Endocrine Abstracts

Background: Insulin-resistance phenomenon is a key factor in the pathogenesis of Metabolic Syndrome (MS). Several reports focus on the identification of a role of Insulin to trigger thyrocytes proliferation in vitro. Thyroid IRS-1 mRNA expression increased progressively during goitrogenesis in vivo. In order to individuate the impact of clinical and biochemical markers of MS on the growth-score of non toxic multinodular goiter (MNG) we evaluated a population of 60 subjects with MNG at onset.

Methods: Of 60 patients (mean age: 50±12 years; F/M: 38/22) with MNG at onset were divided into two groups: Group A affected by MS and MNG; Group B affected by endocrine disease alone. To be included subjects had to have: normal thyroid function, negative titers of antithyroid antibodies and no past history of having received any thyroid medications. All procedures were applied in agreement with the ethical guidelines of our institution. In both groups were evaluated BMI, waist circumference (WC), lipids, fasting insulin and glycemia to assess HOMA-ir and by thyroid ultrasound to measure thyroid volume, number and size of nodules.

Results: HOMA-ir in group A vs B was significantly different (4±2.5 vs 1.32±0.5; P=0.007). Only in group A the Spearman correlation test demonstrates a positive relationship between: WC and the diameter of the biggest nodule (Rho: 0.45; P=0.05); HOMA-ir Index and number of nodules (Rho: 0.48; P=0.01) and with thyroid volume (Rho: 0.473; P=0.01); BMI and thyroid volume (Rho: 0.388, P=0.048).

Conclusion: These data support the role of insulin-resistance in the pathogenesis/progression of MNG. In this light elevated circulating levels of Insulin cause increased thyroid proliferation. Thus established farmacological approaches in metabolic syndrome, such as insulin-sensitizer, may be useful to prevent the progression of goitrogenesis and to control thyroid nodular growth.