ESPE Abstracts (2015) 84 P-3-961

Characterisation of Children Born Small for Gestational Age within the Australian Indications for GH (GH) Therapy: An OZGROW Analysis

Ian Hughesa,c, Mark Harrisb,c & Andrew Cotterillb,c

aMater Reseatch UQ Institute, South Brisbane, QLD, Australia; bLady Cilento Children’s Hospital, South Brisbane, QLD, Australia; cAPEG-OZGROW, Morisset, NSW, Australia

Background: Small for gestational age (SGA) without subsequent catch up growth is an indication for GH treatment in Europe, the US, and Korea but not in Australia. However, many SGA are likely to be included under the ‘short stature and slow growth’ (SSSG) indication. It is unknown to what extent children born SGA are included in the Australian indications or how they differ from non-SGA patients within each indication and gender.

Objective and hypotheses: To characterise and compare birth, parental auxology, and initial GH-treatment data of SGA patients with respect to non-SGA patients by gender and Australian indication. Analyses are confined to SSSG, GH deficiency (GHD), Turner syndrome (TS), and Prader-Willi syndrome (PWS).

Method: SGA was defined as birthweight below the 10th Australian centile for gestation period. Frequencies of SGA for males (M) and females (F) were calculated for each indication. Frequencies were compared to an expected frequency of 10% (Chi square). Means for SGA and non-SGA were calculated for M and F of each indication for gestation period (GP), birth weight S.D. score (BWtSDS), father’s height S.D.s (FHtSDS), mother’s height S.D.s (MHtSDS), mean parental height S.D.s (MPHtSDS), and GH starting age (SAge, years), height S.D.s (SHtSDS), and Dose (SDo, mg/m2 per wk). Means were compared using t-tests.

Results and conclusions: SGA was overrepresented: GHD-22%, PWS-55%, SSSG-41%, TS-48% (P<10−6). SGA BWtSDS was always lower (P<10−10) but GP similar. SGA MPHtSDS was always shorter (P=0.28 (M PWS) – 10−4 (M SSSG)). As was SGA SHtSDS (P=0.4 (F PWS) – 10−8 (M SSSG)). However SAge was similar although younger for SSSG (F 8.7 vs 9.4, P=0.005; M 8.8 vs 9.9, P=10−7). SDo was similar although lower for M SSSG (4.9 vs 5.1, P=10−4). SGA forms a major and significantly different sub-population of Australian GH-patients. Further analyses will address treatment response. SGA-specific GH treatment may be advocated.

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