ESPE Abstracts (2015) 84 P-2-453

Cross-Sectional and Longitudinal Follow-Up of Changes in Glucose Metabolism in Prepubertal GH-Treated SGA-Patients: Results of an Unicentric Study

Carmen Sydlik, Susanne Bechtold, Claudia Weissenbacher, Julia Roeb, Matthias Buckl, Stefanie Putzker & Heinrich Schmidt

Children’s Hospital Ludwigs-Maximilians-University, München, Germany

Background: Several studies show impaired glucose tolerance at a certain number of years after start of growth hormone in SGA-children.

Objective and hypotheses: To perform a longitudinal and cross-sectional evaluation of the oGTTs (glucose-insulin-pairs) in prepubertal GH-treated SGA-children and to evaluate if ISI and HOMA are effective surrogates for glucose tolerance and of prognostic value (0–1 year data).

Method: In 81 prepubertal SGA-children oGTT, HOMA and ISI were determined before start and yearly under GH-treatment until puberty (maximum 4 years of treatment).

Results: In oGTT, highest values for glucose and insulin were seen at 30 min in all years: maximum values for glucose at 0–2 years, for insulin between 1 and 3 years of treatment. Mean glucose/insulin-ratio continuously decreased. HOMA increased until 3 years (0.8±0.5 to 1.6±1.2). ISI continuously decreased from 0 to 4 years (14.9±9.8–6.4±1.2). 3/81 children showed 0-min-glucose values >100 mg/dl indicating impaired fasting glucose (IFG) even before GH-treatment, 7/81 120-min-values >140 mg/dl (IGT) and three elevated fasting insulin (>10 μU/ml). None of them had pathologic oGTTs later. Only 4/81 had pathologic HOMA (>2.5) and/or ISI (<5) at baseline. After 1 year of treatment 7/72 showed IFG, 2/72 IGT, five fasting insulin >10 μU/ml. 5/72 showed elevated HOMA and 8/72 decreased ISI (mostly not the same as at 0 years). 9 of 59 followed for >1 year who had any abnormal value before changed to normal. 16/59 who had completely normal tests at 0 and 1 year showed at least one pathologic value later.

Conclusion: We found continuously raising insulin resistance until at least 4 years of GH-treatment. 30-min-values always were the highest (not represented in ISI-index!). As HOMA and ISI can deteriorate independently of each other, if surveillance of glucose homeostasis shall be performed, determining only the fasting values is not sufficient and in oGTT also the 30-min-results should be considered. Neither baseline nor 1-year-data for HOMA, ISI and/or oGTT are of prognostic value for the further development of glucose tolerance during GH-therapy. In our collective temporarily pathologic values had no therapeutic consequence and none of the patients developed diabetes.

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