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Objectives: An inverse relationship has been shown between body mass index (BMI) and the peak growth hormone (GH) response to stimulation in adults and in children with short stature. This relation is observed even within a normal range of BMI. The aim of this study was to investigate the effect of BMI on the GH response to clonidine in a large number of children with short stature., Design: We conducted a retrospective study on the GH response to clonidine in a single centre., Methods: We studied 202 children with short stature (135 M and 67 F) who underwent clonidine testing from 2007 to 2009., Results: One hundred and twenty-eight patients had a GH peak >10 μg/l. In univariate regression analysis, the peak GH after clonidine was negatively correlated with BMI-standard deviation score (BMI-SDS) and positively correlated with height velocity-SDS and IGF-I-SDS. Only the relationship between peak GH and BMI-SDS remained significant in children with a BMI-SDS from -2 to +2. In the multivariate stepwise regression analysis, BMI-SDS and IGF-I-SDS were the only significant variables in the entire cohort, explaining 19·5% of the variance in peak GH. When only subjects with BMI-SDS between -2·0 and +2·0 were included in the analysis (n = 173), BMI-SDS alone explained 21·4% of the variability in peak GH. The number of patients who failed the clonidine test increased with increasing BMI-SDS., Conclusions: BMI affects the GH response to clonidine in children with short stature and should be considered when interpreting the results to the stimulation test., (© 2011 Blackwell Publishing Ltd.)

Objective: 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. Design and patients: Data were collected retrospectively from 327 children and adolescents with short stature (204 boys and 123 girls, median age 10.5 years (IQR 7.90‐12.40) followed in four Italian Paediatric Endocrine Units (Cagliari, Genova, Napoli and Roma) between 2005 and 2013. Measurements: All children underwent CT as the first GH stimulation test after exclusion of other known cause of their short stature. Results: In 73 prepubertal children and 25 pubertal children, the GH peak after CT was <7 μg/L. GHD was confirmed in 87 (37 organic, 50 idiopathic). Six prepubertal and five pubertal patients showed false positive responses. The median BMI‐SDS in these children was similar to that of children with GH peak ≥7 μg/L, and none were obese. Overall, the prevalence of false‐positive responses was 3.3%. The median (IQR) peak GH after CT was similar between prepubertal and pubertal GHD (3.80 μg/L [1.7‐6.00] vs 3.51 μg/L [0.76‐5.74]) and non‐GHD (13.70 μg/L [10.70‐18.40] vs 12.40 μg/L [9.90‐19.25]) children. Conclusions: Our results show that CT is a reliable and safe GH‐releasing agent in both prepubertal and pubertal children. [ABSTRACT FROM AUTHOR]