Background: It is not established which routinely available clinical parameter best separates endocrine from non-endocrine short stature. We characterised the clinical, anthropometric and hormonal profile of short-statured pre-pubertal children and tested which parameters discriminate between etiological groups.
Methods: Prospective observational study of 100 children aged 6–12 years with height-for-age below the 3rd percentile, over 18 months at a tertiary care centre. All underwent structured history, anthropometry (segment ratios, mid-parental height, height velocity), thyroid function tests, serum IGF-1, cortisol and radiographic bone age; growth hormone (GH) stimulation testing and karyotyping were performed on defined indications. Comparisons used one-way ANOVA with Tukey post-hoc testing, Kruskal–Wallis, t-tests and chi-square/Fisher exact tests.
Results: Mean age was 8.61 ± 1.54 years and 64% were male. Causes were normal variant in 36 (constitutional growth delay 23, familial short stature 13), endocrine in 28, nutritional in 21, chronic/systemic in 9 and genetic in 6; 64% therefore had a pathological cause. GH deficiency was the commonest endocrine diagnosis (18/28, 64.3%). Attained height lay 1.62 SDS below the mid-parental target (95% CI 1.51–1.73; paired t = 28.99, p < 0.001), with 86/100 more than 1 SDS below. Height SDS did not differ across etiological groups (F = 0.931, p = 0.449), but height velocity did (F = 10.49, p < 0.001, η² = 0.31): the endocrine group grew more slowly (3.09 ± 0.71 cm/year) than every other group on Tukey testing (all p ≤ 0.010), with no other pairwise difference. Peak GH separated GH-deficient children from normal responders (5.10 ± 1.86 vs 12.05 ± 2.65 ng/mL, p < 0.001); IGF-1 SDS did not (−2.29 ± 0.54 vs −2.13 ± 0.57, p = 0.452).
Conclusion: Severity of height deficit did not identify the underlying cause; height velocity did, and was selectively reduced in endocrine disease. A single IGF-1 measurement did not distinguish GH-deficient children from normal responders. Height velocity should drive the decision to investigate, and GH stimulation testing remains necessary for diagnosis.