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

Infants of mothers with Graves’ disease (GD) may develop central hypothyroidism (CH) due to exposure of the foetal hypothalamic-pituitary-thyroid axis to higher-than-normal thyroid hormone concentrations, primary hypothyroidism (PH) due to transplacental passage of maternal thyroid stimulating hormone receptor antibody (TRAb), antithyroid drugs (ATD) or thyroid dysgenesis secondary to maternal uncontrolled hyperthyroidism. We describe two infants with PH and four infants with CH born to mothers with poorly controlled Graves' disease. All infants required levothyroxine and had normal developmental milestones. While national guideline consensus for high thyroid stimulating hormone (TSH) on neonatal screening is well-established, thyroid function tests (TFTs) should be serially monitored in infants with low TSH on screening, as not all mothers with Graves’ disease are diagnosed antenatally.
Infant ; Hypothyroidism ; Congenital Hypothyroidism