP,f_{Noni Davis, FRACP,}a_{Julianne Duff, FRACP,}a

Katherine J. Lee, PhD,b,c_{and Lex Doyle, MD, FRACP,}a,c,d_on

behalf of the Victorian Infant Collaborative Study Group

a_{Premature Infant Follow-up Program at the Royal Women}’_s Hospital, Melbourne, Australia; Departments ofb_{Paediatrics, and} d_{Obstetrics and Gynaecology, The University of Melbourne,} Melbourne, Australia;c_{Murdoch Children}’_{s Research Institute,} Parkville, Australia;e_{Mercy Hospital for Women, Melbourne,} Australia; andf_{Monash Medical Centre, Melbourne, Australia}

KEY WORDS

preterm birth, growth, follow-up studies, body height, body weight, BMI

ABBREVIATIONS

CI—conﬁdence interval EPT—extremely preterm MPH—midparental height

Dr Roberts conceptualized and designed the study and drafted the initial manuscript; Dr Opie was involved in acquisition and interpretation of the data; Drs Carse, Davis, and Duff were involved in acquisition of the data; Dr Lee assisted with the data analysis and interpretation; Dr Doyle made substantial contributions to the conception and design of the study and interpretation of the data; and all authors critically revised the manuscript and approved theﬁnal manuscript as submitted. www.pediatrics.org/cgi/doi/10.1542/peds.2012-1135

doi:10.1542/peds.2012-1135 Accepted for publication Oct 1, 2012

Address correspondence to Gehan Roberts, MPH, PhD, FRACP, Centre for Community Child Health, The Royal Children’s Hospital, Flemington Rd, Parkville, 3052, Australia. E-mail: gehan. roberts@rch.org.au

FINANCIAL DISCLOSURE:The authors have indicated they have noﬁnancial relationships relevant to this article to disclose.

FUNDING:This work was partly funded by the Victorian Government and by Project grant 491246 from the National Health and Medical Research Council of Australia. Dr Roberts is supported by National Health and Medical Research Council Postdoctoral Fellowship 607384 and the Centre for Clinical Research Excellence in Newborn Medicine grant 546519.

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gestational age at birth,28 completed weeks).1_{These children are at high risk}

of adverse long-term medical and de-velopmental outcomes.2

Saigal et al3_{reported that adults who}

were born extremely low birth weight have catch-up weight gain during childhood and adolescence, although height disadvantages persist com-pared with term controls. A 2008 re-view of growth in preterm children by Euser et al4_{reported similar}ﬁ_{ndings. A}

limitation of this review is that many studies used birth weight as the se-lection criterion. The use of birth weight, rather than gestational age, as a selection criterion can introduce bias, as more mature growth-restricted infants (who may be at higher risk of future growth disorders) are included with infants who are more premature, but appropriate weight for gestation. As with other outcomes of prematurity, such as neurodevelopment, it is pref-erable to examine growth according to gestational age, rather than birth weight.

Height and weight have been in-vestigated in studies that used gesta-tional age as the inclusion criterion, however. A Dutch national cohort born in 1983 at,32 weeks of gestation was followed-up at 19 years of age, with a response rate of 62%.5_{These young}

adults had mean heights and weights approximating 0.5 of an SD lower than Dutch reference weights and heights. There was no control group, and lim-ited information about growth trajec-tories, as previous measurements had been obtained only at 3 months and 1 year of age. More recent studies have used gestational age as the selection criterion, but have reported growth outcomes only until early childhood.6,7

Others have examined growth out-comes into young-adulthood, but have

Body composition and metabolic risk are of interest in EPT children, given Barker’s fetal origins of adult disease hypothesis.11 _{Low birth weight and}

growth restriction have been shown to be a risk factor for adverse adult car-diovascular outcomes.12–15 _During

childhood, preterm children tend to have reduced fat mass compared with their peers, but have catch-up weight gain during adolescence, although theirﬁnal BMI is not greater than the reference range in most studies.4

There are conﬂicting results with re-spect to the proportion of overweight adults born preterm, with some stud-ies reporting higher-than-expected rates and some lower-than-expected rates.4

Midparental height has traditionally been used to predict adult height in the general population.16 _{Concerns have}

been raised, however, that this method may not be accurate for children with very short stature.17_{For very low birth}

weight children, Trebar et al18 _have

shown that growth during the second year of life is an important predictor of height at age 6, using a prediction model that also included midparental height (MPH), birth weight, and height at age 1 year. To date, MPH has not been compared with early childhood growth as a predictor of ﬁnal height in EPT children.

