Sunitinib Induces Hypothyroidism with a Markedly Reduced Vascularity

被引:62
作者
Makita, Noriko [1 ]
Miyakawa, Megumi [2 ]
Fujita, Toshiro [1 ]
Iiri, Taroh [1 ]
机构
[1] Univ Tokyo, Sch Med, Dept Endocrinol & Nephrol, Bunkyo Ku, Tokyo 1138655, Japan
[2] Toranomon Endocrine Ctr, Tokyo, Japan
关键词
RENAL-CELL CARCINOMA; ENDOTHELIAL GROWTH-FACTOR; THYROID-GLAND; THYROTOXICOSIS; ANGIOGENESIS; VEGF;
D O I
10.1089/thy.2009.0414
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: 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. Summary: 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. Conclusion: Our case study provides compelling evidence that sunitinib induces hypothyroidism by reducing blood flow via capillary regression and constriction.
引用
收藏
页码:323 / 326
页数:4
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