Endocrine Abstracts

Introduction: Numerous thyroid function disturbances have been linked to the administration of growth hormone (GH) to GH-deficient patients. There have been reports of anything from increased energy expenditure and improved peripheral thyroxine (T4) to triiodothyronine (T3) conversion to decreased thyrotropin (TSH) sensitivity to thyrotropin-releasing hormone (TRH) stimulation and induction of hypothyroidism.

Objective: GH has an impact on thyroid structure and function. Although goitre is common in acromegalic patients, it can be challenging to evaluate the consequences of GH deficiency (GHD) because hypopituitarism persons with GH deficiency frequently simultaneously have a partial or total deficit of TSH.

Method: Comparing subjects heterozygous for the same mutation (10 men and 9 women; HET group) and subjects homozygous for the wild-type allele [6 men and 10 women; control (CO) group] to subjects with the homozygous mutation in the GHRH receptor gene (GHRHR), the thyroid morphology and serum levels of thyroid hormones in adult members of a large kindred with untreated isolated GHD was compared. The statistical program SPSS/PC 8.0 was used to conduct the statistical analysis. For qualitative variables, values for continuous variables are given as the mean+sd. For the purpose of comparing the three groups, ANOVA was used. The correlation between TV and its determinants was calculated using the Spearman correlation. Statistics were judged significant at P<0.04.

Result: Thyroid volume (TV) in GHD participants was lower than in HET and CO subjects. Between the GHD and CO groups’ TVs and those of the HET group, it was in the middle. When TV was adjusted for body surface area, the difference between the GHD and HET groups vanished but TV remained less in the GHD and HET groups than in the CO group. When compared to the CO group and HET and CO groups, the GHD group’s serum T3 levels were lower and its free T4 levels were greater.

Conclusions: It is possible that GH plays a permissive role in the growth of the thyroid gland because people with severe untreated GHD caused by a homozygous GHRHR mutation and heterozygous carriers of the same mutation have smaller TV than healthy individuals. Additionally, blood total T3 and free T4 levels in GHD participants were lower, suggesting that the deiodinase system may not be functioning as well.