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In the majority of cases GO is observed in patients with Graves’ hyperthyroidism and, as shown in Figure 1, there is a close temporal relationship between the onset of hyperthyroidism and the onset of GO [2]. In support of a relationship between GO and hyperthyroidism, GO seems to be more severe in patients with untreated hyperthyroidism [7, 8], to worsen more often in Graves’ disease patients undergoing radioiodine treatment more than once [7], and to deteriorate more frequently in patients who undergo relapse of hyperthyroidism after a course of antithyroid drugs [7]. An explanation of how hyperthyroidism may influence GO is related to tissue oxidative stress induced by the excess of thyroid hormones, oxidative stress being one of the factors contributing to the inflammatory changes of the orbit [9]. However, it is also possible that, at least to some extent, the relationship between hyperthyroidism and GO reflects the fact that GO and hyperthyroidism are due to the same alteration of the immune system against thyroid and orbital antigens [7]. In this regard, each autoimmune activation or reactivation against these antigens may correspond to a temporal association between activation or reactivation of both hyperthyroidism and GO. In line with this interpretation, GO can appear in patients who are euthyroid on antithyroid drugs [2], and, as mentioned above, although rarely, GO can occur in the absence of hyperthyroidism, indicating that the latter condition is not necessary for GO to develop [4].

In addition to hyperthyroidism, also hypothyroidism is believed to affect the course of GO. Thus, progression of GO following radioiodine therapy can be to some extent prevented or at least reduced in frequency, if L-thyroxine replacement for hypothyroidism is initiated early [10, 11]. Hypothyroidism may affect GO because it may worsen orbital deposition of glycosaminoglycans, or because of the action of TSH on its receptor in orbital fibroblasts [9, 12].