ESPE Abstracts (2014) 82 P-D-3-1-815

Insulin Tolerance Test and GHRH Plus Arginine in the Reassessment of Pituitary Function at Adult Height Achievement

Natascia Di Iorgia,b, Maria Carolina Salernoc, Marco Cappad, Sandro Lochee, Giorgio Radettif, Donatella Capaldoc, Flavia Napolia, Annalisa Calcagnoa, Anna Elsa Maria Allegria, Ofelia Bianca Iovovicha, Serena Nolia,b, Stefano Parodig & Mohamad Maghniea,b


aGiannina Gaslini Institute, Genova, Italy; bUniversità degli di Studi di Genova, Genova, Italy; cOspedale Federico II, Napoli, Italy; dOspedale Bambin Gesù, Roma, Italy; eOspedale Microcitemico, Cagliari, Italy; fOspedale Regionale, Bolzano, Italy; gInstitute of Electronics, Computer and Telecommunication Engineering, Genova, Italy


Background: There is still need to define permanent GHD after adult height achievement in young adults with childhood-onset GHD (COGHD).

Objective and hypothesis: To reassess GH response during transition.

Method: We present the final data of 129 subjects (71M) recruited from a multicenter cross-sectional observational study, in whom anthropometrics, ITT (n=99), GHRH–arginine (n=122), IGF-1 evaluations were undertaken at a mean age of 17.5±2.1 years. Fifty had idiopathic (iGHD), 49 secondary to brain tumors or LMA (n=1) (TGHD) and 30 congenital GHD (CGHD). Isolated GHD (IGHD) was found in 83 (n=49 iGHD, n=19 secondary GHD (SGHD), n=15 CGHD), and MPHD in 46 (n=1 iGHD, n=30 SGHD, n=15 CGHD). Peak GH values >6 μg/l for ITT and >19 μg/l for GHRH–arginine were considered normal.

Results: As TGHD and CGHD subjects had comparable peak responses to ITT, GHRH–arginine and IGF1 SDS they were combined as secondary GHD (SGHD); this latter showed lower values compared to iGHD subjects (ITT: 5.0±5.3 and 18.7±13.3 μg/l; GHRH–arginine:15.8±19.5 and 49.2±34.7 μg/l; and IGF1 −2.2±2.2 and −0.4±1.3 SDS, respectively; all P’s<0.0001). Patients with SGHD and IGHD showed higher GH responses after GHRH–arginine compared to those with MPHD (P=0.0001). ROC analyses identified a GH value of 5.26 μg/l after ITT discriminating SGHD from iGHD (AUC 0.88, P<0.00001; sensibility (Se), 66% and specificity (Sp), 94%); a GH value of 31.2 μg/l after GHRH–arginine (AUC 0.85, P<0.00001; Se 89%, Sp 74%) and an IGF1 of −1.9 SDS (AUC 0.76, P<0.00001; Se 49%, Sp 96%). The best cut-offs discriminating IGHD from MPHD were a GH value of 5.26 μg/l after ITT (AUC 0.79, P<0.00001, Se 78%, Sp 63%), 13.7 μg/l after GHRH–arginine (AUC 0.86, P<0.00001, Se 79%, Sp 82%) and an IGF1 of −1.5 SDS (AUC 0.75, P<0.00001; Se 69%, Sp 75%). GH responses to ITT and GHRH–arginine were inversely correlated to BMI SDS (r’ −0.44 and −0.40, respectively, P’s<0.00001).

Conclusion: Patients with childhood-onset SGHD and MPHD are at higher risk of permanent GHD compared to iGHD and IGHD. ITT confirms to be reliable in the identification of patients who may need rhGH treatment in adult life. BMI may affect GH response after both stimulation tests.