RESUMO
BACKGROUND: Conflicting data exist on the effects of GH replacement therapy (GHRT) on thyroid function and thyroid volume (TV) in GH-deficient (GHD) patients. AIM: The aim of this study was to assess the effects of GHRT on thyroid function and TV in adults with congenital lifetime isolated GHD (IGHD). SUBJECTS AND METHODS: We studied 20 GH-naïve adults with IGHD due to a homozygous mutation of the GHRH-receptor gene at baseline, after 6-month depot- GH replacement therapy (pGH), and 6-month washout (6mo). Total T(3), free T(4) (FT(4)), reverse T(3) (rT(3)), TSH, IGF-I, SHBG, and TV were measured; body surface area-corrected TV (CTV) was calculated. RESULTS: IGF-I and T(3) increased pGH. T(3) levels remained elevated at 6mo. GHRT did not significantly change FT(4), rT(3), TSH, and SHBG. TV and CTV increased pGH and remained elevated at 6mo. CONCLUSIONS: GHRT in IGHD adults caused an increase in serum T(3) levels and TV, suggesting an important role of the GH-IGF-I axis in thyroid function.
Assuntos
Terapia de Reposição Hormonal/métodos , Hormônio do Crescimento Humano/deficiência , Hormônio do Crescimento Humano/uso terapêutico , Glândula Tireoide/efeitos dos fármacos , Glândula Tireoide/fisiologia , Adulto , Feminino , Homozigoto , Humanos , Fator de Crescimento Insulin-Like I/metabolismo , Masculino , Pessoa de Meia-Idade , Receptores de Neuropeptídeos/genética , Receptores de Hormônios Reguladores de Hormônio Hipofisário/genética , Globulina de Ligação a Hormônio Sexual/metabolismo , Glândula Tireoide/anatomia & histologia , Tireotropina/sangue , Tiroxina/sangue , Resultado do Tratamento , Tri-Iodotironina/sangueRESUMO
GH secretion by the pituitary is the result of the balance between the stimulatory effect of GHRH and the inhibitory effect of SS. Patients with mutations in GHRH receptor (GHRH-R) gene (GHRH-R) offer a unique model to study the mechanism of action of different GH secretion stimuli. In the past, we have demonstrated a small but significant GH response to a GH secretagogue (GHRP-2) in a homogenous cohort of patients with severe GH deficiency (GHD) due to a homozygous null mutation in GHRH-R (IVS1+1G-->A). Now, we sought to determine if we could detect a GH response to hypoglycemia (ITT: insulin tolerance test) or clonidine (CL) in these patients. Nine young GHD subjects underwent both ITT and CL tests, and 2 additional subjects underwent only CL test. There was a small but significant GH increase during ITT, but not during CL test. These results indicate that a minimal albeit significant GH response to ITT can occur despite complete lack of GHRH-R function.
