LAUSR

Graves’ orbitopathy (GO) is believed to reflect an autoimmune aggression against antigens expressed by thyroid epithelial cells and orbital fibroblasts [1]. We report a case of de novo appearance of Graves’ hyperthyroidism (GH) and GO following fine-needle aspiration biopsy (FNAB) of thyroid nodules, possibly reflecting spreading of autoantigens and activation of the immune system against autoantigens expressed by thyroid and orbital tissues. A 48-year-old woman with a normal thyroid function and undetectable anti-thyroid autoantibodies, including anti-TSH receptor autoantibodies (TRAb), underwent FNAB for a thyroid cold nodule, which was cytologically benign. Approximately 6 weeks later she was diagnosed with hyperthyroidism with detectable serum TRAb (20 U/L; n.v. ≤ 1.5). The ophthalmological evaluation suggested the presence of a moderately severe, active GO. Thus, exophthalmometry measurements were 23 mm in the right eye and 22 mm in the left eye and she had inconstant diplopia, conjunctival redness, lagophthalmos, eyelid swelling and erythema, and chemosis. The clinical activity score [1] was 4/7 points. The patient was treated with methimazole and then with total thyroidectomy and high-dose intravenous glucocorticoids. After 6 months, she was euthyroid on replacement therapy with levothyroxine and she had a clear improvement of GO activity in both eyes, with a CAS of 1/3 points. The common pathogenesis of GH and GO is suggested by a number of findings, among which a close temporal relationship between hyperthyroidism and GO and the influence of the underlying thyroid disease and its treatment on GO are included [1]. To our knowledge, there were no previous reports on GH and GO de novo appearance after thyroid FNAB. The case we report suggests a possible cause–effect relationship between FNAB and the occurrence of GH and GO. The tissue damage may provide a possible explanation for this observation, because of the spreading of autoantigens due to the FNAB which, in a predisposed individual, may trigger autoimmunity against these antigens, thereby leading to GH and GO. Obviously, a direct cause–effect relationship between FNAB, GH and GD in our patient is not proved, but it is supported by some similar findings, including the reported relationship between radioiodine treatment and the onset or worsening of GO [1], as the consequence of the massive release of thyroid antigens, which presumably causes the activation or re-activation of the immune system against the same (or similar) antigens expressed by orbital tissues [2]. Thus, although we cannot demonstrate a direct link between FNAB, GH and GO, we believe that this possibility is rather likely, which offers a further little piece of knowledge of the pathogenesis of GH and GO. It is interesting to note that the spread of autoantigen may occur also at the eye level. In this regard, we recently reported the case of a patient with a de novo appearance of GO and then of GH after an eye trauma [3].