No abstract

Individualized GH doses during catch-up growth significantly reduce the proportion of unexpectedly good and poor responders around a predefined individual growth target and result in equal growth responses in children with GHD and ISS.

GH replacement therapy has proved its efficacy and safety in short-term trials and in a few long-term trials with limited number of subjects. In this 1-center study, including 118 consecutive adults (70 men and 48 women; mean age, 49.3 yr; range, 22-74 yr) with adult-onset GH deficiency, the effects of 5 yr of GH replacement on body composition, bone mass, and metabolic indices were determined.The mean initial GH dose was 0.98 mg/d. The dose was gradually lowered, and after 5 yr the mean dose was 0.48 mg/d. The mean IGF-I SD score increased from ؊1.73 at baseline to 1.66 at study end. A sustained increase in lean body mass and a decrease in body fat were observed. The GH treatment increased total body bone mineral content as well as lumbar (L2-L4) and femur neck bone mineral contents. BMD in lumbar spine (L2-L4) and femur neck were increased and normalized at study end. Total cholesterol and low density lipoprotein cholesterol decreased, and high density lipoprotein cholesterol increased. At 5 yr, serum concentrations of triglycerides and hemoglobin A 1c were reduced compared with baseline values. The treatment responses in IGF-I SD score, body fat as estimated by four-and five-compartment body composition models, total body protein and nitrogen, and lumbar bone mineral content and BMD were more marked in men than in women.One patient died during the period, four patients discontinued the study due to adverse events, and one dropped out due to lack of compliance. Four patients were lost to follow-up. However, all patients were retained in the statistical analysis according to the intention to treat approach used.In conclusion, 5 yr of GH substitution in GH-deficient adults is safe and well tolerated. The effects on body composition, bone mass, and metabolic indices were sustained. The effects on body composition and low density lipoprotein cholesterol were seen after 1 yr, whereas the effects on bone mass, triglycerides, and hemoglobin A 1c were first observed after years of treatment. (J Clin Endocrinol Metab 86: 4657-4665, 2001)

Context:The use of levothyroxine to reduce thyroid size in pediatric patients with goiter due to chronic autoimmune thyroiditis (AIT) remains controversial. In overtly hypothyroid patients, reductions in thyroid volume have been reported, whereas the effect in subclinically hypothyroid and euthyroid patients is less clear. Objective:The objective of the study was to evaluate the effect of levothyroxine treatment on thyroid size (determined with thyroid ultrasonography) in children and adolescents with AIT. Design and Setting: This study included patients with AIT treated at a university hospital outpatient clinic between 1987 and 2004.Patients: Ninety children with AIT (73 girls and 17 boys, aged 6.1-17.7 yr) were included in the study.Intervention: Intervention was treatment with levothyroxine for a median 2.8 yr (range 0.5-10.2).Main Outcome Measure: Change in thyroid volume SD score (SDS) during the study period was measured.Results: Median thyroid volume SDS was reduced in patients euthyroid (Ϫ0.4 SDS, P Ͻ 0.001), subclinically hypothyroid (Ϫ1.4 SDS, P Ͻ 0.001), and overtly hypothyroid (Ϫ1.8 SDS, P Ͻ 0.002) at diagnosis of AIT. Both hypothyroid and euthyroid patients with goiter (thyroid volume Ͼ 2.0 SDS) at baseline reduced their median thyroid volume SDS (Ϫ1.6 and Ϫ0.9, respectively, P Ͻ 0.001). Hypothyroid patients without goiter also reduced median thyroid volume SDS (Ϫ1.2, P Ͻ 0.004), whereas no change was noticed in euthyroid children without goiter. Conclusions:Levothyroxine treatment is effective in reducing thyroid volume in pediatric patients and is suggested in treatment of goiter caused by AIT, especially in cases of hypothyroid, but also in euthyroid children.

These findings support the hypothesis that the severe psychomotor retardation and elevated serum T(3) levels in these patients are caused by inactivation of the MCT8 transporter, preventing action and metabolism of T(3) in central neurons.