In this study, our primary aim was to examine the growth outcomes of a geographic cohort of EPT infants fol-lowed into late adolescence, and com-pare their outcomes with matched term controls, recruited at birth. We hy-pothesized that weight disadvantages that are present early in life would disappear over time, although height disadvantages would persist. Our sec-ondary aims were to examine changes in BMI over time and also to examine potential predictors of height at age 18

adolescent height in EPT children, and whether this differed in EPT and term children.

METHODS

Study participants represent all con-secutive EPT survivors born during 1991–1992 in the state of Victoria, Australia. Victoria comprises approxi-mately one-fourth of the population of Australia and has 3 level-III perinatal centers (obstetric referral centers with a NICU, and 1 level-III NICU in a children’s hospital, all of which par-ticipated in the study, enabling re-cruitment of a geographic cohort. Controls comprised randomly selected term births, matched for the mother’s health insurance status, language spoken primarily in her country of birth (English or other), and the child’s gender. Perinatal data were collected, as previously described.19

Height and weight were measured according to standard guidelines.20

Growth data were collected at birth, at discharge from hospital, and at ages 2, 5, 8, and 18 years (corrected for ges-tation).

The Ethics Committees at the Royal Women’s Hospital, Mercy Hospital for Women, and Monash Medical Centre (Melbourne, Australia) approved these follow-up studies. Written informed consent was obtained from parents at all ages, and the subjects themselves at the 18-year follow-up. Early follow-up was considered routine clinical care for children born EPT, but written in-formed consent was obtained from the EPT subjects and their families when they were teenagers.

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were compared with those who were not seen, with respect to perinatal variables, height and weightzscores at age 8, maternal education (as a proxy for social risk), and MPH z score (if known). Dichotomous variables were compared between the 2 groups using

x2

, and continuous variables were compared by usingt tests, assuming unequal variances if Levene’s test for equality of variances was statistically signiﬁcant. BMI was calculated by us-ing the formula (BMI = weight [kg]/ height [m]2_{). Height, weight, and BMI}

measurements were converted intoz scores (standard scores) by using the 1990 British Growth Reference data.21

Mean height, weight, and BMIzscores were compared between EPT and con-trol participants at each time point usingttests, and mean differences and 95% conﬁdence intervals (CIs) calcu-lated, assuming unequal variances as above. Paired t tests were used to

compare mean MPH z scores with

mean age 18 heightzscores for both groups. Regression analyses were used to explore possible predictors of height at 18 years. Initially the re-lationship between heightz scores at 18 years and the main predictors of interest, MPHzscores and age 2 height z scores were presented graphically. R2was used as a measure of the vari-ability in height at 18 years explained by each of these factors. In subsequent analyses, the potential predictors in-cluded prenatal variables (MPH, ante-natal corticosteroids), neoante-natal variables (gestational age, birth weightzscore, postnatal corticosteroids, bronchopul-monary dysplasia (oxygen requirement at 36 weeks corrected gestational age), cystic periventricular leukomalacia), and postnatal variables (heightzscore at age 2 years), with models ﬁtted separately for both EPT and term con-trol groups. These variables were en-tered in the order stated previously, to reﬂect the distal to proximal

tem-poral relationship they have with the outcome measure. A ﬁnal regression analysis was conducted including both EPT and control subjects: height z scores at age 2 years, MPH z scores, EPT or term group status, and in-teraction terms for group with both height z score at 2 years and MPHz scores were examined to determine if there was a differential relationship for these variables between the 2 groups. Again,R2was used as a mea-sure of the variability in height at 18 years explained in the previously men-tioned models.

