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So far, what really triggers GO – and indeed Graves’ hyperthyroidism (GH) itself – is unknown.

Minimal symptoms/signs of GO are very common in GH as suggested by the presence of mild symptoms upon meticulous clinical examination and orbit imaging as well as the exaggerated increase in intraocular pressure in the upper gaze. However, full-blown GO is present in only 25–50% of the patients with GH.

Therefore, there are two questions:

1.What triggers GO?

2.Why is GO more prominent or severe in some patients than in others?

GO onset is not related to hyperthyroidism per se as it can precede, follow or coincide with the development of GH. GO can also occur in conjunction with autoimmune thyroiditis, whatever the thyroid status. It is a common observation, however, that there is a gross correlation between the risk of GO and the duration of active GH.

Three situations/factors appear to precipitate the occurrence of GO:

1.Treatment of GH with ¹³¹I. Treatment of hyperthyroid Graves’ disease (GD) with ¹³¹I can potentially worsen GO (in the case of active GO), especially in smokers and in the presence of markedly elevated T₃ levels [15] and in patients with shorter disease duration [16]. It is likely that GO deterioration results from the well-known exacerbation of thyroid inflammation/autoimmunity which occurs 3–5 months after ¹³¹I irradiation, as evidenced by a rise in blood levels of antithyroid antibodies, including antibodies (TRAbs) against thyroid-stimulating hormone receptor (TSH-R) [17]. Interestingly, glucocorticoid treatment which is able to prevent GO worsening is less efficient in preventing the rise in circulating antibody levels.

2.Occurrence of iatrogenic hypothyroidism. Whatever the treatment modality, but especially after ¹³¹I therapy, iatrogenic hypothyroidism has been recognized as a risk factor for GO [18].

3.Smoking. See “How Do Environmental Factors such as Smoking Increase the Risk and Severity of Graves’ Orbitopathy?” below.

No condition that would protect against or prevent GO has been identified. However, it is noticeable that in children and adolescents both the prevalence and the severity of GO are low. In a series of 83 patients (≤16 years old), lower lid retraction was present in 38.6%, upper lid retraction in 4.8%, and mild proptosis in 12%; overall, GO was scored as class 2 or less in 64% of the cases. In this series, the largest reported so far, no factor that could create a predisposition to GO was identified [19].