Functioning thyroid metastases are a rare cause of hyperthyroidism. Most are follicular carcinoma. Here, we report a case in which a 62-y-old man with a history of right subtotal thyroidectomy for a benign adenoma complained of symptoms of hyperthyroidism associated with left arm pain. Biopsy of a humeral lesion was consistent with papillary carcinoma metastatic from the thyroid. Postoperatively, the patient received a cumulative dose of 14.8 GBq of 131 I with good control of the hyperthyroidism but without eradication of the bone metastasis. Funct ioning thyroid metastases are a rare cause of hyperthyroidism. Fewer than 100 cases can be found in the worldwide literature. Most of them were follicular carcinoma with lung or bone involvement. Only 20 cases of functioning metastases from papillary carcinoma have been reported (1,2).
CASE REPORTA 62-y-old man who had undergone right subtotal thyroidectomy 11 y previously for a benign adenoma had recently presented with symptoms of hyperthyroidism associated with left arm pain. His level of free thyroxine was elevated (68 pmol/L; reference level, 11-25 pmol/L), his level of thyroid-stimulating hormone (TSH) was suppressed (,0.01 mIU/mL; reference level, 0.2-3.2 mIU/mL), and he was negative for TSH-receptor antibody. 99m Tc-sodium pertechnetate planar scintigraphy of the neck and upper chest showed mild uptake in the left thyroid lobe, in contrast to heightened uptake in the left arm (Fig. 1). The planar posterior view and SPECT/CT fusion images showed focal, intense uptake in the fifth thoracic vertebra (Fig. 2), an area of involvement that had been asymptomatic at the first presentation but had become symptomatic within about 50 d. 99m Tc-methylendiphosphonate bone scanning showed a focus of increased uptake in the left humerus and a photopenic area in the right pelvic bone (Fig. 3). No other sites of bone involvement were detected. Biopsy of the left humeral lesion was consistent with papillary carcinoma metastatic from the thyroid. Left subtotal thyroidectomy was therefore performed, but no malignancy was found in the remaining lobe. The clinical course was marked by a rapid onset of medullar compression symptoms. Decompressive laminectomy was recommended, but the patient refused to undergo more surgery. Despite a persistently low TSH level, postablation 131 I whole-body scans showed bone metastases (Fig. 4). Six months after the patient had completed radioiodine therapy (3.7 GBq), the myelopathic symptoms improved but free thyroxine and triiodothyronine remained elevated. In the 48th mo after the diagnosis, he finally received a cumulative dose of 14.8 GBq of 131 I, which controlled the hyperthyroidism well but did not eradicate the bone metastases. Antithyroid drugs were replaced with lifelong TSH suppression.
DISCUSSIONThree criteria on which to base the diagnosis of functioning metastases were present in our patient: failure of thyrotoxicosis to resolve after thyroidectomy, mild iodine uptake in the remnant thyroid lobe, and iodine uptake in metastases (2). Fu...
Antitumor necrosis factor therapies have revolutionized the treatment of some inflammatory diseases. However, the use of these agents is associated with the development of many paradoxical autoimmune diseases. Less well-recognized is the association with sarcoidosis. We report a 55-year-old female with long-standing ankylosing spondylitis who developed persistent dry cough and dyspnea while receiving etanercept therapy. High-resolution computed tomography scanning showed mediastinal lymphadenopathy and multiple nodules in both lung fields developed two months after the administration of etanercept. Lymph node biopsy was not practicable. Histopathological examination of minor salivary gland biopsy revealed noncaseating granulomata, and the serum angiotensin-converting enzyme was very elevated. All infectious studies were negative. Etanercept was discontinued plus a course of corticosteroids with a clinical improvement, and a follow-up high-resolution computed tomography scanning 4 months later showed evident regression of mediastinal lymph nodes and pulmonary nodules. Potential pathogenic mechanisms of this paradoxical effect of tumor necrosis factor-alpha blocking agents are discussed.
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