ESPE Abstracts

Subclinical hypothyroidism (SH) is a biochemical condition defined by increased TSH serum concentration above the upper limit of the reference range associated with normal concentrations of T4 and Free T4. Depending on the degree of TSH elevation SH can be defined mild for TSH values between 4.5-10 mIU/l and severe for TSH levels >10 mIU/l.

The major cause of SH is chronic autoimmune thyroiditis, other causes are persistent neonatal hyperthyrotropinemia, TSH receptor gene mutations, genetic syndromes (Down, Turner, Williams, PHP), Iodine deficiency and excess, drugs (antiepileptic drugs, IFN-a), exposure to ionizing radiation (therapeutic/environmental), obesity and finally SH can be defined as idiopathic when no clear causes can be identified.

SH in children is often a benign and remitting condition. The risk of progression to overt hypothyroidism depends on the underlying cause being autoimmune SH associated with an increased risk of progression to overt hypothyroidism as compared to non–autoimmune SH.

The major concern regarding SH is to establish whether this condition should always be considered an expression of mild thyroid dysfunction. Growth and neurocognitive outcome in children do not appear to be affected by SH, however recent data suggest that mild SH may be associated with subtle pro-atherogenic abnormalities.

The benefits of levothyroxine therapy are far from clear, therefore the optimum management of children with SH remains a matter of debate and depends on the etiology and degree of TSH elevation and should be individually tailored.

Aim of this talk is to give an overview of current evidences on diagnosis and outcomes of mild SH in children and adolescents and to discuss the therapeutic options.