ESPE Abstracts

Introduction: Children born small for gestational age (SGA) represent a heterogeneous population, displaying different phenotypes for both growth and metabolic status. Low birth length and/or weight increases the risks for not only growth impairment but also for metabolic derangements (cardiovascular disease, hypertension and type 2 diabetes), the latter with an even amplified risk in children with rapid postnatal weight gain. Variability in metabolic parameters, catch-up growth and different GH treatment responses are still poorly understood.

Aims: We investigated a possible association between anthropometric/metabolic parameters in SGA children.

Methods: This cross-sectional observational study evaluated a series of 32 children aged between 4 to15.7 years, with birth weight and/or length<-2.0SDS according to INeS Growth Charts. All patients with chronic conditions, GH deficiency, other endocrinopathies and genetic syndromes were excluded. Anthropometric (height-HT, Mid-parental height-MPH, weight, Body Mass Index-BMI, Tanner stage, body composition by Body Structure Analyzer BC-420MA TANITA) and metabolic (fasting glycemia and insulin, glycosylated haemoglobin-HbA1c) parameters were collected. Insulin resistance (HOMA-IR) and sensitivity (QUICKI) were calculated.

Results: Thirty-two SGA patients (F16/32,50%), with a mean age of 9.1±3.0 years were consecutively enrolled. In 18.7% of patients HT was below -2.0SDS. Mean HT was 126.5±15.2 cm, -1.09±1.13SDS according to WHO Growth Charts with a MPH distance (MPH SDS-HT SDS) of 0.62±1.10SDS. As far as glycemic profile was concerned, glycemia was in the normal range in all study patients apart from one with impaired fasting glucose (glycemia 107 mg/dL), mean glycemia was 83.3±8.5 mg/dL, mean HbA1c 34±3.1 mmol/mol, with a median HOMA-IR of 1.6 (IQR 0.9-3.1) and QUICKI of 0.35 (IQR 0.32-0.39). At multiple regression, HbA1c was positively associated with HT SDS (P=0.001) and negatively with MPH distance (P=0.017).

Conclusions: Our results suggest a relationship between postnatal catch-up growth and metabolic impairment, as underlined by the association found between HT and HbA1c, even after correction for MPH. This is only an explorative analysis; we would like to confirm our results on a larger scale. Moreover, considering that Fibroblast Growth Factor-21 (FGF-21), acting with its cofactor β-klotho, has recently emerged as a “starvation hormone” with a key role in the glucose metabolism regulation but also, interacting with GH/IGF-I axis, in longitudinal growth and growth hormone resistance, we ought to investigate FGF-21/β-Klotho system in our cohort in order to eventually bridge the gap between height gain and metabolic impairment in children born SGA.