RESULTS

The follow-up rates for growth mea-surements for the 225 EPT participants at ages 2, 5, 8, and 18 years were 96% (n = 215), 93% (n= 210), 92% (n= 207), and 74% (n = 166), respectively. The equivalent follow-up rates for the 253 controls at ages 2, 5, 8, and 18 years were 90% (n= 228), 86% (n= 217), 84% (n = 213), and 60% (n = 152), re-spectively. Table 1 compares adoles-cents with and without growth data at age 18 on several perinatal and de-mographic characteristics, and height and weight zscores at age 8. The EPT adolescents without growth data were more likely to have cystic periven-tricular leukomalacia and to have parents who were shorter, compared with those with growth data. The con-trols without growth data were more likely to be male and less likely to have mothers who had completed 11 years of schooling, compared with controls with growth data.

The EPT subjects had weight zscores that were signiﬁcantly lower than controls at birth, but the difference was small (Table 2). A larger difference was apparent at discharge after the primary hospitalization, which reduced progressively over time, until by age 18 years the difference between the groups was similar to the difference at

birth. EPT children were shorter than controls at all ages from 2 to 18 years, and, in contrast to the change in weight over the same time, the difference be-tween the groups in heightzscores did not alter greatly over time (Table 2). Of the EPT participants, 15 (9%) had a heightzscore,–2 SD and 48 (29%) had a heightzscore,–1 SD at age 18 years. Of the term participants, how-ever, only 1 child (0.7%) had a heightz score , –2 SD, and 10 (6.6%) had a height z score , –1 SD at age 18 years. BMIzscores were lower in the EPT subjects at ages 2, 5, and 8 years, but the BMI z scores at age 18 were similar between the 2 groups. If the analyses were restricted to only those with growth data at 18 years, no sta-tistical conclusions were altered (data not shown). Imputing missing values of height and weight by substituting height and weight at age 8 years (or at age 5 years if also missing at age 8 years) resulted in additional data for 44 EPT subjects and 59 controls, but resulted in no changes to any statisti-cal conclusions at 18 years (eg, mean difference in height z score between groups was –0.76 with imputation, compared with–0.73 without imputa-tion).

The EPT subjects’heightzscore at 18 years was slightly lower than their MPH z score but this did not reach statistical signiﬁcance (mean differ-ence,–0.17, 95% CI–0.37–0.02,P= .08), whereas the heightzscore of the con-trols was signiﬁcantly higher than their MPH z score (mean difference, 0.41, 95% CI 0.26–0.57,P,.001).

There were strong positive associations between heightzscore at 18 years and both heightzscore at 2 years (Fig 1) and MPHz score (Fig 2) for both EPT and control subjects. Within EPT sub-jects, height z score at 2 years explained a large amount of the vari-ability inﬁnal height (R2= 0.50) com-pared with MPH z score (R2 = 0.18),

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whereas it was the opposite way around for the controls, with MPH z score explaining slightly more of the variability in ﬁnal height (R2 = 0.41), than height z score at 2 years (R2 = 0.37).

For EPT subjects, with all potential predictor variables entered into a sin-gle regression model for heightzscore at 18 years, there was evidence that

MPHzscore (0.27 [95% CI 0.09–0.45,P= .003] increase inzscore at 18 years for each unit increase in MPHzscore) and heightzscore at age 2 years (0.67 [95% CI 0.52–0.82, P , .001] increase in z score at 18 years for each unit increase in z score at 2 years) were both pre-dictive of height z score at 18 years, total model R2 = 0.57. MPH contrib-uted 0.18 and height z score at age

2 contributed a further 0.30 to the R2. Antenatal corticosteroids, ges-tational age, birth weight z scores, postnatal corticosteroids, broncho-pulmonary dysplasia, and cystic periventricular leukomalacia were not signiﬁcant predictors.

