RESUMEN
Introduction: We present the evolution of GHD in adolescent males with persistent growth failure, in whom the diagnosis was established after a second GH stimulation test (GST). Methods: We performed a retrospective chart review of children who presented for short stature (height less < 2SD for mean/mid-parental height) and/or growth failure (sustained growth velocity < 0 SD) to pediatric endocrinology at Mount Sinai Kravis Children's Hospital, New York and who had 2 GSTs. Data collected from electronic medical records were analyzed using SPSS v28.0. Results: Of 53 patients included, 42 were males. Average GH peak on initial GST was 15.48 ± 4.92 ng/ml, at 10.07 ± 2.65 years, mean height -1.68 ± 0.56SD(28% had <2SD), IGF-1 -1.00 ± 0.88SD. After 2.23 ± 1.22 years, at 12.04 ± 2.41years, height SDs decreased to -1.82 ± 0.63SD and IGF-1 was -1.08 ± 0.84SD. At repeat GST, average GH peak was 7.59 ± 2.12 ng/dL, with 36% ≤7 ng/dl and 32% in puberty. 12 males reached adult height of 0.08 ± 0.69 SD with a mean height gain of 1.83 ± 0.56SD(p<0.005), IGF-1 of -1.15 ± 0.81SD after 4.64 ± 1.4 years of GH. Conclusion: We offer evidence for Evolving Growth Hormone Deficiency (EGHD) through repeat GST in children with persistent growth slowdown, even with pubertal progression; emphasizing the need for careful longitudinal follow-up to make accurate diagnosis.
Asunto(s)
Trastornos del Crecimiento , Hormona de Crecimiento Humana , Humanos , Masculino , Hormona de Crecimiento Humana/deficiencia , Adolescente , Estudios Retrospectivos , Niño , Femenino , Estatura , Factor I del Crecimiento Similar a la Insulina/metabolismo , Factor I del Crecimiento Similar a la Insulina/deficiencia , Prueba de Estudio Conceptual , Enanismo Hipofisario/sangreRESUMEN
Two male patients, who presented at 13.5 and 13.9 years of age with growth failure and short stature, were ultimately diagnosed with isolated growth hormone deficiency (GHD). Patient 1 was first evaluated when his height declined from -0.67 SD to -1.3 SD. He had a peak growth hormone (GH) concentration to GH stimulation test (GHST) of 16.9â ng/mL (16.9â µg/L) and remained untreated. As puberty advanced, his height decreased further to -1.65 SD. A second GHST while his serum testosterone was 79â ng/dL (2.74â nmol/L) had a peak GH of 5.4â ng/mL (5.4â µg/L), consistent with GHD. He was treated with GH for 4.8 years and reached adult height of 180.5â cm (0.57 SD), gaining 2.22 SDS. Patient 2, height -2.63 SD, had an unstimulated peak GH concentration of 19â ng/mL (19â µg/L). As puberty advanced, his height decreased further to -2.96 SD. Repeat peak GH concentration was 9.2â ng/mL (9.2â µg/L) when serum testosterone was 83.9â ng/dL (2.91â nmol/L). GH treatment resulted in rapid increase of height velocity from 1.8â cm/year to 11.3â cm/year in 6 months, consistent with GHD. Both patients demonstrate that GHD may develop over time and cannot be excluded by a single GHST. Longitudinal monitoring of children with poor growth as puberty progresses is essential to uncover GHD.