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I.e. finding no significant result when in fact there is a true underlying effect ; may have led to our observation that pubertal timing was not accelerated. Although this study was not powered for the secondary endpoints reported herein, a retrospective analysis indicated that an observed difference in median pubertal onset ages of approximately 0.4 and 1.1 yr in boys and girls, respectively, could have been detected with P 0.05. Results with the lower GH dose used in our study 0.24 mg kg wk ; were similar to those of Leschek et al. 3 ; , who observed no acceleration of pubertal onset or pace compared with placebo-treated controls in patients who began lowdose 0.22 mg kg wk ; GH at mean age of 12 yr. Because our lower dose was similar to that used by Leschek et al. 3 ; , it is unlikely that acceleration of puberty and bone maturation had plateaued at the lower dose in our study which would have rendered further acceleration undetectable at the higher dose of 0.37 mg kg wk GH ; . Our higher GH dose 0.37 mg kg wk ; did not appear to advance bone maturation, with mean ratios of BA CA less than or equal to 1 throughout the study. Importantly, our higher dose did not appear to lead to pubertal onset at an inappropriately early age 711 ; . Results in the literature differ with regard to the influence of GH on pubertal onset and pace. Some of these inconsistencies may be related to small sample size. The first randomized study compared only 10 GH-treated girls with a similar number of untreated controls 25 ; , and more recent randomized controlled studies have included fewer than 20 patients per treatment group 3, 4 ; . Differences in study design may also explain some of the observed inconsistencies regarding the influence of GH on pubertal onset and pace. Less rigorous studies, including those lacking concurrent controls, have demonstrated either no influence of GH on pubertal onset 15, 26 ; or pace 15, 27, 28 ; or, alternatively, acceleration of pubertal onset 29 ; or pace 26 29 ; in children with ISS. Even randomized controlled studies, characterized as having more monitoring and experimental rigor than other study designs, have given differing results 3, 4 ; . Kamp et al. 4 ; observed advancement of pubertal onset and bone maturation in patients who began high-dose 0.5 mg kg wk ; GH at mean age of 8 yr, whereas Leschek et al. 3 ; observed no such effect in patients who began low-dose 0.22 mg kg wk ; GH at mean age of 12 yr. Our patients began treatment at an intermediary mean age of 9.8 yr. Kamp et al. 4 ; suggested that the young age at which their patients began GH therapy may have influenced the effect of GH on pubertal onset 4 ; . However, data from a young cohort of our patients whose age range was similar to that in the study by Kamp et al. 4 ; showed no evidence of acceleration of pubertal onset for the 0.37 mg kg wk dose compared with the 0.24 mg kg wk dose. Thus, the higher GH dose used in the study by Kamp et al. 4 ; seems a more likely explanation for accelerated pubertal onset. Alternatively, type I error i.e. finding a significant result when in fact there is no true underlying effect ; may have led to the authors' observation of accelerated pubertal onset. Using a lower dose of GH 0.37 mg kg wk ; than that used by Kamp et al. 4 ; , we observed ages at pubertal onset that were appropriate compared with the general population 7.

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