ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2019) 63 GP60 | DOI: 10.1530/endoabs.63.GP60

Metabolic outcome in adolescents with growth hormone deficiency during transition phase

Nicola Improda1, Federica Anselmi1, Sara Alfano1, Ida D’Acunzo1, Lorenzo Bufalo1, Donatella Capalbo2 & Mariacarolina Salerno1


1Pediatric Endocrine Unit, Department of Translational Medical Sciences, University of Naples Federico II, Naples, Italy; 2Department of Pediatrics, University of Naples Federico II, Naples, Italy.


Background: There is concern that adolescents with childhood-onset GHD (COGHD) and persistent GH deficiency may be exposed to multiple metabolic risks after GH treatment withdrawal at the attainment of final height (FH).

Aim: Aim of our study is to retrospectively compare growth response and metabolic profile in isolated idiopathic COGHD adolescents with permanent GH deficiency in comparison to GHD subjects who normalized their GH response at transition phase.

Patients and methods: 20 subjects (12M-8F) (age 17.0±1.4 years) with persistent GHD at retesting and 20 adolescents (12M-8F) (age 16.8±1.0 years) with sufficient response to the test (GHS) were enrolled. In all patients the following parameters were evaluated at diagnosis of GHD during childhood and before and after 6 months of GH withdrawal at the attainment of FH: height, weight, body mass index (BMI), waist circumference (WC), hip circumference (HC), waist/hip circumference (WHR), waist/height ratio (WHtR), IGF-1, blood glucose, insulin, HOMA, QUICKI index, total-, HDL- and LDL-cholesterol, triglycerides, atherogenic index (AI), fibrinogen and homocysteine. Height, weight and BMI were expressed in standard deviation score (SDS) according to reference standards.

Results: At diagnosis during childhood, young adults with GHD were younger than GHS subjects (7.0±4.4 vs 10.6±2.9 years) and had lower HSDS (−3.0±1.1 vs −2.2±0.8, P=0.03), HVSDS (−3.6±1.1 vs −2.2±1.5, P=0.007), HDL-C (47.6±12.6 vs 60.1±15.6 mg/dl, P<0.03) and higher levels of AI (3.6±1.1 vs 2.6±0.9, P<0.02), fibrinogen (300.7±46.6 vs 266.3±44.9 mg/dl, P<0.05) and homocysteine (11.8±3.9 vs 8.8±3.4 μmol/l, P<0.04). The groups became comparable for all these parameters during GH treatment. At the attainment of FH the total gain in HSDS was higher in GHD in comparison to GHS young adults (2.2±1.6 vs 1.2±0.4, P<0.03) while all other anthropometric and metabolic parameters were comparable between the two groups. (When subjects were evaluated) After 6 months of GH withdrawal, GHD patients showed higher BMISDS (0.30±1.15 vs −0.67±1.0, P<0.05), WHtR (0.50±0.06 vs 0.45±0.03, P<0.008), total cholesterol (157.7±22.3 vs 141±22.1, P<0.05), AI (3.4±0.5 vs 2.6±0.7, P<0.002), fibrinogen (307±45.7 vs 272.3±46.1 mg/dl, P<0.05) and homocysteine (12.1±4.6 vs 9.2±2.9 μmol/l, P<0.05) and lower levels of HDL cholesterol (47.8±8.8 vs 55.8±10.3 mg/dl, P<0.03) than subjects with sufficient GH secretion.

Conclusions: Discontinuation of GH therapy at attainment of FH in subjects with severe COGHD is associated to the development of metabolic abnormalities which are already evident 6 months after withdrawal thus underling the importance to limit the period of treatment discontinuation during transition phase.

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