Endocrine Abstracts

Introduction: In adolescents with growth hormone deficiency (GHD), continuation of GH therapy beyond final height is often necessary to address persistent metabolic abnormalities. Two adolescents with congenital pan/hypopituitarism who required initiation of adult-dose GH therapy due to symptomatic hypoglycaemia will be presented.

Case 1: A patient presented at age 4 with growth failure. Height was -3.41 SDS, weight -2.49 SDS, BMI -0.2 SDS, target height 1.41 SDS, and bone age 1.5 years. TSH was 2.72 mU/l, free T4 8.4 pmol/l, ACTH 8.1 pmol/l, cortisol 339 nmol/l. Levothyroxine sodium replacement therapy was initiated for central hypothyroidism. Despite achieving euthyroidism, growth velocity remained low (3.4 cm/year); IGF-1 <3.9 nmol/l (-3.36 SDS), GH stimulation tests showed peak levels of 1.75 and 3.26 µg/l. GH therapy was initiated at age 5. Genetic analysis revealed a homozygous PROP1 gene deletion. At age 12, GH was discontinued upon reaching the 25th percentile for adult height. At 15 years, routine labs revealed hypoglycemia; retesting showed a peak GH response of 0.11 µg/l, IGF-1 was <–2 SDS. Off-label adult-dose GH therapy was restarted, the hypoglycaemia improved.

Case 2: Referred in the neonatal period for hypoglycemia, GH levels were undetectable (<0.05 µg/l) during and after the episodes. Investigations revealed central hypothyroidism and low prolactin; adrenal insufficiency was excluded. GH therapy was initiated for neonatal hypoglycemia secondary to GHD. At age 11, she was diagnosed with type 1 diabetes mellitus, confirmed by diabetes-related autoantibodies. The final height was 156 cm. The patient had irregular follow-up visits, experienced recurrent, treatment-resistant hypoglycemia, despite very low insulin requirements (<0.05 U/kg/day). GH retesting revealed a peak <0.03 µg/l. Genetic analysis identified a homozygous POU1F1 mutation and adult-dose GH therapy was reinitiated, resulting in resolution of the hypoglycaemia.

Conclusion: In GHD patients who have achieved final height, the continued physiological roles of GH—such as maintaining glucose homeostasis, lipid metabolism, bone density, and quality of life—must be considered. Structured transition protocols should be developed to guide therapy into adulthood, paediatric endocrinologists should be enabled to prescribe adult dose GH therapy when clinically indicated.