Introduction: The commonest cause of paediatric hyperthyroidism is Graves' disease. Previous studies in the Malaysian context haven’t captured data from Negeri Sembilan. This study aims to describe the demographic and clinical features of children with hyperthyroidism from Hospital Tuanku Jaafar. Methodology: A retrospective cohort study collating socio-demographic and clinical data from electronic medical records was conducted. Statistical analysis was conducted using Microsoft Excel (v2602). Results: Fourteen children between 2015 and 2025 were identified. Females comprised 93% (n = 13). The mean age at diagnosis was 9.76 ± 3.4 years, with 64% (n = 9) aged >10 years. Malay ethnicity comprised 64% (n = 9). Family history was positive in 43% (n = 6). Three (21%) children were detected on routine screening. At presentation, 50% (n = 7) were prepubertal and 36% (n = 5) were underweight, with mean BMI SDS −1.4 ± 1.2. All had high fT4 78.43 ± 72 pmol/L and suppressed TSH TRAb positivity was 86% (n = 12). AntiTPO or anti-thyroglobulin antibodies positivity was 79% (n = 11). In one child, all three antibodies were negative. Thyroiditis was the commonest ultrasound finding. Carbimazole starting dose was 0.6 mg/kg/day and average treatment duration was 3.5 ± 2.4 years, which achieved biochemical euthyroidism in 49 days. Relapse rate on carbimazole was 57% (n = 8). No adverse effects occurred, and none had definitive therapy. Currently, 71% (n = 10) are euthyroid on a mean carbimazole dose of 0.2 mg/kg/ day; one is off carbimazole. Current height is −1.1 ± 1.31 SD and BMI SDS −0.42 ± 1.7 SD respectively. Conclusion Graves’ disease is the commonest form of paediatric hyperthyroidism in Negeri Sembilan, affecting prepubertal Malay females who commonly present with thyrotoxicosis. Carbimazole effectively achieves biochemical euthyroidism with minimal side effects. However, linear growth is affected. Future studies should evaluate the factors associated with these findings.
Child ; Retrospective Studies ; Hyperthyroidism

Introduction: Hyperinsulinemic hypoglycemia of infancy may be congenital or acquired, and rarely due to factitious hypoglycemia imposed by another. A thorough medical and social history, critical sampling, and screening for inborn errors of metabolism are crucial. Case: A 5-month-old, ex-29 weeker, twin female infant, born to a non-consanguineous couple was admitted at 4 months with severe refractory hypoglycemia and seizures requiring a glucose infusion rate (GIR) of 16 mg/kg/min. Critical sampling suggested hypoglycemia due to exogenous insulin: glucose 1.1 mmol/L, ketones 0.2 mmol/L, insulin 1,208 pmol/L (17.8–173), and C-peptide 18.2 pmol/L (366– 1,466). Free fatty acids were not raised; growth hormones were 2.223 µg/L (0.14–6.27) and cortisol >1,000 nmol/L (145.4–619.4). Metabolic and genetic testing excluded glycogen storage disorder. Two months prior, she was admitted with a severe human metapneumovirus and parainfluenza infection, hypoglycemia, lactic acidosis and left ventricular hypertrophy. Her twin had died of sudden infant death syndrome. Examination revealed a small puncture mark on the abdomen, but otherwise it was unremarkable. The GIR dropped dramatically over 3 days and the intravenous dextrose was discontinued. Normoglycemia was maintained on 3-hourly feeds and she tolerated an age-appropriate fast before discharge. No hypoglycemic episodes were reported. Of note, the mother suffered from bipolar disorder and had access to insulin for gestational diabetes mellitus. The infant is currently in foster care, is scheduled to have neuroimaging and continues to have growth and developmental follow-up. Conclusion Factitious hypoglycemia should be suspected when there are red flags in the clinical history and critical sampling demonstrates high insulin levels, suppressed C-peptide in the face of hypoglycem ia with low ketones and low free fatty acids. A multidisciplinary approach involving paediatrics, psychiatry, and child protective services is mandatory
Infant ; Hypoglycemia