Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2015) 37 EP781 | DOI: 10.1530/endoabs.37.EP781

ECE2015 Eposter Presentations Pituitary: clinical (121 abstracts)

Childhood onset GH deficiency: re-evaluation at the point of transition to adult care

Mariana Grace 1 , Stephen O’Riordan 2 , Rose Morissey 2 , Mary Stapeton 3 & Susan O’Connell 2


1Department of Paediatric and Child Health, University College Cork, Cork, Ireland; 2Paediartric Endocrinology Unit, Cork University Hospital, Cork, Ireland; 3Department of Biochemistry, Cork University Hospital, Cork, Ireland.


Childhood onset GH deficiency (CO-GHD) usually presents with aberrant growth. Treatment is recombinant GH (r-GH) to attain target height. The 2005 European Consensus statement on management of CO-CHD at transition indicates that most adolescents will require repeat GH testing at completion of linear growth. Patients with persistent GHD will require continuation of r-GH for wellbeing, optimal body composition and metabolism. However, there is little data supporting predictors of persistent GHD, which include underlying diagnosis (structural pituitary defects or idiopathic, multiple or isolated pituitary hormonal deficiencies) and serum IGFPB3, IGF1 levels on completion of linear growth.

Objectives: To (1.) classify patients according to European Society of Paediatric Endocrinology Classification of Paediatric Endocrine Diagnoses (Cohort 1) (2.) evaluate patients aged >14 years in this cohort (Cohort 2).

Methodology: A retrospective review of all patients receiving GH treatment (n=65) attending a regional tertiary Paediatric Endocrinology centre over an 18 month period, and prospective re-testing of those fulfilling the criteria.

Results: Cohort 1: 47% had primary and 52% secondary growth failure. Cohort 2: 24 patients aged >14 years (75% males), 29% with primary growth failure. 71%had secondary growth failure, of whom 35% had idiopathic GHD (iGHD) (normal pituitary structure), 64% had structural pituitary abnormalities (congenital/ acquired). Four patients fulfilled criteria for retesting, all with normal IGF-1 after one month off GH; two had normal GH levels (iGHD) and two had persistent GHD (1 craniopharyngioma and one suspected genetic aetiology due to family history of CO-GHD).

Conclusion: This is the first study of CO-GHD in an Irish cohort. The results are consistent with international literature. In addition, family history of CO-GHD may be a predictor for persistent GHD. We anticipate that >60% of our cohort will have persistent GHD at the time of transition warranting continuation of GH.

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