Endocrine Abstracts

Introduction: Thyroid hormones influence GH/IGF1 axis, but previous studies reported discrepant results regarding serum IGF1 levels in hyperthyroidism. We have therefore investigated, at diagnosis, the relationship between serum IGF1 levels/IGF1 z scores and clinical and biological characteristics of Graves’ disease (GD) patients. We also compared IGF1 levels/IGF1 z scores, at diagnosis, between GD and autonomous hyperthyroidism patients.

Methods: This cross-sectional study included 119 newly diagnosed hyperthyroid patients (98 with GD and 21 with toxic multinodular goitre) that presented consecutively to our clinic. The main measured parameters: TSH, FT₄, FT₃, TT₃, thyroglobulin, TPOAb, ATA, TRAb, and IGF1. Patients were considered IGF-deficient if IGF1 z score was ≤−2 S.D. from mean for age.

Results: In GD patients men had higher IGF1 levels (P=0.023) and IGF1 z scores (P=0.013) than women. 18.4% of GD patients were, at diagnosis, IGF1 deficient. Compared with patients without IGF1 deficiency, these patients presented, at diagnosis, higher thyroglobulin (median=72.55, IQR=116.02 vs median=11.40, IQR=80.74 ng/ml, P=0.002), FT₃ (median=11.30, IQR=7.64 vs median=7.33, IQR=5.72 pg/ml, P=0.027), and lower ATA (median=20, IQR=0 vs median=34.05, IQR=161 UI/ml, P=0.001) levels. Thyroglobulin was identified as strong predictor for IGF1 deficiency (AUROC=0.732, 95% CI: 0.620–0.844, P=0.002; cut-off for thyroglobulin=50.40 ng/ml, Se=77.8%, Sp=70%). IGF1 status was not influenced by gender (P=0.08), current smoking (P=0.55), goitre size (P=0.53), opthalmopathy (P=0.33), TRAb (P=0.23), and TPOAb status (P=0.36). The prevalence of IGF1 deficiency was higher in GD patients compared to patients with toxic goitre (18% vs 0%, χ²=4.54, P=0.033).

Conclusions: Our study shows, for the first time, the presence of IGF1 deficiency in nearly one-fifth of newly diagnosed GD patients. IGF1 deficiency was associated with lower ATA titres, higher thyroglobulin levels and more severe FT₃ hyperthyroidism. The presence of active GO did not influence IGF1 status. GD patients had higher prevalence of IGF1 deficiency than patients with toxic multinodular goitre.