Graves' Orbitopathy. Группа авторов

and selenium are micronutrients essential to thyroid hormone production and action. Chronic high iodine intake has been associated with an increased frequency of chronic autoimmune thyroiditis, thyroperoxidase antibodies, and autoimmune hypothyroidism. The incidence of moderate-to-severe GO was not changed after iodine fortification of salt in Denmark [3].

Recent epidemiological studies from China provide strong circumstantial evidence that low selenium intake is associated with Hashimoto’s thyroiditis and hypothyroidism, but not with Graves’ disease and hyperthyroidism [35].

      As both deficiency and excess intake of iodine and selenium can be deleterious for thyroid function, dietary advice should aim at maintenance of normal intake.

Does Total Thyroidectomy for Other Diseases than Graves’ Disease Preclude the Development of Graves’ Orbitopathy?

One Korean series and isolated case reports describe mild to moderate-to-severe GO in patients without a history of Graves’ disease, occurring after thyroidectomy or ¹³¹I therapy for nodular goitre or thyroid cancer [36]. Some of these patients had total thyroid ablation with no detectable thyroid tissue and no evidence of prior TSH-R autoantibodies [37].

      The authors hypothesized that radioiodine treatment or thyroid damage during surgery induced thyroid autoimmunity. This pathogenic explanation is less evident in GO cases diagnosed up to 9 years after thyroid intervention in whom the role of other triggers acting on orbital fibroblasts may prevail.

      All but 1 of the above cases were overtreated by thyroid hormones at GO diagnosis, and it is well recognized that euthyroidism is required for GO prevention/improvement. Whether prolonged exogenous hyperthyroidism could promote orbital inflammation by altering local thyroid hormone metabolism needs to be investigated. No case of GO has been described in congenitally athyreotic patients.

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