For the term subjects, with all potential predictor variables entered into a sin-gle regression model for heightzscore at 18 years, there was evidence that MPH z score (0.45 [95% CI 0.29–0.62, P,.001] increase inzscore at 18 years for each unit increase in MPHzscore) and heightzscore at age 2 (0.47 [95% CI 0.31–0.62, P , .001] increase in z score at 18 years for each unit increase inz score at 2 years) were both pre-dictive of height z score at 18 years, a total modelR2 = 0.57. MPH contrib-uted 0.39 and age 2 height a further 0.17 to the R2. Gestational age, and birth weightzscores were not signiﬁ -cant predictors, and antenatal corti-costeroids, postnatal corticorti-costeroids, bronchopulmonary dysplasia, and cystic periventricular leukomalacia were not included, as they were not relevant to the term subjects.

Growth Data at 18;n= 166 No Growth Data at 18;n= 59 Growth Data at 18;n= 152 No Growth Data at 18;n= 101 Perinatal

Antenatal corticosteroids (%) 115 (59) 45 (76) 0 (0) 1 (1)

Male gender (%) 81 (49) 32 (54) 63 (41)a

58 (57)a

Birth weight (g) 892 (174) 888 (183) 3425 (457) 3354 (411)

Mean (SD)

Gestation (wks) 25.8 (1.1) 26.1 (1.0) 39.3 (1.3) 39.3 (1.2)

Mean (SD)

BPDb(%) 68 (41) 29 (49) 0 (0) 0 (0)

Postnatal corticosteroids 64 (39) 27 (46) 0 (0) 0 (0)

Cystic PVLc(%) 7 (4)c 9 (15)c 0 (0) 0 (0)

Demographic

Maternal education$12 y 78/161 (48) 22/46 (48) 104/148 (70)d 29/66 (44)d Midparental heightzscore 20.28 (0.84),n= 123e 20.66 (1.01),n= 39e 20.12 (0.89),n= 104 20.18 (0.91),n= 48 Growth, age 8 y

Weightzscore, mean (SD) 20.27 (1.49) 20.44 (1.48) 0.39 (0.99) 0.32 (1.37) Heightzscore, mean (SD) 20.21 (1.16) 20.61 (1.50) 0.25 (0.88) 0.14 (1.69)

BPD, bronchopulmonary dysplasia; PVL, periventricular leukomalacia. a_{Odds ratio 0.52, 95% CI 0.32}–_0.87,_P,_.05.

b_{Oxygen dependency at 36 wk postmenstrual age and abnormal x-ray.}

c_{Odds ratio 4.1, 95% CI 1.4}–_11.5,_P_{= .005.}

d_{Odds ratio 3.0, 95% CI 1.7}_–_5.5,_P_,_.001.

e_{Mean difference 0.38, 95% CI 0.06}–_0.70.

TABLE 2 Weight, Height and BMIzScores for EPT and Control Participants From Birth to 18 y of Age

Age EPT Controls Mean Difference (95% CI)

Weight

Birth 20.27 (0.87),n= 225 20.06 (0.89),n= 253 20.22 (20.38 to20.06) Discharge 21.65 (1.00),n= 222 20.49 (0.82),n= 227 21.16 (21.33 to20.99) 2 y 20.75 (1.47),n= 215 0.22(1.05),n= 228 20.97 (21.21 to20.73)a

5 y 20.56 (1.53),n= 209 0.30 (1.16),n= 214 20.86 (21.12 to20.60)a

8 y 20.30 (1.48),n= 205 0.38 (1.11),n= 213 20.67 (20.93 to20.42)a 18 y 0.07 (1.52),n= 166 0.45 (1.09),n= 152 20.38 (20.67 to20.09)a Height

2 y 20.44 (1.19),n= 214 0.35 (0.97),n= 216 20.79 (21.00 to20.59)a 5 y 20.29 (1.23),n= 210 0.29 (0.91),n= 217 20.59 (20.79 to20.38)a 8 y 20.29 (1.25),n= 207 0.24(1.18),n= 213 20.52 (20.76 to20.29) 18 y 20.47 (1.14),n= 166 0.26 (0.98),n= 152 20.73 (20.97 to20.50)a BMI

