Abstract:In the New England Journal of Medicine last year, Ross provided an excellent summary of current evidence on use of radioactive iodine (RAI) in the treatment of hyperthyroidism 1 . However, clinical practice with regard to RAI treatment varies widely, with some key differences existing between the North American perspective provided by Ross and what is more widely practiced in Europe. Treatment of hyperthyroidism first requires an accurate diagnosis of the underlying aetiology. Hyperthyroidism refers to any condition in which there is an excessive production of thyroid hormone, which may arise from diffuse autoimmune stimulation in the case of Graves disease (GD) or autonomously functioning nodules including toxic multinodular goitre (TMNG) and solitary toxic adenoma (TA). GD is the commonest cause of hyperthyroidism, but in areas of iodine deficiency the prevalence of TMNG and TA increase with age and therefore are more common than GD in older persons. Spontaneous remission occurs in approximately 30% of patients with GD, but is unlikely to occur in toxic nodules.The rationale for RAI treatment is that iodine is a substrate for thyroid hormone synthesis and is actively transported into thyroid follicular cells, where thyroxine (T4) and triiodothyronine (T3) are formed and then stored within the colloid space. Radioiodine (131I) is similarly processed, and destruction of follicular cells is the result of ?-particle radiation, effectively ablating functional thyroid tissue within a 1-2mm radius 1 . A number of studies have provided reassurance with regard to the safety of RAI. The largest study included over 35,000 patients, followed for a mean of 21 years, and found that radioiodine was not linked to cancer mortality or any specific cancer 2 .The main aim of RAI therapy is to eliminate the hyperthyroid state. However, for patients with GD there are philosophical differences in the approach used to achieve this goal. In the US the goal of RAI in GD is to render the patient hypothyroid. In contrast, the local practice in many Irish centres is to administer a dose of RAI calculated on the basis of an uptake scan with the intent of inducing a euthyroid state. The downside of this approach is that the incidence of persistent hyperthyroidism is higher and some patients may need a second treatment 6 months later.Most hyperthyroid patients will develop normal thyroid function within 4-8 weeks of treatment. Hypothyroidism can occur from 4 weeks, but more commonly arises between 2 and 6 months. For this reason, thyroid function is usually checked at 2, 4, and 6 months post-treatment, and less frequently thereafter. Thyroid stimulating hormone (TSH) levels may remain suppressed for several months following resolution of hyperthyroidism and should therefore be interpreted cautiously and only in association with free T4 and T3 levels. If thyroxine replacement is initiated, the dose should initially be guided by the free T4 level. In contrast to GD, the approach to patients with TMNG or TA is generally the same world ...