Abstract
The multitargeted tyrosine kinase inhibitor sunitinib is known to induce thyroid dysfunction in a substantial proportion of patients treated for advanced renal-cell carcinoma or gastrointestinal stromal tumors. Although sunitinib-induced hypothyroidism seems to be reversible in the majority of patients, some patients develop irreversible thyroid damage resulting in long-lasting thyroid hormone replacement therapy. We report on two cancer patients with a preexisting nodular thyroid gland, who developed thyroid dysfunction and showed marked shrinkage of the thyroid during treatment with the tyrosine kinase inhibitor, necessitating permanent thyroid hormone replacement therapy even after discontinuation of the anticancer agent. Sunitinib treatment in patients with a nodular thyroid can induce a significant decrease in the volume of the enlarged endocrine gland, associated with abnormal thyroid function tests leading to clinical hypothyroidism. The exact pathophysiology remains unknown but we discuss several possible mechanisms of sunitinib-induced thyroid shrinkage. Morphological changes of the thyroid gland can be associated with the well-described adverse biochemical effects of treatment with sunitinib and can be a potential marker of the irreversible organ damage.
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