ESPE Abstracts

Background: The relation between thyroid function and treatment with recombinant human GH (rhGH) has been the subject of many studies which indicate a decrease of fT₄ levels and a compensatory TSH increase at rhGH therapy onset. On the other hand, we have identified a number of patients with documented primary hypothyroidism (either on treatment with L-thyroxine or not) before the onset of rhGH treatment.

Objective and hypotheses: To assess thyroid function in all children treated with rhGH for GH deficiency and detect the percentage of children with primary hypothyroidism before the onset of rhGH.

Method: We retrospectively analyzed thyroid function in all patients receiving rhGH for GH deficiency in our department. Other indications for rhGH treatment (e.g. chronic kidney disease, Turner syndrome, Prader-Willi syndrome) were excluded.

Results: 129 children (77 boys and 52 girls) with GH deficiency on rhGH were identified. 29 (22.5%) were detected to have thyroid dysfunction. Of those, ten patients had central hypothyroidism (in two patients it was secondary due to brain tumor, whereas in the rest eight patients, four had also ACTH deficiency). Patients with additional ACTH deficiency were diagnosed at neonatal age whereas patients with TSH and GH deficiency were diagnosed later in life. 19 children were found to have primary hypothyroidism (TSH values >5 μU/l). Only four (all pubertal boys) out of the 19 patients developed compensated primary hypothyroidism after the onset of rhGH treatment (mean time since rhGH treatment: 28.5 months). Fifteen patients were identified to have primary hypothyroidism before the onset of rhGH treatment. Four patients (three girls and one boy had a confirmed genetic defect) and one girl had clinical and biochemical manifestations of pseudohypoparathyroidism. In one girl, thyroid dysfunction was attributed to treatment with valproic acid. In nine patients, no cause for thyroid dysfunction was identified.

Conclusion: A significant number of patients with GHD (7%) were identified to manifested primary subclinical hypothyroidism of unknown cause before the onset of rhGH.