Turner Syndrome (TS) is a clinical indication for growth hormone (GH) therapy. Nevertheless, height gain in GH-treated TS girls is reduced compared to patients under GH treatment for GH deficiency and for other non-GH deficient syndromes. However, somatic growth depends not only on GH-insulin-like growth factor-I (IGF-I) axis but also on thyroid hormone (TH) status. In TS, serum levels of relevant growth factors are normal and GH treatment induces high IGF-I levels. We previously reported that in the rat supraphysiological IGF-I levels diminished TH action at tissue level by reducing nuclear TH receptor (TR) expression. In this study we aimed at assessing the effect of GH therapy to TS girls on peripheral TH action in order to provide a general estimation of the thyroid status at tissue level. Prepuberal, 10 normal girls (control group), 10 TS girls (TS) and 10 TS girls under GH therapy (TS-GH, 0.33 mg/kg/week for 0.5-2 years) were joint for this study. All groups were age-matched, all girls were clinically and biochemically euthyroid and neither had thyroid antibodies. Blood was collected and after RNA extraction from peripheral blood mononuclear cells (PBMC: tissue accessible for human studies), TR (a1 and b1) mRNAs were co-amplified with ß-actin by RT-PCR. Besides, serum biochemical markers of TH action at tissue level were measured (electrochemiluminescency): thyrotropin (TSH), sex hormone binding globulin (SHBG), osteocalcin (OC) and ß-crosslaps (ß-CL). In addition, iodothyronines (electrochemiluminescency) and IGF-I (IRMA with extraction) were evaluated. Results: No-significant differences were registered in TR mRNAs from PBMC between control and TS. However, a1 and b1 TR mRNAs were significantly reduced in TS-GH vs. control and vs. TS. In turn, serum TSH, OC, ß-CL and IGF-I were increased while SHBG reduced by GH treatment to TS. Conclusions: GH treatment to TS reduced TR expression in PBMC and biochemical serum markers of TH action. These results suggest that GH treatment to TS impaired peripheral TH action at tissue level and prompt a role in the modest growth response to the therapy.
