ESPE Abstracts (2018) 89 P-P2-228

Reliability of Clonidine Testing for the Diagnosis of Growth Hormone Deficiency in Children and Adolescents

Anastasia Ibbaa, Chiara Guzzettia, Letizia Casulaa, Mariacarolina Salernob, Natascia Di Iorgic, Anna Maria Elsa Allegric, Marco Cappad, Mohamad Maghniec & Sandro Lochea


aSSD Endocrinologia Pediatrica e Centro Screening Neonatale, Ospedale Pediatrico Microcitemico ‘A. Cao’, AO Brotzu, Cagliari, Italy; bDipartimento di Pediatria, Università Federico II, Napoli, Italy; cClinica Pediatrica, IRCCS G. Gaslini, Università di Genova, Genova, Italy; dUOC di Endocrinologia Pediatrica, Ospedale Pediatrico Bambino Gesù IRCCS, Roma, Italy


Introduction: The diagnosis of growth hormone deficiency (GHD) is currently based on clinical, auxological, biochemical, and neuro-radiological investigation. Provocative tests of GH secretion using physiological/pharmacological stimuli are required to confirm GHD. The clonidine test (CT) is widely used to assess GH secretory status. In this retrospective study we analyzed the reliability of CT and the effect of puberty in a large number of children with short stature who had been evaluated for suspected GHD.

Subjects and methods: Data were collected from 327 children and adolescents with short stature, and/or poor growth velocity, (204 boys and 123 girls, age 10.04±3.35 SD) followed in four Italian Pediatric Endocrine Units between 2005 and 2013. All children underwent CT as the first GH stimulation test after exclusion of other known causes for their short stature. All children with a GH peak ≥7 μg/L, normal growth velocity for age, and no other recognizable cause for their shortness were considered as non-GHD. Steroid priming was never used in any of the subjects. Children were subdivided into two groups based on pubertal stage according to Tanner (group 1, pre-pubertal Tanner 1, n=223; group 2, pubertal Tanner 2-5, n=104) and into two groups according to diagnosis (GHD vs non-GHD). We then analyzed separately prepubertal vs pubertal GHD children (n=64 and 23, respectively) and prepubertal vs pubertal non-GHD children (n=154 vs 81, respectively).

Results: In 70 prepubertal children and 28 pubertal children the GH peak after CT was <7 μg/L. GHD was confirmed in 87 (37 organic, 50 idiopathic). The remaining 11 (6 pre-pubertal and 5 pubertal) who failed CT, had normal GH responses to a second stimulation test independently of the pubertal status (P=0.66). Mean BMI-SDS in these children was similar to that of the children with GH peak ≥7 μg/L, and none was obese. Overall, the prevalence of false positives was 3.3%. Mean peak GH after CT was similar between prepubertal and pubertal GHD and non-GHD children. Mean IGF-I-SDS was significantly higher in pubertal vs prepubertal non-GHD subjects while there was no difference between prepubertal and pubertal GHD patients.

Conclusions: This study demonstrates that using a validated cut-off of 7 μg/L CT is reliable in the diagnosis of GHD in children and adolescents and that steroid priming is probably not required. The oral CT is a reliable and safe GH releasing agent in both prepubertal and pubertal children.