Growth hormone treatment reduces peripheral thyroid hormone action in girls with Turner syndrome

SUSPERREGUY S, MIRAS MB, MONTESINOS MM, MASCANFRONI ID, MUÑOZ L, SOBRERO G, SILVANO L, MASINI-REPISO AM, COLEONI AH, TARGOVNIK HM, PELLIZAS CG

CLINICAL ENDOCRINOLOGY

Blackwell Publishing

Lugar: Oxford, United Kingdom; Año: 2007

0300-0664

Objective: Turner Syndrome (TS) is an indication for growth hormone (GH) therapy in spite of the modest growth response. Somatic growth depends not only on GH-insulin like growth factor I (IGF-I) axis but also on thyroid hormone (TH) status. We have previously reported that supraphysiological IGF-I levels diminished TH actions in rat tissues by reducing nuclear TH receptor (TR). GH treatment to TS patients induces high IGF-I levels and therefore a reduction of TH action in tissues may be expected. We aimed at evaluating the effect of GH therapy to TS girls on peripheral TH action. Design and patients: We set up a RT-PCR for TR mRNA estimation in peripheral blood mononuclear cells (PBMC) and compared TR mRNA levels from 10 normal, 10 TS and 10 TS girls under GH therapy (0.33 mg/kg/week for 0.5-2 years). Measurements: After RNA extraction from PBMC, TR and ß-actin mRNAs were co-amplified by RT-PCR. Besides, serum biochemical markers of TH action were measured: thyrotropin (TSH), sex hormone binding globulin (SHBG), osteocalcin (OC), ß-crosslaps (ß-CL), iodothyronines (electrochemiluminescency) and IGF-I (IRMA with extraction). Results: TR mRNAs from PBMC were reduced in TS under GH treatment. In turn, serum TSH, OC, ß-CL and IGF-I were increased while SHBG reduced by GH treatment in TS. Conclusions: GH treatment reduced TR expression in PBMC and biochemical serum markers of TH action. These results suggest that GH treatment in TS impaired peripheral TH action at tissue level and prompt a role in the reduced growth response to the therapy.