Growth hormone (GH) treatment reduces peripheral thyroid hormone action in girls with Turner syndrome.
OBJECTIVE
Turner syndrome (TS) is an indication for 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 the 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 in TS girls on peripheral TH action.


METHODS
We set up a reverse transcription-polymerase chain reaction (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).


METHODS
After RNA extraction from PBMC, TR and beta-actin mRNAs were coamplified by RT-PCR. In addition serum biochemical markers of TH action were measured: thyrotropin (TSH), sex hormone binding globulin (SHBG), osteocalcin (OC), beta-crosslaps (beta-CL), iodothyronines by electrochemiluminescency and IGF-I by immunoradiometric assay (IRMA) with extraction.


RESULTS
TR mRNAs from PBMC were reduced in TS patients under GH treatment. In turn, serum TSH, OC, beta-CL and IGF-I were increased while SHBG was reduced by GH treatment in TS patients.


CONCLUSIONS
GH treatment reduced TR expression in PBMC and biochemical serum markers of TH action. These results suggest that GH treatment in TS patients impair peripheral TH action at tissue level and prompt a role in the reduced growth response to the therapy.
Centro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI-CONICET), Departamento de Bioquímica Clínica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Argentina.
S
S
Susperreguy
M B
MB
Miras
M M
MM
Montesinos
I D
ID
Mascanfroni
L
L
Muñoz
G
G
Sobrero
L
L
Silvano
A M
AM
Masini-Repiso
A H
AH
Coleoni
H M
HM
Targovnik
C G
CG
Pellizas
D000199:Actins / Q000235:genetics; D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D002648:Child; D003094:Collagen / Q000097:blood; D003864:Depression, Chemical; D005260:Female; D005500:Follow-Up Studies; D013006:Growth Hormone / Q000627:therapeutic use*; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D015675:Osteocalcin / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012738:Sex Hormone-Binding Globulin / Q000032:analysis; D037021:Thyroid Hormone Receptors alpha / Q000235:genetics; D037042:Thyroid Hormone Receptors beta / Q000235:genetics; D013963:Thyroid Hormones / Q000097:blood*; D013972:Thyrotropin / Q000097:blood; D014284:Triiodothyronine / Q000097:blood; D014424:Turner Syndrome / Q000097:blood / Q000188:drug therapy*
D000199:Actins; D015415:Biomarkers; D010446:Peptide Fragments; D012333:RNA, Messenger; D012738:Sex Hormone-Binding Globulin; D037021:Thyroid Hormone Receptors alpha; D037042:Thyroid Hormone Receptors beta; D013963:Thyroid Hormones; C110762:glutamyl-lysyl-alanyl-histidyl-aspartyl-glycyl-glycyl-arginine; D014284:Triiodothyronine; D015675:Osteocalcin; D007334:Insulin-Like Growth Factor I; D013972:Thyrotropin; D013006:Growth Hormone; D003094:Collagen