ESPE Abstracts (2019) 92 P2-160

Metabolic Outcome in Adolescents with Growth Hormone Deficiency During Transition Phase

Nicola Improda1, Cristina Moracas1, Gian Paolo Ciccarelli1, 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: It is well known that GH deficiency (GHD) in adulthood is associated with detrimental cardiovascular (CV) effects. Although data are controversial, adolescents with childhood-onset GHD (COGHD) and reconfirmed GHD may have increased metabolic risk after GH treatment withdrawal at final height (FH).

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

Patients and Methods: twenty subjects (8 F) (age 17.0±1.4yrs) with reconfirmed GHD at retesting (peak of GH<19 ng/ml after GHRH+Arginine), and twenty adolescents (8 F) (age 16.8±1.0yrs) with sufficient GH 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, height velocity (HV), bone age (BA), waist circumference (WC), hip circumference (HC), waist/hip ratio (WHR), waist/height ratio (WHtR), IGF-1, glucose, insulin, HOMA, QUICKI index, total-, HDL- and LDL- cholesterol, triglycerides, atherogenic index (AI), fibrinogen and homocysteine.

Results: At diagnosis during childhood, subjects with reconfirmed GHD were younger than GHS subjects (7.0±4.4 vs 10.6±2.9yrs, P<0.02) and had lower H SDS (−3.0±1.1 vs -2.2±0.8, P=0.03), HV SDS (−3.6±1.1 vs -2.2±1.5, P=0.007), HDL-C (47.6±12.6 vs 60.1±15.6mg/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±44.9mg/dl, P<0.05) and homocysteine (11.8±3.9 vs 8.8±3.4µmol/L, P<0.04).

The groups became comparable for all these parameters during GH treatment.

At the attainment of FH the total gain in H SDS 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.

Six months after GH withdrawal, GHD patients showed higher BMI SDS (0.30±1.5 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±22.1mg/dl, P<0.05), AI (3.4±0.5 vs 2.6±0.7, P<0.002), fibrinogen (307±45.7 vs 272.3±46.1mg/dl, P<0.05) and homocysteine (12.1±4.6 vs 9.2±2.9µmol/L, P<0.05) and lower levels of HDL cholesterol (47.8±8.8 vs 55.8±10.3mg/dl, P<0.03) than subjects with sufficient GH secretion.

Conclusions: Discontinuation of GH therapy at attainment of FH in subjects with reconfirmed GHD is associated to the development of metabolic abnormalities already 6 months after withdrawal; thus underlying the importance of an early GH restart in young adults with reconfirmed GHD.

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