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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.