Department of Endocrinology and Nephrology, The University of Tokyo School of Medicine, Tokyo, Japan.
Thyroid. 2010 Mar;20(3):323-6. doi: 10.1089/thy.2009.0414.
Sunitinib is a small molecule that inhibits receptor tyrosine kinases, including the vascular endothelial growth factor receptors, and exhibits antiangiogenic and antitumor activity. This molecule has also been reported to cause hypothyroidism at a high frequency, but the mechanism of this is unknown.
A 60-year-old woman was administered sunitinib for the treatment of metastatic renal cell carcinoma. One week later, she displayed overt hypothyroidism with an atrophic thyroid and a marked reduction in vascularity as determined by ultrasonography, despite high levels of thyrotropin. In contrast, during the off-periods in the sunitinib treatment cycles, the volume of her thyroid recovered with an increase in vascularity despite a low level of thyrotropin. These results suggest that thyroid function and volume may depend on the vascularity, which is negatively regulated by sunitinib.
Our case study provides compelling evidence that sunitinib induces hypothyroidism by reducing blood flow via capillary regression and constriction.
舒尼替尼是一种小分子，可抑制受体酪氨酸激酶，包括血管内皮生长因子受体，并具有抗血管生成和抗肿瘤活性。该分子还被报道以高频率引起甲状腺功能减退症，但机制尚不清楚。
一名 60 岁女性因转移性肾细胞癌接受舒尼替尼治疗。一周后，尽管促甲状腺激素水平很高，但她表现出明显的甲状腺功能减退症，甲状腺萎缩，超声检查显示血管明显减少。相比之下，在舒尼替尼治疗周期的停药期间，尽管促甲状腺激素水平较低，她的甲状腺体积仍随着血管增多而恢复。这些结果表明，甲状腺功能和体积可能取决于血管，而血管受到舒尼替尼的负调控。
我们的病例研究提供了有力的证据，表明舒尼替尼通过毛细血管退化和收缩减少血流来诱导甲状腺功能减退症。
