Introduction: Precocious puberty is increasingly recognized in children. Effect of gonadotropin-releasing hormone agonist (GnRHa) on height velocity (HV) and body mass index (BMI) during treatment of Central Precocious Puberty (CPP) is not welldocumented. Methodology: Records of all patients treated with GnRH for CPP who attended the paediatric endocrine clinic over a 5-year period (2021–2025) [N1.1] were reviewed retrospectively for HV and BMI changes for 3 consecutive years. Basal luteinizing hormone levels ≥0.3 IU/L or stimulated levels ≥5 IU/L are considered diagnostic of CPP. Results: Twenty patients were reviewed and median age at the start of study was 7.8 years (4.3–10.3). Majority were female (n = 18, 90%) with median Tanner Stage 3 and of Malay origin (n = 18, 90%[N2.1]). Median chronological age was 7.8 years (4.3–10.3) with bone age 10.3 years (5.8–13.4). Causes of CPP were idiopathic (n = 16, 80%), CNS lesion (n = 2, 10%) and poorly controlled congenital adrenal hyperplasia (n = 2, 10%). Nine (82%) of the 11 patients who had MRI brain done had normal findings. After 1 year of treatment, the median HV SDS was −0.83 (range −2.45 to 2.42), and BMI SDS was 0.45 (−1.94 to 2.15). After 2 years (n = 12), HV SDS declined to −1.3 (−3.44 to 0.69), with BMI SDS of 0.13 (−1.16 to 1.79). After 3 years (n = 9), HV SDS declined further to −1.51 (−3.52 to 3.13), and BMI SDS was 0.16 (−0.12 to 1.25). After 1 year of treatment, 20% (n = 4) of patients were overweight and 10% (n = 2) were obese. By 3 years, 22% (n = 2) remained overweight, and none were obese. Conclusion Premature growth plate senescence induced by prior estrogen exposure may lead to HV decline. Although obesity is a risk factor for the onset of CPP, whether GnRHa treatment directly increases BMI remains controversial as our cohort’s BMI change reveals otherwise.
Child ; Body Mass Index ; Puberty, Precocious ; Hormones

Introduction: Clonidine is frequently utilized as a stimulus of growth hormone secretion to diagnose growth hormone deficiency in children. This clinical audit evaluates the efficacy and safety profile of clonidine as a sensitive, first-line screening agent to exclude GHD in children. Methodology: A clinical audit was conducted on seven patients (4 females, 3 males) aged 7.1 to 12.3 years (median age 11.1) evaluated with clonidine stimulation test. The cohort included one prepubertal and six post-pubertal (highest tanner 2) children. Bone age was delayed at BA/CA ratio at 0.63–0.9 (median 0.8). Baseline IGF-1 levels ranged from 56 to 264 ng/mL. None of the children received sex steroid priming. A peak GH threshold of >10 ng/mL was utilized to exclude GHD. Safety profiles, specifically hemodynamic stability and level of consciousness, were actively monitored. Results: Clonidine effectively stimulated GH secretion and excluded GHD in six out of seven patients, yielding peak GH levels between 10.3 and 20.6 ng/mL. One patient with peak GH of 7.6 ng/mL with clonidine, and subsequent test with insulin tolerance test (ITT), confirmed GHD with a peak GH of 7.4 ng/mL. All participants (n = 7) experienced drowsiness. Hemodynamic adverse events were notable. Three patients experienced mild hypotension, and three patients developed clinically significant hypotension requiring normal saline fluid bolus. Conclusion Clonidine is a highly effective, sensitive first-line screening agent to exclude GHD, as it reliably stimulates GH peaks above diagnostic thresholds. However, close supervision is required due to drowsiness and the potential for severe hypotension requiring fluid resuscitation. Clinical judgment remains essential as secondary testing with another GH secretagogue is warranted when clinical suspicion persists.
Child ; Clonidine ; Clinical Audit ; Growth Hormone