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Riedel’s thyroiditis, also termed “invasive fibrous thyroiditis,” is the rarest form of autoimmune thyroiditis and can be associated with systemic fibrotic processes, Hashimoto thyroiditis (1, 2), and Graves’ disease (3). A case of hyperthyroidism followed by spontaneous hypothyroidism and Riedel’s thyroiditis has been reported (4). Two previously reported patients from our institution had invasive fibrous thyroiditis that evolved from antecedent Graves’ disease, as indicated by thyroid dysfunction, bilateral ophthalmopathy, and positive TSH receptor-stimulating autoantibodies (5). We present a new case. In 2004, a 26-yr-old woman presented with a mass in the left thyroid lobe, pain, and respiratory distress. Thyroid function was normal. A tracheostomy and biopsy showed Riedel’s thyroiditis. Therapy with corticosteroids and tamoxifen stabilized the disease. After 1 yr, the tracheostomy was closed. In 2008, her TSH level was less than 0.01 mIU/liter, her free T4 was 4.5 ng/dl (58 pmol/liter; normal, 0.8–1.8 ng/dl or 10–23 pmol/liter), and her serum was strongly positive for TSH receptor antibodies (52%; normal, <16%). The diagnosis of Graves’ hyperthyroidism was made. Her 24-h iodine-131 uptake was 33% (upper limit of normal, 29%). She was treated with 19.7 mCi iodine-131. Computed tomography of the neck, performed in 2004 and 2008, showed left lobe thyroid enlargement and compression of the trachea (Fig. 1). Ultrasonography of the thyroid in 2008 (Fig. 2) showed hypervascularity in the areas not affected by Riedel’s thyroiditis; the absence of vascularity in the hypoechoic areas of the left lobe corresponded to Riedel’s involvement, as shown by computed tomography.
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McIver et al. (2010) studied this question.
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