Appearance of Graves’ disease after percutaneous ethanol injection for the treatment of hyperfunctioning thyroid adenoma

Abstract

In this report we describe an unusual patient with hyperfunctioning thyroid adenoma in whom percutaneous ethanol injection (p.e.i.) therapy was followed by typical Graves' disease. His history revealed the presence of a sister with Hashimoto's thyroiditis. 99-mTc thyroid scintiscan showed focal uptake in the nodule, with suppression of extranodular parenchyma. P.e.i. therapy was followed by the development of severe hyperthyroidism. One month after a second p.e.i. cycle, recurrence of hyperthyroidism associated with diffuse 99-mTc uptake by the gland was observed. TSH-receptor and thyroglobulin autoantibodies were undetectable before p.e.i. therapy, appeared during the first cycle, and showed a further increase after the second p.e.i. therapy cycle. Though spontaneous switch to Graves' disease cannot be excluded in patients with toxic nodules, the massive release of thyroid materials from follicular cells, among these TSH-receptor antigenic components partially denatured by ethanol, may indeed trigger an autoimmune response to the TSH-receptor, thus accounting for this observation. Patients with possible autoimmune disposition, as selected by familiar history and/or laboratory markers should be carefully monitored during p.e.i. treatment.

(131)I and thyroid-associated ophthalmopathy

“…In these patients an induction of a Graves'-like disease, including development of TRAb was seen 3±6 months after 131 I therapy (24±26). A similar induction of GD has been described related to subacute thyroiditis (27,28) and ethanol injection of hyperfunctioning autonomous thyroid adenoma (29,30), representing other treatments causing destruction of the thyroid cells and release of thyroid antigen. Accordingly, release of thyroid antigen has been demonstrated in relation to subacute thyroiditis (31) and in relation to thyroid resection for thyrotoxicosis or non-toxic goiter, a drastic increase in circulating levels of thyroglobulin was seen (32,33).…”

Serum Levels of the Cytokines IL-1β, IL-6 and ICAM-1 After131I-Treatment of Graves' Disease and Nodular Goiter

“…A similar immunological response including a de novo Graves' like disease has recently been demonstrated during events causing destruction of thyroid cells potentially leading to release of thyroid auto-antigens. This is 1311-treatment of nodular goiter [2,3,12] subacute thyroiditis [13,14] and alcohol injection into a thyroid nodule [15,16]. Further, it has been debated whether 1311-treatment by releasing thyroid auto-antigen, could induce ophthalmopathy in patients with Graves' disease.…”

Two Cases-Report of Mild Graves?Disease Following Subacute Thyroiditis: More Evidence of the Role of Thyroglobulin in The Pathogenesis of Autoimmune Thyroid Disease?

“…Iodinated peptides in Tg as well as iodine-induced apoptosis/necrosis of thyrocytes trigger autoimmune thyroid disease [25]. Increased release of Tg temporarily increases anti-Tg level, and has been reported after thyroid surgery [26], RAI administration [27], and ethanol administration in toxic adenomas [28,29]. In our cases, during the acute phase of SAT, serum Tg levels were increased, whereas anti-Tg was normal, which was followed by development of increased anti-Tg levels 3 months later, with the appearance of GD.…”