ESPE Abstracts

A small number of GH deficient patients can be recognized before age 3, and only few of them are diagnosed during work-up for hypoglycemia. Data comparing clinical and laboratory characteristics of hypoglycemic vs non-hypoglycemic population of children with early onset GH deficiency is scarce. The aim of this study is to assess long-term follow-up of growth hormone therapy in early onset GH deficiency, and compare pre-treatment and treatment related factors with respect to history of hypoglycemia.

Methods: Twenty-three children with early onset GH deficiency in whom GH treatment was initiated before 3 years of age were included. Patients were grouped according to history of hypoglycemia. We retrospectively analyzed pre-treatment clinical and laboratory parameters such as birthweight, initial growth factor and GH as well as other pituitary hormone levels, and longitudinal growth and weight indices of patients. Diagnosis of GH deficiency was based on decreased growth velocity and low peak GH level in two GH stimulation tests, or low GH in a critical sample during hypoglycemia in cases with neonatal hypoglycemia.

Results: Thirteen children (seven females) out of 23 (ten females) had history of hypoglycemia. Eighteen children (ten hypoglycemic) had combined pituitary hormone deficiencies. Birth weight, gestational age at birth, initial length Z-score, weight for length Z-score, growth velocity Z-score, IGF1 and peak cortisol levels were similar in the two groups. Hypoglycemic patients were diagnosed, and received GH and thyroid hormone replacements at an earlier age than non-hypoglycemic patients (P: 0.02, <0.01, 0.02, respectively). Prolactin levels were lower in hypoglycemics than non-hypoglycemics (P: 0.01). Initial mean length Z-score improved significantly in the course of GH replacement in the whole group (−3.51 at onset, and 0.6 at 5^th year of treatment), however there was no significant difference between the two groups. Only two patients were obese at onset (one hypoglycemic), during follow up seven patients (six hypoglycemic) developed obesity, suggesting an increased tendency for obesity in hypoglycemics in comparison to non-hypoglycemics (P:0.08). Weight for length/height Z-score increased at 36th month of treatment in the whole group (P: 0.073), which was attributed to the hypoglycemics (P: 0.04) rather than non-hypoglycemics (P: 0.83).

Conclusion: GH deficient children with history of hypoglycemia are more prone to develop obesity in the face of a similar growth response to GH treatment. Further studies are needed to explain this finding.