ESPE Abstracts (2016) 86 P-P2-646

ESPE2016 Poster Presentations Growth P2 (47 abstracts)

Metabolic Parameters and Glucose Homeostasis in Childhood Onset Growth Hormone Deficiency at Time of Initial Evaluation and Retesting

M Ahmid , M McMillan , S F Ahmed & M G Shaikh

Developmental Endocrinology Research Group, Royal Hospital for Children, School of Medicine, University of Glasgow, Glasgow, UK

Background: It is well known that growth hormone (GH) brings about several effects, involving bone, body composition, lipids and glucose homeostasis. However, the complex interplay between these parameters is rather poorly studied in children with childhood-onset-GH deficiency (CO-GHD).

Objective and hypotheses: To investigate lipids, adipokines (leptin- adiponectin- resistin) and glucose homeostasis and their relationship with bone and body composition in children and adolescents with CO-GHD at time of diagnosis and retesting at final height.

Method: A cross-sectional study of children undergoing GH stimulation tests for short stature (total −25, GH deficiency −15, median age (range) 10.9 years (5.6–16.0)) and biochemical revaluation at final height after GH therapy (total – 11, GH deficiency – 7, age 16.7 years (14.9–18.6)).

Results: At time of diagnosis and retesting, lipid profiles, adipokines and glucose homeostasis in both groups were within the normal range with no differences between those with GHD and those who had normal GH levels. Leptin levels in both groups correlate positively with fat mass (r=0.9, P<0.001), and with osteocalcin positively at diagnosis (r=0.5, P=0.01) but inversely at retesting (r=−0.9, P<0.001). In retesting group, those who were older at the time of diagnosis CO-GHD and had a shorter duration of GH therapy were more likely to have higher cholesterol (r=0.9, P<0.001), LDL(r=0.9, P<0.001), and leptin (r=0.8, P<0.001), and lower osteoclacin (r=−0.7, P=0.01) at final height.

Conclusion: Metabolic profiles and glucose homeostasis are not significantly different between those with GH deficiency and those with normal GH levels at times of initial evaluation and retesting at final height. Timing and duration of childhood treatment may influence adiposity parameters and bone formation biomarkers seen in adolescents with CO-GHD. Differences in relationship between leptin and osteoclacin at diagnosis and retesting may be related to active growth. Further studies are still required to clarify the relationship between adipokines, bone and CO-GHD.

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