ESPE Abstracts

Objectives: Among adverse effects of GH, a particular attention should be given to glucose homeostasis. The aim of the study was evaluate the effect of GH therapy on glucose homeostasis in children with GHD after 10 years of treatment.

Methods: 30 patients (8 M/22 F, age 7.00 ± 2.61 years) with GHD at diagnosis and 30 healthy children comparable to patients for age, sex and BMI were enrolled. Glucose, insulin, HOMA-IR and HbA1c were evaluated in patients and controls at study entry. All the evaluations were repeated in patients and controls after 1 and 10 years of treatment or follow-up respectively.

Results: at study entry no significant differences were detected between GHD and controls in glucose (76.40 ± 9.23 vs 75.38 ± 8.45 mg/dl), insulin (6.83 ± 5.44 vs 6.15 ± 2.97 µU/ml), HbA1c (5.5 ± 1.38 vs 5.27 ± 0.34 %), and HOMA-IR (0.96 ± 1.17 vs 0.94 ± 0.44). After the first year of treatment, insulin (11.04 ± 4.8 vs 6.83 ± 5.44 µU/ml, P=0.03) and HOMA-IR (1.84 ± 0.88 vs 0.96 ± 1.17, P=0.011) values significantly increased in GHD children. Furthermore, these values were significantly higher than those of controls evaluated after 1 year of follow-up (7.01 ± 2.42, P<0.05). After 10 years of GH treatment, patients showed a slight reduction in insulin levels in comparison to year 1 (8.63 ± 2.16 vs 11.04 ± 4.8 µU/ml), although the difference did not reach statistical significance. At the same time point, controls showed a significant increase of insulin values compared to year 1 (9.87 ± 2.64 µU/ml vs 7.01 ± 2.42, P<0.001), thus becoming similar to patients’ values. Fasting glucose and HbA1c values did not change in patients or controls throughout the study.

Conclusions: Our results suggest that long-term treatment with GH is not associated with significant impairment in glucose homeostasis. GH replacement therapy is associated with a transient insulin resistance (IR), already evident after 1 year of treatment. Insulin values do not further increase after 10 years of GH therapy and the slight IR obsereved in GHD subjects in adolescence is comparable to that physiologically occuring during puberty.