Growth Hormone Response to Glucagon Stimulation Test in Transitional Age

Daniela Fava; Barbara Vanorio; Chiara Santucci; Stefano Parodi; Alessia Pepe; Agnese Repetto; Claudia Caridi; Lucia Acquarone; Erica Data; Silvia Merlo; Flavia Napoli; Caterina Tedesco; Alessia Angelelli; Marta Panciroli; Emilio Casalini; Iorgi Natascia Di; Mohamad Maghnie

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ESPE Abstracts (2024) 98 FC7.4

ESPE2024 Free Communications GH and IGFs (6 abstracts)

Growth Hormone Response to Glucagon Stimulation Test in Transitional Age

Daniela Fava ¹ , Barbara Vanorio ² , Chiara Santucci ² , Stefano Parodi ³ , Alessia Pepe ² , Agnese Repetto ² , Claudia Caridi ² , Lucia Acquarone ² , Erica Data ² , Silvia Merlo ² , Flavia Napoli ¹ , Caterina Tedesco ¹ , Alessia Angelelli ¹ , Marta Panciroli ² , Emilio Casalini ² , Natascia Di Iorgi ² & Mohamad Maghnie ²

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¹Pediatric Endocrinology Unit, Department of Pediatrics, IRCCS Istituto Giannina Gaslini, Genova, Italy. ²Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genova, Italy. ³Epidemiology and Biostatistics Unit, Scientific Directorate, IRCCS Istituto Giannina Gaslini, Genova, Italy

Context: In the diagnosis of permanent GH deficiency (GHD) during the transition phase, the 2019 AACE guidelines recommended peak GH-cutoffs of ≤3µg/L and ≤1µg/L for the glucagon test (GST), while a recent investigation identified a value <5.8μg/L as a suitable gold standard (Fava et al, Journal of Clinical Endocrinology and Metabolism, 2024). However, the clinical applicability of this cutoff remains to be confirmed and the potential confounding by Body Mass Index (BMI) needs to be assessed.

Objective: Aim of the study was to evaluate the response to GST in patients with childhood-onset GHD (CO-GHD) at adult height achievement in relation to pre-test probability and BMI.

Patients and Methods: A consecutive cohort of 171 patients with CO-GHD without type 2 diabetes (median age, 17.44 years, IQR 15.96;18.62) underwent GST (1 mg I.M.); 76 childhood cancer survivors (CCS), 72 idiopathic (I), 61 moderate organic (OM) (1-2 hormone deficiencies-HDs) and 38 severe organic (OS) GHD (≥3 HDs). Association between peak GH to GST and GHD severity, adjusted by BMI SDS, was evaluated by multiple linear regression analysis, and by logistic regression using GST with a cut-off <5.8μg/L.

Results: GH peak to GST was lower in OS (0.76 μg/L, IQR 1.2;1.87) and OM groups (2.64 μg/L, IQR 1.14;5.67) compared to I (12 μg/L, IQR 9.83;20.16, P <0.001). BMI SDS was higher in OS (1.35, IQR 0.45;2.33) and OM (0.62, IQR -1.0;1.68) patients compared to I (0, IQR -0.9;0.73, P <0.001). Obesity (BMI≥2 SDS) was observed in 24 patients (14%): 13 OS (34.2%), 7 OM (11.5%) and 4 I (5.6%). Eighy-five patients (49.7%) showed a GH peak≥5.8 μg/L, who included 3 OS (3.5%), 15 OM (17.6%) and 67 I (78.8%). Among the 86 patients with GH peak<5.8 μg/L, 21 had obesity: 13 OS (62%), 7 OM (33.3%) and 1 I (4.7%), respectively. An inverse correlation was observed between peak GH and BMI SDS (r =-0.44, P <0.001). Both the severity of GHD and the BMI SDS were independently inversely associated with the GH peak to GST in both linear and logistic regression analysis. Odds Ratio (OR) at a GH peak<5.8 μg/L for OM and OS, compared with I patients, were 37.1 and 104.9, respectively (P <0.001); for BMI>2SDS the OR was 1.6 (P = 0.013).

Conclusion: A GH peak to GST<5.8 μg/L is an accurate diagnostic cut-off for young adults with CO-GHD and high pre-test probability of permanent GHD.