2 y 20.81 (1.22),n= 211 20.10 (1.07),n= 214 20.70 (20.90 to20.50)a 5 y 20.62 (1.44),n= 209 0.16 (1.15),n= 214 20.78 (21.03 to20.53)a

8 y 20.06 (1.41),n= 205 0.37 (1.16),n= 213 20.42 (20.67 to20.18)a

18 y 0.40 (1.42),n= 166 0.42 (1.08),n= 152 20.03 (20.31 to 0.25)a

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In the final analysis that included all participants as well as the interaction terms examining differential group effects, there was evidence that MPHz score at age 2 (0.28 [95% CI 0.12–0.44, P= .001] increase inzscore at 18 years for each unit increase in MPHzscore), and heightzscore at 2 years (0.65 [95% CI 0.53–0.77, P , .001] increase in z score at 18 years for each unit increase in height z score at 2 years) were predictive of outcome, with a main ef-fect of group (controls 0.36 [95% CI 0.16–0.57] higher than EPT subjects). Neither of the interaction terms was significant, although there was a trend toward a weaker association between heightzscore at 2 years and 18 years (interaction coefficient–0.18 [95% CI– 0.39–0.03;P= .09], and a stronger as-sociation between MPH z score and height at 18 years (interaction co-efficient 0.18 [95% CI –0.05–0.42; P= .13], in controls compared with EPT subjects.

DISCUSSION

On average, EPT subjects were lighter and shorter than their term peers throughout childhood and into late adolescence. Differences in weight z scores between groups were largest at the time of initial discharge, and gradually reduced over time. Height differences between groups persisted over time with no evidence of catch-up between 2 and 18 years of age. Because EPT subjects showed more rapid weight gain over time, compared with their height, than did the controls, by 18 years of age the BMI scores were not different, on average, between the 2 groups. The other majorﬁnding is that heightz scores were strongly related to both heightzscores at 2 years of age and MPHzscores in both EPT and term controls, as would be expected. The interesting and novelﬁnding, however, is that the relationship between height zscore at 18 years with heightzscore

FIGURE 1

Relationship between heightzscore at age 18 and heightzscores at age 2 years.

FIGURE 2

Relationship between heightzscore at age 18 and midparental heightzscores.

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ﬂ

parents as measured using the MPHz score.

The growth results are consistent with previous studies examining growth in cohorts selected using gestational age as the primary inclusion criterion, al-though differing selection of control groups and ages at follow-up make direct comparisons difﬁcult. The EPI-Cure study group assessed all children born in the UK and Ireland at,26 weeks of gestation at age 6, compared with classroom controls, and reported that the EPT children were 1.2 SD lighter and 0.97 SD shorter than the controls, with approximately 0.4 SD catch-up in both weight and height since age 2.6_In

our study, which included more mature children, the differences between EPT and control subjects were not as large for either weight or height, and any small gain in height between 2 and 5 years had disappeared by 18 years. A single-center study by Jitka et al reported growth outcomes at age 2 and 5 for a cohort of children born at ,28 weeks of gestation. There was no control group and results were com-pared against local published stan-dards.7_{Mean weight and height were}

∼1.0 SD lower than the population mean for children at,26 weeks and ∼0.7 SD lower for children at 26 to 28 weeks. Similar to our study ﬁndings, they noted more catch-up weight gain compared with height gain from 2 years of age.7

It could be considered reassuring that there was little difference in mean BMI between the EPT and term cohorts at age 18; however, to reach this point, the EPT cohort had more rapid weight gain during childhood, which may place them at higher metabolic risk. This in-creased risk has been described by Eriksson et al,13 _{who reported that}

children born in the 1920s and 1930s in

in later childhood, had a greater risk of death due to coronary disease in adulthood. As individuals born preterm have a higher risk of “metabolic pro-gramming”toward adverse metabolic outcomes, compared with term con-trols,15_{it is important that metabolic}

outcomes are examined carefully in the growing number of young adults who were born preterm. We do not have any metabolic data on our subjects.

