Sunitinib (SUO11248; Sutent®, Pfizer, New York, NY), a multiple tyrosine kinase inhibitor, was approved in January 2006 by the FDA as monotherapy for the treatment of advanced renal cell carcinoma and imatinib-resistant gastrointestinal stromal tumors, and is currently in wide clinical use for these indications. Sunitinib has also demonstrated clinical activity in phase II clinical trials for neuroendocrine tumors, breast cancer, and colon cancer (1). Sunitinib has antitumor and antiangiogenesis activity through inhibition of multiple receptor tyrosine kinases (2, 3). Angiogenesis inhibition is mediated through modulation of vascular endothelial growth factor (VEGFR 1–3) and platelet-derived growth factor receptors (PDGFRa and PDGFRb). Other important targets of the drug belonging to the tyrosine kinase family include stem cell growth factor (c-KIT), fetal liver tyrosine kinase receptor FLT3, colony-stimulating factor 1 (CSF-1), and ret proto-oncogene (RET). Recent studies have reported sunitinib-induced hypothyroidism (4–9), but associated pathologic changes have not been previously described. We present here a patient treated with sunitinib for metastatic renal cell carcinoma who developed lymphocytic thyroiditis accompanied by a brief episode of increased, rather than decreased, thyroid hormone release.

A 48-year-old Asian male was diagnosed in September 2006 with renal cell carcinoma of the right kidney metastatic to the lungs, spine, and brain. He underwent right nephrectomy. Sorafenib therapy was initiated, but was discontinued after 1 week because of severe anasarca and a hand–foot syndrome. After developing right arm weakness, the patient was diagnosed with a brain lesion, which was managed with high-dose dexamethasone and gamma-knife radiation.