Department of General Medical Oncology, University Hospitals Leuven, Leuven Cancer Institute, Leuven, Belgium.
Thyroid. 2010 Mar;20(3):317-22. doi: 10.1089/thy.2009.0125.
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.
多靶点酪氨酸激酶抑制剂舒尼替尼在治疗晚期肾细胞癌或胃肠道间质瘤的患者中，已知会导致相当一部分患者发生甲状腺功能障碍。尽管舒尼替尼诱导的甲状腺功能减退症在大多数患者中似乎是可逆的，但一些患者会发生不可逆转的甲状腺损伤，导致长期的甲状腺激素替代治疗。
我们报告了两名患有结节性甲状腺的癌症患者，他们在接受酪氨酸激酶抑制剂治疗期间出现了甲状腺功能障碍，并表现出甲状腺明显缩小，即使在停止抗癌药物治疗后，仍需要进行永久性甲状腺激素替代治疗。舒尼替尼治疗结节性甲状腺可导致内分泌腺肿大显著减少，同时伴有甲状腺功能试验异常，导致临床甲状腺功能减退。确切的病理生理学尚不清楚，但我们讨论了舒尼替尼诱导甲状腺缩小的几种可能机制。
甲状腺形态学的变化可能与舒尼替尼治疗的不良生化效应有关，并且可能是不可逆器官损伤的潜在标志物。