In EPT young adults, the ﬁnding that height at age 2 was a stronger predictor of height at age 18 years than MPH is interesting. As expected, MPH was a good predictor of height at age 18 in the term-born controls. In the EPT adolescents, however, height at age 2 explained more of the variability in height at age 18, compared with MPH. These results suggest that medical risk factors during the early years may be more important predictors of adult height than genetic predisposition in EPT individuals. Medical risk factors are more common in preterm children, compared with term children, and may impair growth in infancy and early childhood. These include, but are not limited to, poor nutrition, respiratory illnesses, and increased hospitaliza-tion.4_{Trebar et al}18_{have demonstrated}

that a prediction model including early growth parameters and MPH can be used to predict growth at age 6 in very low birth weight children. The results from the current study show that the common clinically used prediction tool of MPH should be used with caution in EPT children, but that if growth is sat-isfactory in early childhood, families can be reassured that their EPT child is likely to follow expected growth tra-jectories over time.

The strengths of the current study in-clude longitudinal follow-up, at multiple time points, of a large geographic

co-follow-up rate at age 18 years, which is consistent with other follow-up stud-ies that have recruited participants during young adulthood.4 _Length

data were also incomplete at birth and discharge, so that comparisons could not be made with height at later ages.

CONCLUSIONS

EPT children remain at a height disad-vantage compared with term controls at 18 years of age, although the weight disadvantage reduces steadily over time. More research into growth dif-ferences in preterm children at later gestational ages is needed, as is

re-search into the metabolic

con-sequences of these altered growth trajectories.

ACKNOWLEDGMENTS

This work is published on behalf of the Victorian Infant Study Group, which was involved in data collection at the various study sites.

The Victorian Infant Study Group conve-nor was: Lex W. Doyle, MD, FRACP (Pre-mature Infant Follow-up Program at the Royal Women’s Hospital; Departments of Obstetrics and Gynaecology, and Pae-diatrics at the University of Melbourne; and Murdoch Childrens Research Insti-tute).

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BSc, PhD (Premature Infant Follow-up Program at the Royal Women’s Hos-pital and Department of Obstetrics and Gynaecology at the University of Melbourne); Julianne Duff, FRACP (Pre-mature Infant Follow-up Program at the Royal Women’s Hospital); Marie Hayes, RN (Monash Medical Centre); Esther Hutchinson, BSc (Hons) (Prema-ture Infant Follow-up Program at the Royal Women’s Hospital); Elaine Kelly, MA (Premature Infant Follow-up Pro-gram at the Royal Women’s

Hospi-tal and Mercy HospiHospi-tal for Women); Marion McDonald, RN (Premature In-fant Follow-up Program at the Royal Women’s Hospital); Gillian Opie, FRACP (Mercy Hospital for Women); Gehan Roberts, MPH, PhD, FRACP (Premature Infant Follow-up Program at the Royal Women’s Hospital; Department of Ob-stetrics and Gynaecology at the Uni-versity of Melbourne; and Murdoch Childrens Research Institute); Linh Ung, BSc (Hons) (Premature Infant Follow-up Program at the Royal

Wom-en’s Hospital); Andrew Watkins, FRACP (Mercy Hospital for Women); Amanda Williamson (Mercy Hospital for Women); and Heather Woods, RN (Mercy Hospital for Women).

The following Victorian Infant Study Group participants were successful applicants for Project grant 491246 from the National Health and Medical Research Council: Lex Doyle, Peter Anderson, Stephen Wood, Colin Robertson, Sarah Hope, Doug Hacking, Jeanie Cheong.

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DOI: 10.1542/peds.2012-1135 originally published online January 6, 2013;

2013;131;e439

Pediatrics

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Duff, Katherine J. Lee, Lex Doyle and on behalf of the Victorian Infant Collaborative

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Growth of Extremely Preterm Survivors From Birth to 18 Years of Age Compared With Term Controls