OBJECTIVE: Although recombinant human growth hormone (rhGH) can unmask central hypothyroidism, few studies have investigated prevalence, predictors and growth consequences of evolving hypothyroidism in children receiving rhGH based on therapeutic indication. We hypothesized that children with GH deficiency (GHD) and greatest severity of GHD would be most likely to develop central hypothyroidism and decreased growth velocity (GV). DESIGN: Retrospective chart review. PATIENTS: Children currently receiving rhGH with data available for at least 24 months after rhGH initiation (n=119). Indications included GHD, Prader-Willi syndrome, Turner syndrome, and idiopathic short stature (ISS) and SGA (n=60, 20, 19 and 20 respectively). METHODS: We categorized patients as those hypothyroid at baseline (HYPO-B; n=13), those who developed hypothyroidism over 24-months of rhGH (HYPO-24; n=16), and those never hypothyroid (NO-HYPO; n=90). Groups did not differ for age or gender. RESULTS: Central hypothyroidism developed in 25% of GHD patients. For all patients on rhGH, baseline IGF-1 (p=0.007), IGFBP-3 (p=0.006) and peak GH (p=0.02) differed between groups. HYPO-24 had lower baseline IGF-1, IGFBP-3 and peak GH than NO-HYPO, but did not differ from HYPO-B. Peak GH was <7 ng/ml in 100% of HYPO-24, 77% HYPO-B, and 71% NO-HYPO (p=0.01). GV SDS decreased between the first and second years in HYPO-24 in HYPO-24 compared with NO-HYPO. CONCLUSION: Evolution of central hypothyroidism is more likely in patients receiving rhGH for GHD than other indications, becomes more likely with greater severity of GHD and is associated with a reduction in GV SDS.
OBJECTIVE: Although recombinant humangrowth hormone (rhGH) can unmask central hypothyroidism, few studies have investigated prevalence, predictors and growth consequences of evolving hypothyroidism in children receiving rhGH based on therapeutic indication. We hypothesized that children with GH deficiency (GHD) and greatest severity of GHD would be most likely to develop central hypothyroidism and decreased growth velocity (GV). DESIGN: Retrospective chart review. PATIENTS: Children currently receiving rhGH with data available for at least 24 months after rhGH initiation (n=119). Indications included GHD, Prader-Willi syndrome, Turner syndrome, and idiopathic short stature (ISS) and SGA (n=60, 20, 19 and 20 respectively). METHODS: We categorized patients as those hypothyroid at baseline (HYPO-B; n=13), those who developed hypothyroidism over 24-months of rhGH (HYPO-24; n=16), and those never hypothyroid (NO-HYPO; n=90). Groups did not differ for age or gender. RESULTS:Central hypothyroidism developed in 25% of GHD patients. For all patients on rhGH, baseline IGF-1 (p=0.007), IGFBP-3 (p=0.006) and peak GH (p=0.02) differed between groups. HYPO-24 had lower baseline IGF-1, IGFBP-3 and peak GH than NO-HYPO, but did not differ from HYPO-B. Peak GH was <7 ng/ml in 100% of HYPO-24, 77% HYPO-B, and 71% NO-HYPO (p=0.01). GV SDS decreased between the first and second years in HYPO-24 in HYPO-24 compared with NO-HYPO. CONCLUSION: Evolution of central hypothyroidism is more likely in patients receiving rhGH for GHD than other indications, becomes more likely with greater severity of GHD and is associated with a reduction in GV SDS.