The incidence and mechanism of sunitinib-induced thyroid atrophy in patients with metastatic renal cell carcinoma

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Background: In order to elucidate the incidence and the mechanisms of sunitinib-induced thyroid atrophy, we investigated the serial volumetric and functional changes, and evaluated histological changes of the thyroid gland in metastatic renal cell carcinoma patients who received sunitinib. Methods: Thyroid volume measured by CT volumetry and thyroid function were measured at baseline, during the treatment, and at post-treatment periods. Histological evaluation of thyroid gland was performed in 4 autopsied patients. Results: The median reduction rate in thyroid volume at last evaluation during sunitinib treatment was 30% in all 17 patients. The incidence of hypothyroidism during sunitinib treatment was significantly higher in the high reduction rate group (n=8; more than 50% reduction in volume) than in the low reduction rate group (n=9; less than 50% reduction in volume). Half of patients in the high reduction rate group exhibited a transient TSH suppression suggesting thyrotoxicosis during sunitinib treatment. Histological evaluation demonstrated atrophy of thyroid follicles and degeneration of follicular epithelial cells without critical diminution of vascular volume in the thyroid gland. Conclusion: Thyroid atrophy is frequently observed following sunitinib treatment and may be brought about by sunitinib-inuced thyrotoxicosis or the direct effects of sunitinib that leads to degeneration of thyroid follicular cells.
2011-01-18