Endocrine 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, the latter with an even amplified risk in children with rapid postnatal weight gain. Variability in metabolic parameters, catch-up growth as well as different GH treatment responses are still poorly understood.AimsWe investigated a possible association between anthropometric/metabolic parameters in SGA children.MethodsThis cross-sectional observational study evaluated a series of 58 children aged between 4 and 15.7 years, with birth weight and/or length<-2.0 SDS according to INeS Growth Charts. All patients with underlying chronic conditions, GH deficiency, other endocrinopathies and known genetic syndromes were excluded. Anthropometric (height-HT, Mid-parental height-MPH, weight, weight gain at 24 months, Body Mass Index-BMI, Tanner stage, body composition by Body Structure Analyzer BC-420MA TANITA) and metabolic (fasting glycemia and insulin, glycosylated hemoglobin-HbA1c) parameters were collected. Insulin resistance (HOMA-IR) and sensitivity (QUICKI) were calculated.ResultsFifty-eight SGA patients (F 33/58, 57%), with a mean age of 9.5±2.9 years were consecutively enrolled. In 22.4% of patients HT was below -2.0 SDS. Mean HT was 129.8±17.7 cm, -0.88±1.29 SDS according to WHO Growth Charts with a MPH distance (MPH SDS-HT SDS) of 0.70±1.36 SDS. As far as glycemic profile was concerned, glycemia was in the normal range in all study patients apart from one with impaired fasting glucose (107 mg/dL), mean glycemia was 82.7±7.9 mg/dl, mean HbA1c 35±3 mmol/mol, with a median HOMA I of 1.45 (IQR 0.74-2.7) and QUICKI of 0.36 (IQR 0.32-0.39). At multiple regression, HbA1c was positively associated with HT SDS (P=0.005), even after correction for MPH (P=0.01). Moreover, weight gain at 24 months was positively associated with HT SDS (P=0.021). No association was found between weight gain and metabolic parameters.

Conclusions: Our results suggest a possible relationship between postnatal height catch-up growth and metabolic impairment, as underlined by the association found between HT and HbA1c, even after correction for mid-parental height. This is only an explorative analysis; we would like to confirm our results on a larger scale in order to eventually bridge the gap between height gain and metabolic impairment in SGA children.