ESPE Abstracts (2016) 86 P-P1-613

Glucose Dysregulation in Children with Growth Hormone Deficiency (GHD), Turner Syndrome (TS) or Born Small for Gestational Age (SGA) Treated with GH: A Report from the NordiNet International Outcome Study (IOS)

Primoz Kotnika, Tilman Rohrerb, Birgitte Tønnes Pedersenc, Effie Pournarad & Henrik Christesene


aUniversity of Ljubljana, Ljubljana, Slovenia; bUniversität des Saarlandes, Homburg/Saar, Germany; cNovo Nordisk A/S, Søborg, Denmark; dNovo Nordisk Health Care AG, Zurich, Switzerland; eUniversity of Southern Denmark, Odense, Denmark


Background: The prevalence of glucose dysregulation in children treated with GH is not well established.

Objective and hypotheses: To evaluate the prevalence of glucose dysregulation in children with growth disorders (GH deficiency (GHD), Turner syndrome (TS), small for gestational age (SGA)) treated with GH (Norditropin, Novo Nordisk) enrolled in NordiNet International Outcome Study (IOS) (NCT00960128), a non-interventional study evaluating safety and effectiveness of Norditropin in clinical practice.

Method: Diabetes was identified based on reports of: clinical diagnosis; diabetes reported as an adverse event; treatment with antidiabetic medication. A subgroup of 1659 children without diabetes at baseline was evaluated for ΔHbA1c (2-year change). Data are mean (s.d.).

Results: Diabetes prevalence in NordiNet IOS was 0.34% (45/13,134 patients): Type 1: n=29 (n=reported before/after GH): (GHD, n=15/3; TS, n=4/2; SGA n=4/1); Type 2: n=10 (GHD, n=4/3; TS, n=0/1; SGA, n=0/2). Unspecified diabetes: n=6 (GHD, n=2/2, SGA, n=2/0). In the subgroup analysis (GHD, n=915; TS, n=191; SGA, n=553) children born SGA were younger (7.7 (3.2) years) and leaner (BMI SDS, –1.06 (1.24)) than children with GHD (9.8 (3.8) years; BMI SDS, –0.21 (1.34)) or TS (8.4 (3.6) years, BMI SDS, 0.33 (1.08)). Mean GH dose (μg/kg per day) over 2 years was lower in GHD, 32.6 (8.3), and higher in TS, 45.0 (10.5) and SGA, 38.6 (10.4). Two patients (GHD, n=1; SGA, n=1) with normal baseline HbA1c (<5.7%) developed type 2 diabetes, and two patients (GHD, n=1; SGA, n=1) had HbA1c >6.5% at year 2. Mean ΔHbA1c was 0.08(0.36)% for SGA, 0.06(0.46)% for GHD and 0.05(0.55)% for TS. The proportion of patients with an increase in HbA1c from normal (<5.7%) to prediabetes/high-normal (5.7%–6.5%)) at 2 years was 12.2%, 10.6% and 6.5% for GHD, SGA and TS, respectively.

Conclusion: With this report we present the prevalence of glucose dysregulation in children with growth disorders before and after short-term GH treatment. These findings warrant further analysis and comparison to measures within population-based diabetes studies.

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