Sunitinib 투여 환자에서 발생하는 갑상선기능저하증
Sunitinib-induced hypothyroidism
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초록
Sunitinib malate is a multi-targeted tyrosine kinase inhibitor used for gastrointestinal stromal tumor and renal cell carcinoma. It is also under phase II trial for use in advanced colon cancer, non-small cell lung cancer and breast cancer. Sunitinib-induced thyroid dysfunction, mainly hypothyroidism is very common and is reported around 50～85% of sunitinib treated patients. The proposed mechanisms of sunitinib-induced hypothyroidism are 1) inhibition of thyroid peroxidase, 2) inhibition of sodium iodide symporter, and 3) destructive thyroiditis due to reduced vasculature through inhibition of VEGFR by sunitinib. Although nearly one third of patients with sunitinib-induced hypothyroidism would benefit from thyroid hormone replacement therapy, one should be cautious about use of thyroxine replacement therapy because hypothyroidism itself is associated with good prognosis in patients with various kinds of advanced cancer. Because of high prevalence of thyroid dysfunction observed with sunitinib, it is recommended to evaluate thyroid function before starting and during the use of sunitinib and thyroid hormone replacement should be considered both on the basis of patient’s symptom and laboratory value. Future prospective studies to address the issue of prevalence, mechanism and treatment of sunitinib-induced hypothyroidism and its association with prognosis of advanced cancer is expected.
Abstract
Sunitinib malate is a multi-targeted tyrosine kinase inhibitor used for gastrointestinal stromal tumor and renal cell carcinoma. It is also under phase II trial for use in advanced colon cancer, non-small cell lung cancer and breast cancer. Sunitinib-induced thyroid dysfunction, mainly hypothyroidism is very common and is reported around 50～85% of sunitinib treated patients. The proposed mechanisms of sunitinib-induced hypothyroidism are 1) inhibition of thyroid peroxidase, 2) inhibition of sodium iodide symporter, and 3) destructive thyroiditis due to reduced vasculature through inhibition of VEGFR by sunitinib. Although nearly one third of patients with sunitinib-induced hypothyroidism would benefit from thyroid hormone replacement therapy, one should be cautious about use of thyroxine replacement therapy because hypothyroidism itself is associated with good prognosis in patients with various kinds of advanced cancer. Because of high prevalence of thyroid dysfunction observed with sunitinib, it is recommended to evaluate thyroid function before starting and during the use of sunitinib and thyroid hormone replacement should be considered both on the basis of patient’s symptom and laboratory value. Future prospective studies to address the issue of prevalence, mechanism and treatment of sunitinib-induced hypothyroidism and its association with prognosis of advanced cancer is expected.
참고문헌 (15)
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