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

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