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A 63-yr-old woman was admitted for a painful goiter. She had no medical history, except a renal carcinoma. She developed pulmonary metastases 2 yr after diagnosis. Administration of sunitinib (50 mg/d) included six repeated cycles with 4 wk of treatment followed by 2 wk without treatment. A swelled and painful neck appeared 5 months after treatment with sunitinib. The patient had no signs of thyrotoxicosis but had an irregular goiter. TSH was suppressed (0.06 mU/liter; normal, 0.27–4.20), with elevated free T4 (131 pmol/liter; normal, 12.0–22.0) and free T3 (9.2 pmol/liter; normal, 3.5–6.5). Antithyroid antibodies were absent. C-reactive protein level was 3.27 mg/ml (normal, <5), sedimentation rate was 35 mm/h (normal, 0–20), and thyroglobulin level was 42.3 ng/ml (normal, 2.5–30). Contrast computed tomography (CT) revealed an unusual aspect of the thyroid [36 Hounsfield unit (HU) density] (Fig. 1, A–C). Ultrasonography confirmed goiter (65 cm3) (Fig. 1D). Beta-blockers were started. After 10 d, free T4 and free T3 decreased (7.91 and 1.78 pmol/liter, respectively), TSH increased (17.31 mU/liter), thyroid peroxidase antibody emerged (81 U/ml; normal, <60), sedimentation rate was 24 mm/h, and thyroglobulin was 27.9 ng/ml. Ultrasonography didn't change. l-Thyroxine was required (75 μg/d) and normalized thyroid function. Sunitinib is a tyrosine kinase inhibitor with antiangiogenic and antiproliferative effects (1). Sunitinib is one of the first-line treatments of advanced renal carcinoma (2). Thyroid dysfunction due to sunitinib is usual, but mechanisms remain unclear. Hyperthyroidism was reported in 25% of patients preceding hypothyroidism. Increased thyroglobulin level, decreased iodine uptake, and cytological data suggested destructive thyroiditis (3–5). In this observation, a thyroid cytotoxic or ischemic effect of sunitinib could explain the transient thyrotoxicosis and CT scan picture.

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Special features > Special Features - Image in Endocrinology
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